Luglio 2020 - Odontoiatria neuromiofasciale

Management of OSAS: The ELIBA® Device Can Help the Patient?

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2020 Mar 4

Eleonora Ortu, Davide Pietropaoli, Alessandra Mummolo, IAPNOR, Mario Giannoni, and Annalisa Monaco

Abstract

Obstructive sleep apnea syndrome (OSAS) is one of the most challenging diseases to treat in medicine. Here, the authors describe a case of OSAS treated with a lingual elevator of Balercia (ELIBA®). The patient, a forty-five-year-old Caucasian male, had a chief complaint of numerous episodes of nocturnal apnea. After several visits with specialists, a polysomnographic examination was performed, in which the patient’s apnea hypopnea index (AHI) was 30.4, and a lingual elevator was prescribed. The lingual elevator helped to keep the patient’s tongue in the correct position and prevented the tongue from reverting back to the soft tissue spaces in the mouth. After six months of treatment with the lingual elevator and dietary adjustments, the patient’s AHI decreased to 11.6. This simple yet customizable approach is a comfortable and easy option for patients to reduce night apnea episodes.

1. Introduction

OSAS is characterized by repeated episodes of complete, partial, and/or prolonged obstruction of the upper airway during sleep, normally associated with a reduction in blood oxygen saturation. It occurs in all ages and it is certainly more common in males [1]. Patients present a high number of apneas during the night and complain of excessive sleepiness during the day. Other common symptoms are headache upon waking up, snoring reported by the partner as intermittent (because interrupted by apnea), reduced memory capacity, reduced ability to concentrate, hypertension, and dry mouth upon waking up [2, 3]. The airways can be blocked in several ways. For example, a large tongue, associated with normal muscle relaxation and consequent soft tissue collapse that occurs during sleep, may be one of the causes of apnea [3–5]. Further, overweight or obese people have a predisposition for apnea; symptom severity often increases with increased body weight. Another major risk factor for apnea is nasopharyngeal abnormalities that reduce the upper airway diameter. Though generalized narrowing is common in adults and in children, anatomopathological anomalies such as adenotonsillar hypertrophy can increase the risk of apnea, and deviations of the nasal septum are often observed [6]. A fundamental premise for the treatment of OSAS is an accurate and multidisciplinary diagnosis: the reference centers for sleep medicine usually have a team that includes, in addition to the sleep doctor (specialist in pneumology or neurology) who coordinates activities, other specialists (maxillofacial specialist, orthodontist, otolaryngologist, and nutritionist) who each deal with their own skills to best treat this disease [3, 7]. To reach a correct diagnosis, the clinical work-up requires the association of comprehensive clinical evaluation (anamnesis, physical examination) and nocturnal polysomnography [8]. The last one uses a simultaneous recording of several physiological parameters during the night, using a polysomnograph. Normally, during the test, two or more electroencephalography channels, various electromyographic channels, chest and abdomen movements, oronasal flow, and oxygen saturation in the blood are recorded [9]. There is a variety of treatments for obstructive sleep apnea syndrome, which depends on the medical history of the individual, the severity of the disorder and, mainly, the specific cause of the obstruction. Although there are various oral devices to treat OSAS, many of these devices are cumbersome for patients to use at night because they act to advance the position of the jaw [10–12].

2. Case Report

A forty-five-year-old male Caucasian patient had a chief complaint of numerous episodes of nocturnal apnea and daytime sleepiness. The patient had no history of diabetes and asthma. The dental history was insignificant. The patient’s body mass index was 29 (overweight), and he was being treated by a nutritionist to improve alimentation and lose weight [13]. The patient’s arterial blood pressure was 120/80 mmHg, his pulse was 95 beats/min, and his respiratory rate was 20 breaths/min. The results of the laboratory (i.e., complete blood count, hematocrit, mean corpuscular value, erythrocyte sedimentation rate, and lipid panel) examinations were normal. Chest X-ray, respiratory function tests, and bronchoscopic test results were also normal. The upper airway appeared normal in ear-nose-throat and laryngoscopy examinations. The patient’s neck and tongue muscles were enlarged. Written consent was obtained from the patient.

Upon polysomnographic examination, the subject was diagnosed with positional preference obstructive sleep apnea syndrome (OSAS), with 70% of episodes occurring while the patient was in the supine position (Figure 1). During the test, he had 96 apneas, 3 of which were central. The patient’s apnea hypopnea index (AHI) was 30.4, a value that meets the criterion for severe sleep apnea [14, 15]. Treatment options for reduction of the OSAS, including a lingual elevator by Balercia (ELIBA® device that properly spaces the orolingual space for better breathing) and continuous positive airway pressure (CPAP) therapy, were discussed with the patient. Because the patient refused CPAP therapy due to discomfort, the patient was prescribed an ELIBA®, which is a small, comfortable to wear device that does not change the position of the jaw.

Figure 1

Polysomnographic report before treatment with the ELIBA® device. The apnea hypopnea index (AHI) was 30.4.

Briefly, dental stone models of the dental arches and Myoprint impressions of the physiological free orolingual space were made using Bosworth Sapphire acrylic resin (custom acrylic material; Bosworth Company) under ultra-low-frequency-transcutaneous nervous stimulation (ULF-TENS) [16–20]. The low-frequency neurostimulator (J5 Myomonitor® TENS Unit, Myotronics-Noromed Inc., Tukwila, WA) generated a repetitive, synchronous, and bilateral stimulus through pulsed currents delivered at 1.5 s intervals and a frequency of 0.66 Hz. The two TENS electrodes (Myotrode SG Electrodes®, Myotronics-Noromed Inc., Tukwila, WA) were then placed bilaterally over the cutaneous projection of the fifth pair of cranial nerves notch, which was located between the coronoid and condylar processes. This location was determined by manual palpation of the zone anterior to the tragus (Figures 2(a) and 2(b)). A third grounding electrode was placed in the center of the back of the neck [21, 22] (Figure 2(c)). Central nervous system stimulation was produced by sensory stimulation of cranial nerves V and VII with low-frequency TENS [18]. Typically, low-frequency ULF-TENS is applied to bring the mandible in a neutral position that can obviate the need for occlusal adjustments [19]. Once the threshold of sensory stimulus is identified, identified by the sensation of tingling at the level of the electrodes, the stimulus is administered with the ULF-TENS. The patient is asked to rest the apex of the tongue against the back incisive papilla and keep it relaxed in this position for the duration of the procedure. When the resin reached a solid but elastic consistency, before complete hardening, it was extracted from the oral cavity and inserted into the master model to complete its hardening. The clinician indicated to the dental laboratory (enabled to manufacture) the distal lateral limits for the construction of the artifact and the most suitable retentive devices for the stabilization of ELIBA®. ELIBA® must be totally passive and must not touch the oral mucosa [4–9, 19, 23–27] (Figures 3(a)–3(d)).

Figure 2

Application of TENS electrodes. (a, b) The two TENS electrodes are placed bilaterally over the cutaneous projection of the fifth pair of cranial nerves notch, which is located between the coronoid and condylar processes. (c) A third grounding electrode is placed in the center of the back of the neck.

Figure 3

ELIBA® construction phases and oral aspect of the device. (a) Marking of the lateral/distal borders of the ELIBA® device, as specified by the clinician. (b) The ELIBA® appliance on the plastic cast and impression of the ELIBA® device. (c) Enlargement of the device ELIBA® applied on the plastic cast with hooks in front area in cobalt chrome. (d) Intraoral views of the ELIBA® appliance fitted to the oral cavity of the patient.

After six months of using the ELIBA® device, the patient’s apnea improved, and the second polysomnographic examination revealed only six apnea episodes, two of which were central. The patient’s AHI decreased to 11.6 after implementation of the ELIBA® device (Figure 4). Moreover, the patient’s overall health improved owing to dietary adjustments. He lost ten kilograms, and his body mass index decreased to 25. The patient appeared satisfied with the results of the ELIBA® and dietary adjustments.

Figure 4

Polysomnographic report after treatment with the ELIBA® device. The apnea hypopnea index (AHI) decreased to 11.6.

3. Discussion

The patient described in this case was treated with an ELIBA® device, in strict accordance with the principles of neuromyofascial occlusal dynamics. The ELIBA®, which was designed to treat atypical swallowing and yields better patient compliance than those prescribed CPAP, modifies the position of the tongue by acting on the inner component of the trigeminal system and partly on the autonomic nervous system. ELIBA® seizes the patient’s physiological free orolingual space, defined anteriorly and laterally by the lower jaw, inferiorly by the tongue floor, and superiorly by the ventral surface of the tongue. The Medium Longitudinal File, which allows a direct connection between the various cranial nerves, can provide a way to link the upper spinal cord to the mesencephalus. The ELIBA® works by way of proprioception and interception, in which it stimulates the trigeminal system and, consequently, activates the oculomotor system to help maintain appropriate tongue position and movement [28]. Contact of the tongue apex with its designated spot during the night together with perioral muscle-generated centripetal force is indicative of functional improvement. The tongue and neck muscles are related by way of proprioception via a common trunk from the ansa cervicalis through the hypoglossal nerve [29]. Currently, tongue position studies have suggested that it may not be possible to improve OSAS, at least not without difficult-to-use devices, because it is related to a subcortical abnormality, specifically in the ventral part of the rostral brainstem [30, 31].

The ELIBA® is a simple, customizable device that is comfortable for patients to wear and does not have any contraindications in children or adults. In the current case study, ELIBA® implementation combined with dietary changes improved the patient’s sleep quality while maintaining patient comfort [32]. The patient was satisfied with the outcome of the ELIBA®. The authors hope to treat further patients with this approach to understand more about its advantages and possible limitations.

Disclosure

This article was written in agreement and courtesy of the IAPNOR association, as the ELIBA® device is a registered patent c/o the Italian Ministry of Economic Development, patent office.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

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Standard Correction of Vision Worsens EMG Activity of Pericranial Muscles in Chronic TMD Subjects

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2020 Apr 13

Annalisa Monaco, Eleonora Ortu, Mario Giannoni, Pierdomenico D’Andrea, Ruggero Cattaneo, Alessandra Mummolo, and Davide Pietropaoli

Abstract

Recent studies showed an evident correlation between the stomatognathic system and the visual system. These results suggest that subjects who are affected by both temporomandibular (TMD) disorders and refractive disorders present with altered control of pericranial musculature tone and higher open-eye electromyographic (EMG) values. The objective of this work was to evaluate the effects of standard vision correction on EMG in subjects suffering from TMD compared with application of the same vision treatments to non-TMD subjects. 40 subjects were enrolled in this study. The test group included 20 myopic subjects and also included patients with TMD. The control group included 20 healthy myopic subjects. All of the participants underwent a complete ocular examination and a sEMG analysis. The results showed that TMD subjects with vision disorders that are corrected with standard glasses present EMG values that are significantly higher than those presented by non-TMD subjects with vision disorders and standard glasses. Infact, in TMD subjects, eye correction did not have a positive effect on the stomatognathic or pericranial musculature.

1. Introduction

A correlation between the stomatognathic system and the visual system has been suggested on the basis of clinical and instrumental observations. For example, it has been observed that myopia occurs more frequently in subjects with second class 1^st division, while astigmatism is more characteristic in subjects with a crossbite [1]. However, from an electromyographic (EMG) point of view, opening of the eyes frequently determines alterations in signals that occur at the level of the stomatognathic musculature [2]. It is also interesting to note that for children with functional lateral deviation, there are data that indicate that the correction of vision defects with standard eye techniques can lead to an increase in EMG values of the stomatognathic musculature [3]. In healthy adults that are not affected by temporomandibular disorders (TMD) and sight defects, EMG values of their stomatognathic system and neck muscles do not show significant variations if taken when the individuals have their eyes closed versus open [4]. These observations indicate that visual input, per se, does not induce an increase or a significant change in the electric activity of the muscles correlated to the stomatognathic system in healthy individuals. In contrast, under rest conditions and with their eyes closed, adult individuals suffering from masticatory muscle pain show an increase in their EMG activity [5]. While such feedback appears to be of greater statistical importance than clinical importance, there are data that suggest that these values are higher when eyes are open [6]. Therefore, the characteristic of individuals with myogenic pain appear to be related to difficulties in adapting to variations in their visual input rather than absolute values of a single test or condition (e.g., eyes closed or open). In general, we propose that a relationship exists between refractive disorders, vision disorders, the stomatognathic system, and EMG hyperactivity, as described in a recent literature review [7]. It has been reported that the prevalence of vision disorders in the general population is high, and it is increasing in Europe and elsewhere worldwide [8, 9]. There is also a high prevalence of TMD in the general population (affecting approximately 5–20% annually) [10]. Moreover, for those in the general population who suffer from headaches, these individuals have up to a 15-fold higher probability of developing TMD compared with the general population [11].

Refractive disorders are often associated with muscular disorders involving eye movement. Correspondingly, individuals suffering from refractive and oculomotor dysfunctions tend to be more affected by headaches than individuals who are not affected by such disorders [12–14]. Furthermore, individuals with tension headaches present with higher EMG pericranial muscular activity than individuals who do not suffer from tension headaches, similar to individuals who suffer from TMD and exhibit a high incidence of tension headaches [15–18]. The above considerations suggest that subjects who are affected by both TMD and refractive disorders present with altered control of pericranial musculature tone and higher open-eye EMG values. To the best of our knowledge, the influence of standard vision correction on the activity of pericranial and stomatognathic muscles in TMD subjects has not been investigated. Thus, we hypothesize that the state of muscular activation induced by opening of the eyes, especially in TMD subjects, is clinically relevant to investigations of the effects of standard vision correction on EMG. Therefore, the aim of this work was to evaluate the effects of standard vision correction on EMG in subjects suffering from TMD compared with application of the same vision treatments to non-TMD subjects.

2. Materials and Methods

2.1. Selection of Subjects

This study was carried out in accordance with the fundamental principles of the Declaration of Helsinki and was approved by the Internal Review Board (IRB) of the University of L’Aquila (Number 16137/2016). Written informed consent was obtained from all the participants. A total of 75 myopic patients and patients with corrective glasses for myopia (40 females and 35 males) with a mean age of 27 ± 1.5 years were examined by the same dentist. Next, all of the subjects underwent an eye examination that was conducted by an expert ophthalmologist who was blinded to the TMD subjects and control subjects, as well as the purpose of the visits. In order to reduce operators bias, the same calibrated dentist performed TMD diagnosis (RC) according to DCTMD. According to DC/TMD, the enrolled patients had myofascial pain and TMD pain [19]. Subjects who had a discrepancy between eye standards and the glasses they were wearing, subjects with systemic diseases, as well as epileptic subjects, were excluded from this study. Consequently, a total of 40 subjects were enrolled in this study, and the test group included 20 myopic subjects. The glasses worn by the latter subjects were verified by an ophthalmologist to be correct. The test group also included patients with TMD, based on diagnostic criteria (DC) [19]. The control group included 20 healthy myopic subjects (10 males and 10 females) with a mean age of 25 ± 2 years.

All of the participants in this study underwent a complete ocular examination that consisted of a slit-lamp bio-microscopy, a fundus examination, and an evaluation of intraocular pressure. The best-corrected visual acuity (BCVA) for all of the participants was 10/10. In addition, Snellen and ophthalmologic examinations were normal for all of the participants. All of the subjects completed a central sensitization inventory (CSI) questionnaire and subsequently underwent an EMG examination and a sEMG analysis. SCAN 9 with muscle tone was evaluated with the subjects’ eyes closed with and without glasses and with the subjects’ eyes open with and without glasses in order to identify specific muscle activity (e.g., masseters, anterior digastrics, sternocleidomastoid, and anterior temporalis) in a resting position.

2.2. Eye Standard

Eye standard corresponds to the ability of the eye to see distinctly within a field of vision a figure placed at a given distance. Visual acuity is evaluated by recognizing signs or symbols called Snellen’s optotypes or tables. A subject must recognize a set of letters and the subject’s vision is determined based on the ratio of the size of the letters correctly read to the size of reference letters (in the European system, the size of the symbols in the 10^th row is used as reference letters). Visual acuity is inversely proportional to the height of the alphabetical letters read. For example, 1/10 visual acuity is conventionally considered to correspond to the ability to read a letter size of 75 mm at a distance of 5 m. For 10/10 visual acuity, the size of the letters is 7.5 mm. In general, a young subject can see 5 mm letters at a distance of 5 m [20, 21].

2.3. Electromyography Instrumentation

EMG activity was recorded with an eight-channel Myotronics K7 Evaluation System (Seattle, WA, USA) equipped with bipolar electrodes with an interelectrode distance of 20 mm. Before positioning the electrodes, each patient’s skin was thoroughly cleaned with alcohol. Electrodes were positioned on the left and right masseter muscles (LMM and RMM, respectively) and on the left and right anterior temporal muscles (LTA and RTA, respectively), as described by Castroflorio et al. [22, 23]. Electrodes were also placed on the left and right anterior digastric muscles (RDA and LDA, respectively) [24] and on the left and right sternocleidomastoid muscles (LSC and RSC, respectively) bilaterally parallel to the muscular fibers and over the lower portion of the muscle to avoid the innervation point, as described by Falla et al. [25].

Electrical signals were amplified, recorded, and digitized with the K7 clinical software package (Myotronics Inc., http://www.myotronics.com/). Root mean square (RMS) values (in µV) were used as indices of signal amplitude. Each EMG epoch lasted 15 s. Muscle tone (SCAN 9) was evaluated with eyes closed with and without glasses and with eyes open with and without glasses. It should be noted that the subjects were instructed about the tests they were to complete and that they needed to open their eyes without forcing their eyelids, wrinkling their forehead, or squeezing their eyes. The EMG test was carried out only after the subjects had repeated the tests and demonstrated that they were able to perform the test correctly [26, 27].

Here is a summary of the protocol used:

Subject closes eyes and is without glasses. The third screen in which the values are stable is used to calculate average values. No function artifacts (e.g., swallowing) or movement should occur.
Subject is asked to open their eyes (they are still without glasses) when they reach approximately halfway down the screen that was shown in (1). An operator ensures that opening of the eyes has occurred without wrinkling of the forehead or visible displacement of the head.
At this point with the subject’s eyes open, the following period is considered valid. During the open-eye test, the subject is invited to read silently the first, second, and third lines, with the subsequent lines covered, of a standard Snellen optotype. The subject is positioned 3 m away from the optotype, which corresponds to vision acuity of 1/10, 2/10, and 3/10, respectively.
The sequence from 1 to 3 is subsequently repeated with the subject’s glasses on. Then, the subject is asked to silently read the fifth, sixth, and seventh lines (with the remaining lines covered), which corresponds to vision acuity of 5/10, 6/10, and 7/10, respectively.

The level of optotype reading and the distance from the subject (less than 5 m) were chosen so that the subjects would not be expected to perform at the maximum capacity of their vision.

2.4. DC

Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) were previously proposed by Dworkin and LeResche for research efforts regarding orofacial pain [28]. We applied an updated version of these criteria, DC/TMD [19, 28, 29], to clinical data in the present study.

2.5. CSI

To evaluate central sensitization, such as cutaneous allodynia and hyperalgesia in the trigeminal and extratrigeminal areas, a CSI was administered. Central sensitization (CS) is a proposed physiological phenomenon in which neurons of the central nervous system become hyperexcitable, thereby resulting in hypersensitivity to both noxious and nonnoxious stimuli [30].

Central sensitivity syndrome (CSS) describes a group of medically indistinct (or nonspecific) disorders, such as fibromyalgia, chronic fatigue, and irritable bowel, for which CS may be a common etiology. Our patient’s CSI total score was 55.4, thereby revealing a severe form of central sensitization [30, 31].

2.6. Statistics

Acquired data were tested for normality with the Shapiro–Wilk test as a parametric approach. Single muscle sEMG activity was calculated for the healthy and TMD groups according to experimental settings (e.g., eyes closed (EC), eyes open (EO), eyes closed with glasses (ECWG), and open eyes with glasses (EOWG)). Total sum of sEMG activity was derived in the same manner. A paired t-test was used to compare between experimental settings, while an unpaired t-test was used to compare differences between groups. Differences in CSI were also tested with an unpaired t-test. Statistical significance was set at p < 0.05. All of the statistical analyses were performed with public domain R libraries. Plots were generated with the “ggplot” library.

3. Results

Table 1 and Figure 1 show the CSI values obtained for the TMD and control subjects in our cohort. The average values for the TMD subjects are significantly higher than those of the control subjects (55.40 vs. 32.95, respectively). Values greater than 50, which were received by the TMD subjects, are indicative of severe CS status. Meanwhile, values less than 40 are indicative of a normal or sub clinical status of CSI. There were no significant differences observed between the male and female subjects within each group.

An external file that holds a picture, illustration, etc. Object name is PRM2020-3932476.001.jpg

Figure 1

Distribution of CSI scores for the TMD (red) and healthy (blue) groups.

Table 1

CSI scores.

Group	CSI TMD value (±SD)	CSI healthy value (±SD)	p value
Total	55.4 (6.62)	32.95 (7.22)	≤0.001
Female	56.4 (7.35)	32.8 (7.11)	≤0.001
Male	54.4 (6.02)	33.1 (7.72)	≤0.001
Female vs. male	0.92	0.51

Intergroup comparisons between the EMG values of individual muscles for EC versus EO conditions. No significant differences were observed among the two groups (Table 2).

Table 2

EMG values for specific muscles in the TMD and healthy subjects with eyes open (EO) versus eyes closed (EC).

Muscle group		EC			EO
Muscle group		N	Mean	SD	N	Mean	SD	t value	p value
TMD group	LTA	20	2.65	0.5	20	2.83	0.7	0.936	0.355
	RTA	20	2.78	0.8	20	2.94	0.8	0.632	0.531
	LMM	20	2.02	0.6	20	2.37	0.8	1.565	0.126
	RMM	20	2.21	0.5	20	2.53	0.6	1.832	0.075
	LSM	20	2.36	0.8	20	2.62	0.7	1.094	0.281
	RSM	20	2.87	0.6	20	2.95	0.7	0.388	0.700
	LDA	20	2.01	0.5	20	2.26	0.6	1.431	0.160
	RDA	20	1.98	0.4	20	2.05	0.6	0.434	0.667

Healthy group	LTA	20	1.54	0.5	20	1.55	0.5	0.063	0.950
	RTA	20	1.63	0.4	20	1.64	0.3	0.089	0.929
	LMM	20	1.78	0.4	20	1.79	0.4	0.079	0.937
	RMM	20	1.81	0.6	20	1.82	0.5	0.057	0.955
	LSM	20	1.95	0.8	20	1.97	0.9	0.074	0.941
	RSM	20	1.85	0.3	20	1.86	0.5	0.077	0.939
	LDA	20	1.13	0.3	20	1.16	0.4	0.268	0.790
	RDA	20	1.15	0.2	20	1.16	0.2	0.158	0.875

Table 3 presents the sum of the sEMG values recorded for our cohort. The sum of the EMG values was significantly higher for TMD subjects that had their eyes open versus closed (18.88 vs. 20.55, respectively; p ≤ 0.001). In contrast, the difference in EMG values between the control subjects with their eyes open versus closed was not significant (12.84 vs. 12.95, respectively).

Table 3

EMG values with eyes closed versus eyes open for the two groups.

sEMG sum	EC			EO
sEMG sum	N	Mean	SD	N	Mean	SD	t value	p value
TMD	20	18.88	0.5875	20	20.55	0.6875	8.258565	≤0.001
Healthy	20	12.84	0.4375	20	12.95	0.4625	0.772703	0.444

When EMG values were compared for closed eyes with and without glasses, there were no significant differences in the TMD and control groups (Table 4).

Table 4

EMG values with eyes closed and with glasses on.

Muscle group		CE			CEWG
Muscle group		N	Mean	SD	N	Mean	SD	t value	p value
TMD group	LTA	20	2.65	0.5	20	2.55	0.6	0.573	0.570
	RTA	20	2.78	0.8	20	2.69	0.6	0.402	0.690
	LMM	20	2.02	0.6	20	2.12	0.5	0.573	0.570
	RMM	20	2.21	0.5	20	2.31	1.1	0.370	0.713
	LSM	20	2.36	0.8	20	2.45	0.6	0.402	0.690
	RSM	20	2.87	0.6	20	2.77	1.1	0.357	0.723
	LDA	20	2.01	0.5	20	2.1	1.1	0.333	0.741
	RDA	20	1.98	0.4	20	1.48	0.8	2.500	0.017

Healthy group	LTA	20	1.54	0.5	20	1.54	0.6	0.000	1.000
	RTA	20	1.63	0.4	20	1.69	0.9	0.272	0.787
	LMM	20	1.78	0.4	20	1.71	1.1	0.267	0.791
	RMM	20	1.81	0.6	20	1.56	0.5	1.431	0.160
	LSM	20	1.95	0.8	20	1.89	1	0.210	0.835
	RSM	20	1.85	0.3	20	1.85	0.8	0.000	1.000
	LDA	20	1.13	0.3	20	1.12	0.6	0.067	0.947
	RDA	20	1.15	0.2	20	1.17	0.5	0.166	0.869

There was also no significant difference in the sum of EMG values between the subjects with their eyes closed with and without glasses for both the TMD and control groups (Table 5).

Table 5

EMG values with eyes closed with and without glasses on.

sEMG sum	EC			ECWG
sEMG sum	N	Mean	SD	N	Mean	SD	t value	p value
TMD group	20	18.88	0.5875	20	18.47	0.8	1.847338	0.072
Healthy group	20	12.84	0.4375	20	12.53	0.75	1.59668	0.119

Table 6 shows the EMG values obtained for individual muscles between the TMD and normal groups that were evaluated with eyes open with and without glasses. Significantly higher values were obtained for the TMD subjects wearing glasses for all of the muscles examined (e.g., LTA, RTA, LSM, RSM, LDA, and RDA), with the exception of the right and left masseter muscles (LMM and RMM). Meanwhile, in control subjects, none of the muscles exhibited significantly different EMG values with or without glasses.

Table 6

EMG values of the individual muscles with eyes open with and without glasses on.

Muscle group		EO			EOWG
Muscle group		N	Mean	SD	N	Mean	SD	t.value	p value
TMD group	LTA	20	2.83	0.7	20	3.95	0.9	4.393	≤0.001
	RTA	20	2.94	0.8	20	4.78	1	6.426	≤0.001
	LMM	20	2.37	0.8	20	3.12	0.9	2.785	0.008
	RMM	20	2.53	0.6	20	2.41	0.8	0.537	0.595
	LSM	20	2.62	0.7	20	3.66	1.8	2.408	0.021
	RSM	20	2.95	0.7	20	3.57	1.1	2.127	0.040
	LDA	20	2.26	0.6	20	3.11	0.5	4.867	≤0.001
	RDA	20	2.05	0.6	20	3.38	0.9	5.499	≤0.001

Healthy group	LTA	20	1.55	0.5	20	1.71	0.2	1.329	0.192
	RTA	20	1.64	0.3	20	1.58	0.8	0.314	0.755
	LMM	20	1.79	0.4	20	1.58	0.3	1.878	0.068
	RMM	20	1.82	0.5	20	1.51	0.6	1.775	0.084
	LSM	20	1.97	0.9	20	1.85	0.2	0.582	0.564
	RSM	20	1.86	0.5	20	1.92	0.5	0.379	0.706
	LDA	20	1.16	0.4	20	1.16	0.6	0.000	1.000
	RDA	20	1.16	0.2	20	1.17	0.3	0.124	0.902

Furthermore, the sum of EMG values for the individual muscles was significantly greater with eyes open with glasses than without glasses in the TMD group (20.55 vs. 27.61, respectively). Conversely, the sum of the EMG values of the individual muscles was significantly lower in the control subjects group with and without glasses (12.95 vs. 12.48, respectively), and there was no significant difference (Table 7).

Table 7

EMG values with open eyes with and without glasses.

sEMG values	EO			EOWG
sEMG values	N	Mean	SD	N	Mean	SD	t-value	p-value
TMD group	20	20.55	0.6875	20	27.98	0.9875	27.61517	≤0.001
Healthy group	20	12.95	0.4625	20	12.48	0.4375	3.30155	0.002

In Figure 2, a visual representation of the individual muscle data described above for the TMD and control groups are presented. Differences between the two groups are particularly obvious for the EC and EO versus EOWG for the two groups.

An external file that holds a picture, illustration, etc. Object name is PRM2020-3932476.002.jpg

Figure 2

Results of electromyographic values in the two groups.

Thus, the following observations were made based on the data analyzed:

For all of the tested conditions, the TMD subjects exhibited significantly higher EMG values than the control subjects.
The TMD subjects showed significant increases in EMG values between closed eyes and open eyes without glasses, and more so between open eyes with and without glasses.
The control subjects did not show significant increases in their EMG values between closed eyes and open eyes without glasses, yet the EMG values were lower when the subjects’ eyes were open and glasses were worn. The latter data contrast with the corresponding data for the TMD subjects.
The CSI values were significantly higher for the TMD subjects compared to the control subjects. Moreover, the former values are indicative of a serious CS condition, while the values for the control subjects indicate a normal or subclinical CS condition.

Finally, the electromyographic traces are shown in Figure 3(a)–3(e).

An external file that holds a picture, illustration, etc. Object name is PRM2020-3932476.003.jpg

Open in a separate window

Figure 3

(a–e) Five different cases involving detection of EMG reactions upon opening of the eyes. (a) A trace representing a bilateral increase in an EMG signal from the anterior temporal musculature. (b) A trace representing a monolateral increase in the EMG signal from the left sternocleidomastoid. (c) A trace representing a bilateral increase in the EMG signal from the sovraioidea musculature (anterior abdomen of the digastrics). (d) A trace representing a monolateral decrease in the EMG signal from the RTA. (e) A trace representing the EMG signal from opening of the eyes.

4. Discussion

The data obtained in this study indicate that TMD subjects with vision disorders that are corrected with standard glasses present EMG values that are significantly higher than those presented by non-TMD subjects with vision disorders and standard glasses. While the relationship between EMG and TMD remains a topic of debate, our results are consistent with those previously reported, which suggest that resting EMG data of subjects suffering from TMD differ from control subjects [5, 32–34]. However, it should be noted that some authors have indicated that EMG data are insufficient for clinical and research purposes [35]. Discrepancies can arise due to differences in techniques and tools of analysis, study protocols, and in the selection of subjects. Yet, regardless of the reliability of surface EMG values for a diagnosis of TMD, their application in the present study was not to support a diagnosis of TMD, but rather they were used to examine a possible direct correlation between variations in EMG values from opening of the eyes, which, in most cases, is an easily observed phenomenon on EMG traces as shown in the figures.

In the present study, a bilateral increase from the anterior temporal musculature, a monolateral increase from the left sternocleidomastoid, and a bilateral increase from the sovraioidea musculature (anterior abdomen of the digastrics) were more frequently observed in the TMD subjects, while a monolateral decrease from the RTA and from opening of the eyes were observed in the control subjects. These results are consistent with accumulating evidence that indicates that subjects suffering from TMD exhibit dysregulation of the systems that control the response of the autonomous and somatomotor systems to sensory stimuli [36]. Furthermore, it has been hypothesized that this dysregulation in TMD patients represents a form of CS [37–41]. In fact, our CSI data indicate that TMD subjects receive high scores, and this is consistent with a role for central involvement that is not observed in control subjects. In previous studies of central dysregulation in TMD, a notable observation is that the pupil system of TMD subjects responds in a dysregulated manner to teeth clenching in response to administration of ultra-low-frequency transcutaneous electrical nervous stimulation (ULF-TENS) with sensory amplitude, which represents a central action mechanism [27, 37, 42–44]. In the present study, opening of the eyes was found to have a significant effect on EMG values only when TMD subjects opened their eyes while wearing glasses that provided standard eye correction. In contrast, EMG values for healthy subjects and from tests conducted with the eyes open without glasses did not significantly vary. Considering that in the protocol used, there were no differences observed between the two groups in terms of epidemiology or type of vision disorder, and that all subjects had a vision correction that was confirmed to meet ophthalmological standards, the only variable that differentiates the two groups is a TMD condition. The TMD subjects, on average, exhibited an increase in EMG values from the pericranial muscles upon opening of the eyes, and when the same subjects were wearing corrective glasses, the increase was even greater.

The aforementioned effect cannot be considered peripheral because possible connections of the visual/oculomotor system are not directly related to the position of the jaw and to the activity of the investigated stomatognathic muscles. Such relationships may be indirect and require a circuit that leads from sight and ocular motion centers to the nuclear trigeminal complex, and further to trigeminal/hypoglossal/facial motor nuclei (e.g., a central circuit). In animal studies, projections from the superior colliculus were observed to spread to a large part of the trigeminal sensory complex [45, 46]. The superior colliculus plays an important role in the orientation of the head and the eyes towards a salient visual stimulus [47, 48], it has a critical role in managing the visual structures of the neck and face in response to an unexpected object in the visual field, and it plays an important role in generating saccades and in the mechanisms of object tracking [49, 50]. Correct functioning of collicular transmission is, in part, related to structures that govern the state of attention and arousal [50]. At the same time, the superior colliculus receives somatosensory afferents from neurons in the main and spinal trigeminal nucleus that are connected to various somato-sensory orofacial structures [51].

The relationships that have been identified between the superior colliculus and the trigeminal nuclear complex suggest that these two nervous structures collaborate in organizing defensive and behavioral responses and appropriate control of motor responses to intercept and evaluate objects that appear, even suddenly, in the visual field. To optimize one’s ability to discriminate sensory stimulation, to interpret its meaning and value, and to respond with a valid motor behavior with an adequate state of arousal is indispensable. This arousal state is partly modulated by central structures, including catecholaminergic nuclei which are present in the trunk of the brain and in reticular formations and the locus coeruleus [52]. Tonic and phasic discharge modes of the locus coeruleus, in particular, have been associated with the behavioral states of arousal and hyperarousal. In the latter case, an altered coupling between a sensory somato/sensory stimulus and an adequate motor and behavioral response is possible [53, 54]. Activity of the pupil muscles is related to that of the locus coeruleus [55], and both are related to exploration activity and attention to an environment [56]. Furthermore, the activity of noradrenergic arousal systems can influence the phasic tonic activity of muscles that are innervated by trigeminal and hypoglossal nuclei [56–58].

Voluntary teeth clenching and rubber mastication in humans can modify pupil dynamics, probably indirectly, via stimulation of the locus coeruleus and the ascending systems of arousal [59]. Alterations in occlusal status or chronic pain disorders of the trigeminal region are associated with dysregulation of arousal-related systems [42, 60]. By 1949, Moruzzi and colleagues demonstrated the importance of trigeminal afferents in maintaining an arousal status, and these afferents were later shown to be essential for proper functioning of the arousal system. Projections from the main spinal and mesencephalic nucleus of the trigeminal to the various noradrenergic nuclei of the encephalic trunk are widespread, and they are responsible for modulation of the arousal state through an ascending reticular activating system and through structures that control the tonic state of the musculature of the head, neck, and ocular motion [61–64].

TMD, as previously noted, are categorized as CSSs and are sometimes referred to as hyperarousal syndromes which are characterized by dysregulation of the arousal state and difficulty in responding adequately to visceral somatosensory stimuli [65, 66]. This categorization suggests the existence of an altered response mode to peripheral inputs, including those coming from the visual system where the balance between visual and trigeminal structures can be altered. In this case, and when arousal systems are dysregulated, it is possible that standard vision correction induces an exaggerated activation in some TMD subjects due to CS. This activation could be interpreted as overstimulation of the associated trigeminal areas, and their response could result in an unbalanced activation of tone for muscles that are innervated by the trigeminal nuclear system. The observation in the present study that the control subjects had lower EMG values and improved quality of visual sensory information when opening their eyes with standard vision correction is consistent with our original hypothesis. Furthermore, these data can be attributed to the best visual acuity for the subjects when interpreting the “nature” that surrounded them because it favors the selection of salient stimuli, which is typical of a state of arousal suitable to a no-alarm circumstance as occurred during the study session.

5. Conclusion

A limitation of the present work is that a speculative hypothesis mainly based on indirect data obtained from the literature is used to explain phenomenon observed at the EMG level. However, research data from various fields are consistent with the hypothesis that chronic TMD belongs to a broad category of chronic pain disorders in which pathogenesis of a central type, rather than a peripheral type, plays a key role. Thus, the present work supports an indirect relationship of a probable central nature between visual and stomatognathic musculature that are not directly related to one another. Another limitation of the present study is that the number of analyzed subjects is not large. We applied strict inclusion criteria to obtain TMD patients and healthy subjects that were only affected by myopia and not other types of vision disturbances. Consequently, it is possible that our results are influenced by this selection and that the results may differ for TMD subjects with other vision pathologies. However, our goal was not to create a new nosography that correlates visual defects with the behavior of the stomatognathic musculature or to demonstrate a differentiated impact based on the visual defect associated with TMD. Rather, the aim of the present study was to test the hypothesis that correction of vision according to ophthalmological standards improves tone of the stomatognathic musculature. In healthy subjects, this hypothesis was confirmed. However, in TMD subjects, eye correction did not have a positive effect on the stomatognathic or pericranial musculature. Thus, it remains to be evaluated whether the EMG activity of TMD subjects can be improved with “nonstandard” visual corrections.

Acknowledgments

The authors wish to thank all the staff of The Dental Clinic of L’Aquila.

Data Availability

The data used to support the findings of this study have not been made available because they are private.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Authors’ Contributions

AM and RC conceived and designed the study. AM, PDD, and RC performed all the experiments and acquired data. DP performed the statistical analysis. EO, AM, and MG wrote the first draft. AM and CR supervised the drafting of the final version of the manuscript. AM and CR are responsible for the data acquisition and interpretation of the results. All the authors read and commented on the manuscript.

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Presentation of a keratocystic odontogenic tumor with agenesis: a case report

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2014 Apr 9

Mariano Lacarbonara, Giuseppe Marzo, Vitantonio Lacarbonara, Annalisa Monaco, and Mario Capogreco

Abstract

Introduction

We analyzed the etiopathogenetic, clinical, radiographic, and histopathologic aspects of keratocystic odontogenic tumors, particularly in association with dental anomalies of number, with the aim of providing useful information for their correct diagnosis, treatment, and prognosis within a multidisciplinary approach.

Case presentation

A 14-year-old Caucasian girl presented for observation of bilateral agenesis of the upper incisors, which was diagnosed by orthopantomography. Approximately one year after starting orthodontic treatment, the patient went to the emergency department because of a phlegmonous tumefaction of the lateroposterior upper left maxillary region. Diagnostic orthopantomography and axial computed tomography scan results of the facial skeleton revealed a large lesion occupying the left maxillary sinus, rhizolysis of dental elements 26 and 27, and dislocation of dental element 28. The lesion and infected sinus mucosa were removed through surgical antral-cystectomy with the Caldwell-Luc approach. Histological examination of the lesion confirmed the suspected diagnosis of keratocystic odontogenic tumor. The 12-month follow-up orthopantomography and computed tomography scan results showed good trabecular bone formation in the lesion area. The 24-month follow-up results showed optimal healing in the area of the lesion, positive pulp vitality tests for teeth 26 and 27, and good periodontal tissue healing, as verified through periodontal probing.

Conclusions

Combined with our observations from a careful review of the literature, the results of the case study suggest that keratocystic odontogenic tumor and dental agenesis probably do not develop through a common genetic cause. More likely, they are caused by related environmental factors. Management of this case required the multidisciplinary collaboration of different specializations and careful planning to devise a correct therapeutic protocol and reach a favorable prognosis.

Introduction

The classification of maxillary cysts by the World Health Organization (WHO) in 1992 categorized keratocysts as maxillary cysts of dysembryonic odontogenic origin. In 2005, the WHO defined keratocysts as benign, uni- or multi-cystic intraosseous neoplasms of odontogenic origin (for example, arising from epithelial residues of the dental lamina). Keratocysts typically have a thick, parakeratinized, stratified, squamous epithelial lining, and a potentially aggressive and infiltrating behavior [1–3]. The well-known aggressive evolution of keratocysts, their histology, and new findings in genetics led the WHO (year 2005) to reclassify these lesions as keratocystic odontogenic tumors (KCOTs) [3,4].

KCOTs can develop in single or multiple form. Multiple keratocysts are characteristic of Gorlin-Goltz or nevoid basal cell carcinoma syndrome. Single keratocysts have a frequency of 5 to 15 percent, compared to 5 percent for multiple keratocysts. The frequency of recurrence ranges from 25 to 30 percent for single keratocysts, and is higher for multiple keratocysts. The likelihood of recurrence is currently predicted on the basis of histology; recurrence is rarely associated with orthokeratosis, but frequently found in parakeratosis. KCOTs have equal prevalence in males and females. They can affect individuals of all ages, with peaks in the second and fourth decades of life. They are more common in the posterior mandible (65 to 70 percent of cases), especially in the posterior body and ascending ramus [5,6].

Clinically, a keratocyst manifests as a fast-growing aching tumefaction, with infiltration and expansion in the cortical bone. It may cause rhizolysis and dental dislocation. On radiography, a keratocyst appears as a uni- or multi-locular radiotransparency. A unilocular keratocyst can be connected to the tooth apex, simulating a periapical cyst. Alternatively, it can surround the crown of an impacted tooth, potentially being confused with a dentigerous cyst. If the keratocyst is localized between tooth roots, it may be misdiagnosed as a lateral periodontal or lateral radicular cyst. A KCOT that develops along the midline simulates a nasopalatine duct cyst. Unilocular keratocysts and ameloblastomas are indistinguishable on X-ray [6].

The aim of this report was to study the etiopathogenetic and clinical manifestations of KCOTs, particularly in association with dental anomalies of number. The overall goal was to provide useful information for the correct diagnosis, treatment, and prognosis of these lesions, within a multidisciplinary approach [7–9].

Case presentation

Here, we report the case of a 14-year-old Caucasian girl, who presented with bilateral agenesis of the upper incisors, diagnosed via orthopantomography (OPG) (Figure 1) and skull X-ray in the laterolateral projection. Approximately one year after starting orthodontic treatment, our patient came to the emergency department because of a phlegmonous tumefaction of the lateroposterior upper left maxillary region. A careful intraoral examination revealed remarkable swelling and mobility of teeth 26 and 27, which were positive to vitality tests. OPG (Figure 2) revealed a large area of unilocular osteolysis, with a calcific peripheral edge in the left maxillary sinus; radicular resorption of teeth 26 and 27; and the absence of tooth 28, which had been present in the previous radiographic examination (Figure 1).

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Figure 1

Orthopantomography with agenesis of 1.2 and 2.2.

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Figure 2

Dental panoramic radiograph.

To determine the origin of the lesion and the best surgical approach, an axial computed tomography (CT) scan of the facial skeleton was requested. The coronal section showed complete opacity of the left maxillary sinus, involvement of ethmoidal cells (Figure 3), and dislocation of tooth 2.8 in the sinus. The axial projection showed a large, oval-shaped area of osteolysis, measuring 3.6 × 4.3mm, with deformation and erosion of the buccal cortical bone (Figure 4). Considering this erosion, we immediately performed a needle biopsy of the lesion. The lesion was hemorrhagic and purulent, typical of an infected cyst. After a careful evaluation, we chose antral-cystectomy with the Caldwell-Luc technique, under general anesthesia, as the treatment for removal of the lesion and the infected sinus mucosa.

Figure 3

Computed tomography scan: coronal sections.

Figure 4

Computed tomography scan: axial sections.

A large mucoperiosteal incision was made to create a mixed flap (marginal-paramarginal) from the central contralateral incisor to the maxillary tuberosity (Figure 5). Removing the flap revealed a large opening in the cortical bone. The maxillary sinus was emptied through complete enucleation of the keratocyst and removal of the ethmoidal membrane, including the eighth. The removed lesion (Figure 6) was immersed in 10 percent formalin and sent to a pathologist for histological examination. Teeth affected by the lesion were stabilized by interocclusal splinting with wrought metal wire. A histological diagnosis of ‘odontogenic keratocyst with a specific flogistic and chronic focus’ confirmed the clinical suspicion.

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Figure 5

Opening of the flap.

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Figure 6

Macroscopic findings.

The KCOT showed a typical undulated pattern in the epithelium, accompanied by parakeratinization and exfoliation of keratin in the lumen (Figure 7). Clinical and imaging follow-ups at 6, 12, and 24 months showed good bone trabeculation in the area of the KCOT (Figures 8, ,99 and and10),10), and positive pulp vitality results for teeth 2.6 and 2.7. Probing indicated healing of the periodontal area. Teeth neighboring the missing teeth were subjected to radicular torque, and internal hexagon implants (3.5 and 4mm in diameter) were inserted (Figure 11). Temporary rehabilitation was performed. Loading was deferred for 30 days after implant insertion (Figure 11).

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Figure 7

Histological findings.

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Figure 8

Orthopantomography follow-up after 6 months.

Figure 9

Computed tomography axial projection at 12 months.

Figure 10

Computed tomography coronal projection at 12 months.

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Figure 11

Details of implant on 2.2.

The orthodontic braces were removed, resulting in an increased gum volume and ‘gummy smile’. Therefore, we performed gingivectomy using an Nd: YAG laser source (Figure 12).

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Figure 12

Gingivectomy with Nd:YAG laser.

Sixty days after implant insertion, the peri-implant soft tissues were determined to be in an excellent condition, and the final prosthetic rehabilitation with a ceramic implant-crown system was performed (Figure 13). At the 24-month follow-up visit, there was no recurrence, and the vitality of the dental elements was confirmed (Figure 14).

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Figure 13

Completed case.

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Figure 14

Orthopantomography examination at 24 months.

Discussion

In this manuscript, we present the case of a patient with a KCOT, an infrequent pathology of the maxillary sinus, associated with a dental anomaly (hypodontia). We primarily focused on the etiopathogenesis of the lesion, to detect a possible causal relationship between KCOT and agenesis.

Keratocyst: malformation or neoplasm?

No predisposing factors for keratocysts are known. Like other odontogenic tumors, keratocysts usually appear de novo. In rare cases, they develop on odontogenic cysts. Approximately 200 genes are involved in tooth development. Among them, fibroblast growth factor (FGF) and sonic hedgehog (SHH) are the most frequently altered genes in odontogenic neoplasms.

The question of whether keratocysts are malformations or neoplasms has been the subject of long debate. Whereas some authors claim that a keratocyst develops from a distal extension of the dental lamina, others think it is derived from the basal layer of the oral epithelium. Most authors agree that the neoformation shows an expanding growth type, similar to maxillary cysts [10,11]. Keratocysts have an actively proliferating epithelium. They exhibit high numbers of cells positive for Ki67, proliferating cell nuclear antigen (PCNA), and p53 compared to other odontogenic cysts [12]. PCNA and Ki67 are proliferation markers that are expressed during mitosis. The oncosuppressor p53 favors cell apoptosis, and is frequently mutated or overexpressed in neoplasms. From these observations, we can deduce that B-cell lymphoma-2 (Bcl-2), matrix metalloproteinase (MMP)-2 and -9, transforming growth factor (TGF), and interleukin (IL)-1a and -6 are overexpressed in keratocysts.

Patched (PTCH) is the receptor for secreted sonic hedgehog (SHH) protein. Normally, PTCH forms a receptor complex with the product of the oncogene Smoothened (SMO), through the SHH ligand. The interaction between PTCH and SMO inhibits translation of the growth signal. If the normal functioning of PTCH fails, then the proliferation-promoting effects of SMO become dominant [7,9]. SMO is an oncosuppressor that is important for the embryonic development of neural tubes, skeleton, limbs, lungs, hair follicles, and teeth. Mutations of SMO can be found in keratocysts in Gorlin-Goltz syndrome, as well as in sporadic keratocysts. The above findings constitute clinical and molecular evidence for the conclusion that keratocysts are neoplasms characterized by local aggressiveness (see [3]), and should be referred to as ‘keratocystic odontogenic tumors’ [1–3,13,14].

Dental agenesis: genetic and/or environmental etiology

Concerning the etiopathogenesis of dental agenesis, the hereditary theory (Brook [15]; Magnusson [16]; Graber [17]; Ahmed et al.[18]) highlights a dominant autosomal transmission, with reduced penetrance and variable expression in terms of the number and region of the missing teeth. Genetic surveys of members of families with dominant autosomal oligodontia highlighted mutations in two transcription factors: Msh homeobox 1 (MSX1) in chromosome 4 (4p.16), and Paired box gene 9 (PAX9) in chromosome 14 (14q.21q.13) [15–18]. Functional deletion of these genes in rats arrested tooth development and caused tissue alterations [19,20]. Other recent studies suggested a possible relationship of agenesis with deletion of the gene TGF alpha (TGFA) [20].

Some authors have suggested that a recessive autosomal transmission may be possible (Grahnen [21]; Ahmad [22]). Suarez and Spence [23] stated that agenesis may result from a polygenic or multifactorial heredity model, rather than from a single dominant gene. Brook [24] supported a multifactorial model, in which polygenic factors played a fundamental role, but without excluding environmental factors [25].

Studies agree on the importance of pathology during the maturation and migration processes of cells involved in dental gem formation (that is, after 120 embryonic days, for the permanent dental elements). Environmental factors can prevent follicle formation, due to internal factors (for example, pathologies of the hypophysis, thyroid, or parathyroid, and so on) or external factors (for example, maxillary trauma or surgery, early infection, serious nutritional insufficiency, radiotherapy, and so on) [19,26]. Arrest of dental development has been attributed to environmental factors, on a background of genetic predisposition to agenesis (Schalk Van Der Weide) [27–29]. Thus, KCOT and dental agenesis are likely not due to a common genetic cause, but are probably related to casual environmental factors.

Case study of KCOT with dental agenesis

The present study concentrated on clinical, imaging, and histological diagnosis, as well as on the therapy of the lesion and agenesis. Initially, healing the KCOT was the most important concern. We applied an aggressive approach (that is, enucleation of the lesion with maxillary antrostomy, using the Caldwell-Luc technique), which prevented recurrence and encouraged bone repair. From a radiological perspective, this approach led to a progressive increase in trabecular bone formation during later follow-ups.

The final phase of the intervention concentrated on the bilateral agenesis of the upper incisors through an implant-supported prosthetic treatment. From the biological, functional, and esthetic perspectives, implant therapy was considered to be the most desirable treatment. Prior to implant insertion, orthodontic treatment was used to achieve and maintain the space necessary for the implant-supported prosthetic reconstruction.

Conclusions

The management of this case required multidisciplinary collaboration between different specializations. It necessitated careful planning to devise the ideal therapeutic protocol for a favorable prognosis, including absence of KCOT recurrence. Good functionality and esthetics were obtained through the implant-supported prosthetic rehabilitation of dental agenesis.

Consent

Written informed consent was obtained from the patient’s legal guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Abbreviations

CT: computed tomography; KCOT: keratocystic odontogenic tumor; OPG: orthopantomography.

Competing interests

All authors declare that they have no competing interests.

Authors’ contributions

ML and VL contributed to the conception and design of the study, the analysis and interpretation of the data, and drafted the manuscript. ML, VL, and MC made the diagnosis of KCOT and established the treatment. AM, GM, and MC were involved in the data interpretation, and contributed to the revision of the drafted manuscript. All authors read and approved the final manuscript.

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Comparison Between Sensory and Motor Transcutaneous Electrical Nervous Stimulation on Electromyographic and Kinesiographic Activity of Patients With Temporomandibular Disorder: A Controlled Clinical Trial

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2013 May 15

Annalisa Monaco, Fabrizio Sgolastra, Davide Pietropaoli, Mario Giannoni, and Ruggero Cattaneo

Abstract

Background

The purpose of the present controlled clinical trial was to assess the effect of a single 60 min application of transcutaneous electrical nervous stimulation (TENS) at sensory stimulation threshold (STS), compared to the application of motor stimulation threshold (MTS) as well as to untreatment, on the surface electromyographic (sEMG) and kinesiographic activity of patients with tempormanbibular disorder (TMD).

Methods

Sixty female subjects, selected according to the inclusion/exclusion criteria, suffering from unilateral TMD in remission were assigned to MTS, STS or untreatment. Pre- and post-treatment differences in the sEMG activity of temporalis anterior (TA), masseter (MM), digastric (DA) and sternocleidomastoid muscles (SCM), as well in the interocclusal distance (ID), within group were tested using the Wilcoxon test, while differences among groups were assessed by Kruskal-Wallis test; the level of significance was set at p ≤ 0.05.

Results

Significant pre- and post-treatment differences were observed in MTS and STS groups, for TA and MM of both sides; no significant difference was detected between MTS and STS groups. Kinesiographic results showed that the vertical component of ID was significantly increased after TENS in MTS and STS groups.

Conclusions

STS TENS could be effective, as well as MTS, in reduce the sEMG activity of masticatory muscles and to improve the ID of TMD patients in remission. Future studies are needed to confirm the results of the present study. Clinical relevance. The present study demonstrates that the application of TENS is effective in reduce the sEMG activity, as well as in increasing the ID of patients with TMD; our study did not support superior effectiveness of MTS or STS.

Trial registration

ClinicalTrials.gov: NCT01832207

Keywords: Surface electromyography, Kinesiography, Temporomandibular disorder, Transcutaneous electrical nervous stimulation

Background

Temporomandibular disorder (TMD) is a collective term that embraces a number of clinical problems that involve the masticatory muscles, the temporomandibular joint and the associated structures. [1] The diagnosis of TMD is mainly based on clinical examination, even if additional auxiliary tools are available for a supplemental clinical investigation. Among those, surface electromyography (sEMG) has been proposed as supplemental tool in TMD diagnosis: despite the fact that the reliability of sEMG recordings from masticatory muscles is still lacking general consensus [2,3], since several issues, which are related to selectivity, reliability, and interpretation of sEMG signals, remain to be resolved [4,5], it has been suggested that sEMG could provide an objective recording of muscular activity [6–8], at rest and during functional activity, in a non-invasive way.

Transcutaneous electrical nervous stimulation (TENS) has been suggested as a treatment strategy in the therapy of TMD [9–11], since it has been showed to produce an antalgic effect in symptomatic patients and a positive relaxing effect on the masticatory muscles [12]. In clinical practice and research investigation, TENS has been administered at a variety of intensities as well of threshold of stimulation, both for antalgic [13,14] and relaxing purposes [15–17]. However, the effectiveness of TENS in reducing the sEMG activity of masticatory muscles, in patients with TMD, is still a debated question: differences, in terms of settings and types of TENS applications, among studies have been suggested to play an important role in explaining the contrasting findings, that have been observed in the literature [18–20]: interestingly, two controlled studies [15,17], that recruited patients with symptomatic and asymptomatic TMD, respectively, using the same treatment design, that consisted of a 60 min application of low intensity TENS with a motor threshold of stimulation (MTS), reported a significant reduction of sEMG activity of masticatory muscles; in contrast, another controlled study, that recruited patients with symptomatic TMD [16], using a 45 min application of high intensity TENS with a sensorial threshold of stimulation (STS), observed a significant reduction of pain intensity, and reported no significant differences with regard to the muscular activity in the group receiving TENS application.

Interestingly, Moran and coworkers [21] showed that TENS-mediated pain relief has a dose–response relationship, suggesting that intensity as well as threshold stimulation could influence the effectiveness of TENS application. These observations, could have important implications in clinical practice and research, since no optimal dosage as well as threshold of stimulation have been defined in the treatment of patients with TMD. Accordingly, no study is available to compare the effect of different threshold of stimulation on muscular activity of patients with TMD.

Previously [17], we showed that MTS is effective in reducing the sEMG activity of masticatory muscles; in the present study we assess, the effect of motor threshold of stimulation (MTS) TENS, compared to sensory threshold application (STS) TENS on the muscular activity of masticatory and neck muscles, of patients with TMD.

Methods

Subjects

This study was conducted in accordance with the Declaration of Helsinki. The Committee on Ethics in Science of the University of L’Aquila, L’Aquila, Italy approved the study and informed consent was obtained from each subject.

Sixty female subjects suffering from unilateral TMD in remission at least from 3 months, aged 24 to 30 years-old (median age = 26 years), were recruited and divided into three groups: twenty patients were assigned to a single session of 60 m of MTS TENS; twenty patients undergone a single session of 60 m of STS TENS; twenty patients received a delayed TENS treatment after the end of the study, and, therefore, this group received no treatment during the entire duration of the study and acted as control.

Selection criteria

Considering that jaw elevator muscle activity can be influenced by oro-facial pain [22], gender [23], age [24], occlusion [25], and hemispheric-dominance [26], only patients that fulfilled the following inclusion criteria were included in the study: age less than 30 years; female gender; right-handed (7–10 points in Edinburgh inventory) [27]; presence of complete permanent dentition, with the exception of the third molars; normal occlusion; and diagnosis of unilateral arthrogenous TMD on the Research Diagnostic Criteria for TMD (RDC/TMD) [28,29], Axis I, groups II and III. Patients were excluded from the study if they met one or more of the following exclusion criteria: having pacemaker or other electrical devices, previous experience of TENS or biofeedback, systemic diseases, history of local or general trauma, neurological or psychiatric disorders, muscular diseases, cervical pain, bruxism, diagnosed by the presence of parafunctional facets and/or anamnesis of parafunctional tooth clenching and/or grinding; pregnancy, assumption of anti-inflammatory, analgesic, antidepressant or myorelaxant drugs, fixed or removable prostheses, fixed restorations that affected the occlusal surfaces, or previous or concurrent orthodontic or orthognathic treatment.

sEMG, TENS and kinesiographic measurements

All examinations were performed by one examiner (A. M.), using an 8-channel surface electromyograph with simultaneous acquisition, common grounding to all channels, and filters of 50 Hz electromyography (K7/EMG, Myotronics-Noromed, Inc., Tukwila WA, USA), with disposable electrodes (Duotrode, bipolar surface electrodes Ag-AgCl, 20 mm center to center distance, Myotronics-Noromed, Inc., Tukwila WA, USA), for sEMG recording. The right masseter (RMM), left masseter (LMM), right anterior temporal (RTA), left anterior temporal (LTA), right digastric (RDA), left digastric (LDA), right sternocleidomastoid (RSCM), and left sternocleidomastoid (LSCM) muscles were recorded. The sEMG recordings and muscle activity was expressed as the root mean square (RMS) of the amplitude, expressed in μV [30]. Kinesiographic recordings were performed using a kinesiograph (K7/CMS; Myotronics-Noromed, Inc., Tukwila, WA, USA) that measures jaw movements with an accuracy of 0.1 mm. An array of lightweight (113 gr) with multiple sensors and containing 8 magnetic sensors, tracked the motion of a magnet (CMS Magnet; Myotronics-Noromed, Inc., Tukwila WA, USA), that was attached at the lower inter-incisor point. The kinesiograph was interfaced with a computer for data storage and subsequent software analysis (K7 Program, Myotronics-Noromed, Inc., Tukwila WA, USA).

Positioning of sEMG, TENS electrodes and kinesiographic array

The electrodes determine, to a large extent, the quality of the recordings [31]. Electrodes were positioned on LMM, RMM, LTA and RTA, as described by Castroflorio et al. [6], as well on RDA, LDA [32], LSC and RSC [33,34], A template was used to enabled the exact reposition of the electrodes, in the occurrence of malfuctioning. The ground electrode, which was larger than the others and ensured a very good contact with the skin, was positioned on the subject’s forehead to ensure a common reference to the differential input of the amplifier. The kinesiographic array was mounted on the subject’s head, and the optimal position of the magnet for the recording of kinematic movements was monitored by software.

Due to the noise inherent with the sEMG recording, a special attention was paid to obtain reproducible and standardized recordings; approximately 15% of the electrodes required a relocation after new degreased, dry, jelly, and electrode fixation; however, to obtain a reliable sEMG recording, the reliability of signal captation of each electrodes was tested by a noise test software (K7 Program, Myotronics-Noromed, Inc., Tukwila WA, USA): only when the software gave the absence of noise (corresponding to the value provided by the software of 0.0), the sEMG recording was started.

Stimulation procedure

For TENS application a J5 Myomonitor TENS Unit device (Myotronics-Noromed, Inc., Tukwila, WA, USA), with disposable electrodes (Myotrode SG Electrodes, Myotronics-Noromed, Inc., Tukwila, WA, USA) was used: this low-frequency neurostimulator generates a repetitive synchronous and bilateral stimulus, delivered at 1.5 s intervals, with a variable amplitude of approximately 0–24 mA, a duration of 500 μs and a frequency of 0.66 Hz. The two electrodes for TENS were placed bilaterally over the cutaneous projection of the notch of the V pair of cranial nerves, that is located between the coronoid and condylar process and was retrieved by manual palpation of the zone anterior to the tragus; a third grounding electrode was placed in the center of the back of the neck [15]; however, since in the area of application of TENS, fibers of VII pair of cranial nerves are present, MTS TENS resulted in the motor stimulation of jaw elevator and facial muscles.

The stimulation procedure was performed under kinesiographic recording, in order to assess the achievement and the absence of motor stimulation in the MTS and STS group, respectively. In both MTS and STS groups the amplitude of TENS stimulation was reached starting from 0, with the stimulator turned on and the rheostat, which controls amplitude, positioned on 0; thus, the amplitude of stimulation was progressively increased of 0.6 mA/s: in the MTS group the stimulation was progressively increased until the contraction of the elevator muscles of the jaw was observed on the kinesiographic track.

In the STS group, the stimulation was progressively increased until the patients reported the sensation of pricking: a particular attention was paid to avoid the reaching of the threshold of motor stimulation: indeed, in this group, if any movement of the investigated muscles was observed during the kinesiographic recording, the patients was excluded from the study.

Recording procedure

Electromyographic and kinesiographic recordings were conducted with patients comfortably seated on a wooden chair with a straight back; patients were asked to assume a relaxed position of the head. The measurements were performed in a silent and comfortable environment. For sEMG recording, three consecutive tracks, with a duration of 15 s, and withouth any interposing phasic event, such as swallowing, voluntary movement or clenching, were acquired with the mandible of the patient in rest position. During the recordings, each subject was asked to keep his/her eyes closed, maintaining a slight contact between his/her lips. The participants received these instructions before the recordings. For each patient, sEMG and kinesiographic measurements were recorded before and immediately after the application of TENS. Patients in the control group received no treatment, and underwent sEMG and kinesiographic recording at baseline and immediately after TENS.

For kinesiographic recording, the patients were asked to close their eyes and, starting from the mandible rest position, to occlude teeth; after 2 s from occlusal contact, the patients were asked to quickly open and return in occlusal contact (tap-tap phase); for each patient, at least 3 consecutive tap-tap phases were recorded; the achievement of occlusal contact during each tap-tap phase was defined as the presence on the vertical component (Figure 1, Blu line) of the kinesiographic tracing of an horizontal line located at the same height of the first occlusal contact (Figure 1). After the tap-tap phase, the patients keep their habitual occlusal position for at least 1 s, then, they were asked to protrude the mandible. Kinesiographic recording was started at the end of the TENS session.

Figure 1

Kinesiographic track. Ver (Verticality/Blu line) refer to vertical component of the interocclusal distance; AP (Anterior-Posteriority/Red line) refer to anterio-posterior component of interocclusal distance. Lat (Laterality/Green line) refer to lateral component of interocclusal distance. Line at the beginnig of the track refer to basal position of the mandible at rest position.

For kinesiographic measurements, the interocclusal distance (ID) was recorded in its threedimensional component: verticality (defined as the difference between basal and the highest level of the blue line) (Figure 1), anterior-posteriority (defined as the difference between basal and highest level of the red line) (Figure 1), and verticality/anterior-posteriority (V/AP) ratio.

Study design

TENS electrodes were placed in all patients, but the stimulation was performed only in the MTS AND STS groups. The stimulation procedure was performed by the same operator who placed the electrodes (Figures 2 and and33).

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Figure 2

sEMG and TENS electrodes positioning.

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Figure 3

K7 electromyographic and kinesiographic instruments.

Sample size calculation

The sample size calculation determined that 16 subjects per treatment arm would provide a 80% power to detect a true difference of 0.6 μV among the three study groups using the reduction in the mean RMS between LTA and RTA as the primary outcome variable, assuming that the common standard deviation is 0.6 μV. Accordingly, a sample of 20 subjects per arm was recruited to overcome the possibility of dropouts.

Statistical analysis

Statistical analysis was performed using STATA 10 (StataCorp LP, College Station, TX, USA). The level of significance was assumed to be p ≤ 0.05 for all tests.The Shapiro-Wilk test indicated a non normal distribution of the sEMG and kinesiographic data, as well of the patient’s age in the three groups; therefore, pre- and post-treatment within group differences in the sEMG and kinesiographic data were analyzed using the Wilcoxon test. Differences in the sEMG, kinesiographic data and age among the three groups, were assessed by Kruskal-Wallis test. Kinesiographic and sEMG data are expressed as means and standard deviations (SD). Intraclass coefficient correlation (ICC) was calculated to estimate the intra- and inter-sessional reproducibility, according to the protocol suggested by Castroflorio and coworkers [35].

Results

All sixty female patients completed the study and no droput occurred. The mean age was 25.5±1.3 in MST group, 26.3 ± 1.2 in STS group and 25.4 ± 1.1 in the control group; no significant differences were observed in age among the three groups (p > 0.01).

Reproducibility

At the first sEMG recording, the mean ICC for investigated muscles was 0.832, while in the second recording the mean ICC was 0.803; globally, the ICC was 0.814.

SEMG and kinesiographic findings

At baseline, no significant difference in sEMG and kinesiographic measurements was observed among the three groups. In the MTS group, motor stimulation was reached in 15–20 s, while in the STS the group sensory stimulation was reached in 5–10 s.

Immediately after TENS, a reduction in RMS was observed for all investigated muscles in MTS and STS groups; in the control group, only RMM, LDA and RDA showed a reduction in RMS values, even if these changes were not statistically significant. Significant pre – post-treatment differences were observed in the MTS and STS groups, for LTA RTA LMM and RMM. Kruskal-Wallis test revealed that RMS values of LTA RTA LMM and RMM in the MTS and STS groups were significantly reduced, in comparison with control group; however, no significant differences were observed between MTS and STS groups at baseline or at post-treatment timepoint (Table 1).

Table 1

Values of sEMG activity in the MTS, STS and control group

	MTS group		STS group		CONTROL group
	Baseline	After TENS	Baseline	After TENS	Baseline	After TENS
LTA	2.79 (1.69)	1.62 (1.08) ^a,b	2.91 (1.48)	1.70 (0.99) ^a,b	2.69 (1.25)	3.18 (1.93)
RTA	2.87 (1.76)	1.71 (1.13) ^a,b	2.83 (1.46)	1.64 (1.07) ^a,b	2.93 (1.57)	3.36 (1.67)
LMM	1.59 (0.91)	1.17 (0.64) ^a,b	1.59 (1.17)	1.12 (0.78) ^a,b	1.37 (1.19)	1.39 (1.26)
RMM	1.47 (1.01)	1.11 (0.77) ^a,b	1.50 (1.19)	1.14 (0.54) ^a,b	1.51 (1.19)	1.42 (1.33)
LSM	2.44 (1.81)	2.23 (2.40)	2.51 (1.71)	2.52 (2.05)	2.19 (1.30)	2.38 (1.97)
RSM	2.28 (1.74)	2.24 (2.74)	2.39 (2.33)	2.27 (2.26)	2.46 (1.92)	2.65 (1.81)
LDA	1.99 (1.17)	1.79 (1.11)	1.91 (1.12)	1.82 (0.75)	1.79 (0.76)	1.64 (0.68)
RDA	2.16 (1.26)	1.95 (1.25)	1.98 (1.21)	1.76 (089)	1.94 (1.35)	1.89 (1.09)

Legend: MTS, motor threshold of stimulation; STS, sensorial threshold of stimulation; LTA, left temporalis anterior; RTA, right temporalis anterior; LMM, left masseter muscle; RMM, right masseter muscle; LSM, left sternocleidomastoi muscle; RSM, right sternocleidomastoi muscle; LDA, left digastric anterior; RDA, right digastric anterior.

Letters refer to significant change pre-post treatment (a) or among groups (b).

Kinesiographic results showed that the vertical component of ID, as well as V/AP ratio were significantly increased after TENS, in both MTS and STS groups; significant differences were found for MTS and STS groups in comparison with control group (Table 2); no significant differences for any kinesiographic parameter was observed between MTS and STS groups.

Table 2

Kinesiographic values in the MT TENS, ST TENS and control group

	MTS TENS		STS TENS		CONTROL
	Baseline	After TENS	Baseline	After TENS	Baseline	After TENS
Verticality	1.23 (0.72)	3.03 (1.17)^a,b	1.25 (0.74)	2.94 (1.14) ^a,b	1.25 (0.79)	1.27 (1.09)
Anterior-posteriority	0.61 (0.36)	0.78 (0.51)	0.58 (0.47)	0.70 (0.38)	0.59(0.44)	0.64 (0.39)
V/AP Ratio	2.36 (1.18)	4.42 (3.06) ^a,b	2.15 (1.23)	4.20 (2.97) ^a,b	2.24 (1.18)	2.09 (1.46)

Legend: MTS, motor threshold of stimulation; STS, sensorial threshold of stimulation; V/AP, verticality – anterior-posteriority ratio.

Letters refer to significant change pre-post treatment (a) or between test (MST or SST) and control group (b).

Discussion

In the present study, the effect of two different types of TENS stimulation on the sEMG activity as well on the kinesiographic pattern of patients with TMD in remission was investigated; the results suggest that both MTS and STS are effective in reducing the activity at rest of LMM, RMM, LTA and LTA, as well in increasing the inter-occlusal distance; furthermore, no significant difference was found between MTS and STS. These findings are in agreement with those achieved by other studies [15,16,35,36]; in particular Cooper and Kleinberg [15] found that MTS application reduced the sEMG activity of masticatory muscles, as well as symptoms; however, even if the effect of MTS on sEMG values were evaluated before and immediately after the MTS application, changes in symptoms were evaluated after one and three months, during which patients underwent an additional treatment with orthosis; therefore, it is difficult to define the amount of reduction in sEMG activity as well in symptoms, that could be attributed to MTS application. Rodrigues et al. [16] evaluated the effects of TENS on sEMG activity and pain of 19 patients suffering from TMD: a significant reduction on pain level, as well on the sEMG activity of LTA and RTA, at rest, was observed; however, this study used a high intensity STS with a time of application of 45 min.; therefore, the discrepancies in the settings of TENS make impossible comparisons with our findings.

Some concerns have been claimed on the validity of the sEMG recording in the diagnosis and monitoring of TMD [2,3,37]; these concercens are mainly related to the reliability of the sEMG recording and to its reproducibility: in the present study, the reproducibility of the sEMG measurements was assessed through the protocol suggested by Castroflorio et al. [38]; accordingly, a mean ICC of 0.814 was obtained; this value is in agreement to that reported by Castroflorio et al.[38] and could be considered as indicative of an excellent reproducibility [39].

With regard to the condition of the sEMG recording, no general consensus has been reached in the literature on what condition should be the most appropriate and reliable for the reproducibility of the sEMG recording: even if clenching has been suggested to be a more reliable and standardized condition for sEMG recording, than rest position [7], it has been observed that in situations of chronic muscular pain, muscular contraction ability is reduced due to the decrease in activity of the agonist muscles and the increase in activity of the antagonist muscles [40–42]; in the present study we selected only asymptomatic patients, that were in remission from chronic pain accordingly and did not use clenching as the condition for sEMG recording, but rest position of the mandible, that has been suggested to be more reliable in asymptomatic patients [43].

To enhance the internal validity of the study and to obtain an homogeneous sample, we used strict and rigorous inclusion/exclusion criteria in the selection of patients, and performed a sample size calculation, which indicated that a minimum of 16 patients per group would be required; it has been reported that TMDs occur more frequently in women than man [44]: this potential confounding factor, as well as other like age, ethnicity, gender, hemispheric-dominance, missing teeth, occlusal alteration, the presence of systemic condition that could affect the activity of muscles, nervous system and joints, has been excluded to homogenize all groups under study. These strict inclusion criteria were required considering that the present was a pilot study.

The present study has an important limitation, since it was not a randomized double-blind clinical trial: the randomization process is performed to assign participants to study groups, such that the groups are balanced for known and unknown risk factor, to minimize bias; the absence of randomization may have introduced a bias into the study.

Based on the findings of the present study, the application of a single session of 60 min of STS is as effective as MTS, in reducing the sEMG activity of LTA, RTA, LMM and RMM at rest and in increasing the ID in patients with TMD in remission. However, further studies are required to assess the effect of STS, compared to MTS, on the sEMG and kinesiographic pattern of patients with symptomatic TMD.

Conclusions

Abbreviations

TMD: Temporomandibular disorder; sEMG: Surface electromyography; TENS: Transcutaneous electrical nervous stimulation; MTS: Motorial threshold of stimulation; STS: Sensorial threshold of stimulation; V/AP: Verticality/antero-posteriority; ID: Interocclusal distance; LTA: Left temporalis anterioris; RTA: Right temporalis anterioris; LMM: Left masseter muscle; RMM: Right masseter muscle; RSCM: Right sternocleidomastoid; LSCM: Lfet sternocleidomastoid; RDA: Right digastric; LDA: Left digastric.

Competing interest

The authors declare that they have no competing interests.

Author’s contributions

GM conceived the study. AM and FS collected the data. DP performed the surface electromyographic evaluation and RC performed the statistical analysis. All the authors concepted the manuscript and were involved in writing the paper. All authors read and approved the final manuscript.

Pre-publication history

The pre-publication history for this paper can be accessed here:

http://www.biomedcentral.com/1471-2474/14/168/prepub

Acknowledgments

No fund was used for the realization of the study.

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Dysregulation of the Autonomous Nervous System in Patients with Temporomandibular Disorder: A Pupillometric Study

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Published online 2012 Sep 18

Annalisa Monaco, Ruggero Cattaneo, Luca Mesin, Irma Ciarrocchi, Fabrizio Sgolastra, and Davide Pietropaoli

Abstract

The role of the autonomic nervous system (ANS) was recently investigated in Temporomandibular disorders (TMD). Several authors argue that in subjects with TMD there is a dysregulation of ANS. Recent literature support that Pupillometry is a simple non-invasive tool to study ANS. The aim of this study was to investigate the relationship between TMD and ANS activity using pupillometry recording in Infrared light at rest Mandible Position (RP); Infrared light at Forced Habitual Occlusion (FHO); Yellow-green light at RP; Yellow-green light at FHO. Forty female subjects were enrolled: 20 case patients showed TMD based on the Research Diagnostic Criteria for TMD, and 20 control patients, aged matched, had no signs or symptoms of TMD. Statistical analysis was performed on average pupil size. Ratio between pupil size in FHO and RP (FHO/RP ratio) and yellow-green and infrared (light/darkness ratio) lighting were carried out. Within group differences of pupil size and of “ratio” were analyzed using a paired t test, while differences of pupil size between groups were tested using an unpaired t test. Statistical comparisons between groups showed no significant differences of absolute values of pupil dimension in RP and FHO, both in yellow-green and in infrared lighting. In addition, there were no significant differences within groups comparing RP and FHO in yellow-green light. In within group comparison of pupil size, differences between RP and FHO were significant in infrared conditions. Control subjects increased, whereas TMD patients decreased pupil size at FHO in infrared lightening. FHO/RP ratio in darkness and light/darkness ratio in RP were significantly different between groups. Taken together, these data suggest that TMD subjects have an impairment of the sympathetic-adrenergic component of the ANS to be activated under stress. The present study provides preliminary pupillometric data confirming that adrenergic function is dysregulated in patients with TMD.

Introduction

The role of the autonomic nervous system (ANS) was recently investigated in Temporomandibular Disorders (TMD). Several authors argue that in subjects with TMD there is a dysregulation of ANS [1], [2], [3]. Such a dysregulation is in part based on genetics [4]. It implies that the patients’ enhanced sympathetic drive inhibites normal catecholamine release resulting in significant effects on peripheral target organs and functions of the ANS, which would become less efficient in adapting to the needs of environmental and physiologic demands [5].

Some authors demonstrated the influence of the sympathetic branch of ANS on the muscles and dynamics of the jaw in animals and humans [6], [7], [8], [9], [10].

The control of contraction and dilation of the pupil is due to the sympathetic nerve centers (Budge’s ciliospinalis centre) and parasympathetic centre (Edinger- Wesphal Nucleus). The first promotes the pupil dilation (mydriasis), the second the constriction (miosis) according to the light stimulation.

Pupillometry is a simple and non-invasive tool to assess the size of the pupil. It is considered a reliable tool in the study of pupil effects of drugs [11], [12], [13] and literature supports that it is a valid method to study the ANS [14].

Pupil diameter significantly correlated with heart rate variability [15] and showed its usefulness for assessing the ANS dysregulation in clinical conditions in which the ANS is involved [16], [17], [18], [19], [20], [21].

The aim of this work is to study the effect of light condition and of dental occlusion on ANS behavior through the study of the pupil in subjects with TMD. The hypothesis is that these subjects exhibit a reduced ability to adapt and are less able than control subjects to modify the response of the pupil to activation induced by occlusal and light variations.

Materials and Methods

Subjects

Inclusion/Exclusion Criteria

20 patients that fulfilled the following criteria were included in the study: age less than 30 years; female gender; presence of complete permanent dentition, with the possible exception of the third molars; normal occlusion; and diagnosis of unilateral arthrogenous TMD, based on the Research Diagnostic Criteria for TMD (RDC/TMD) [22] Axis I, groups II and III in remission at least from 3 months.

Patients were excluded from the study if they met one or more of the following criteria: having systemic or metabolic diseases; eye diseases or visual defects; history of local or general trauma; neurological or psychiatric disorders; muscular diseases; cervical pain; bruxism, diagnosed by the presence of parafunctional facets and/or anamnesis of parafunctional tooth clenching and/or grinding; pregnancy; assumption of anti-inflammatory, analgesic, anti-depressant, opioid or myorelaxant drugs; smoking; fixed or removable prostheses; fixed restorations that affected the occlusal surfaces; either previous or concurrent orthodontic or orthognathic treatment.

Control Group consisted of 20 young women scheduled for a routine checkup at University Clinic, aged matched, without signs or symptoms of TMD, who fulfilled the inclusion and exclusion criteria.

Pupillometry

Pupillometry was performed with a table-mounted infrared pupillometer (Oculus system, Inventis srl, Padova, Italy), which is composed by two infrared CCD cameras (resolution of 720×576 pixels, 256 grey levels) mounted on a light helmet (1.5 kg), with sampling frequency of 25 frame/s. To stabilize accommodation, the subjects were asked to focus their eyes on the light point into the pupillometer [23]. Assessment of pupil size was performed in light conditions, illuminating the eyes with a yellow-green led with 740 nanometer of wave-length, and under dark conditions that were obtained with an infrared diode with 880 nanometer of wave-length.

Pupillometric recordings were acquired in digital form and processed through the algorithm of Tarjan (of strongly connected components) [24] to measure frame by frame the area of pupil, expressed as number of pixels. A template was positioned on the computer screen allowing to correct the position of the eyes to avoid errors due to different positions of the pupil.

Pupillometry was performed with the subjects in horizontal supine position, on a bed for clinical examination. Room temperature (21°C) and relative humidity (50%) were maintained constant. Any external or internal source of noise was excluded. Before any pupillometric recording session, patients were invited to lie on an examining table with open eyes for at least 3 minutes, to adapt to the temperature and humidity of the room, as well to reduce the anxiety status. Then the pupillometer was applied and maintained until the end of the recording session.

Recording Procedure

The subjects underwent to 4 subsequent recordings of 30 s each:

Infrared light at Rest Mandible Position (RP);
Infrared light at Forced Habitual Occlusion (FHO);
Yellow-green light at RP;
Yellow-green light at FHO.

The sequence of tests was assigned randomly. At the end of each test, a period of 1 minute followed in which subjects were asked to stay with eyes closed. Each new acquisition started 15 seconds after the opening of the eyes.

FHO was standardized by surface electromyography (SEMG). Disposable electrodes (Duotrode, bipolar surface electrodes Ag-AgCl, 20 mm center to center distance, Myotronics-Noromed, Inc., Tukwila WA, USA) were used for SEMG recording on right and left masseter. The electrodes were connected to SEMG equipment (K7/EMG, Myotronics-Noromed, Inc., Tukwila WA, USA). A pretest established, for each subject, the value of SEMG amplitude (Averaging) corresponding to maximum voluntary clenching. During FHO tests, SEMG values were maintained with verbal instructions from the operator between 30 and 50% of the maximum voluntary clenching.

Statistical Analysis

Statistical analysis was performed using STATA 10 (StataCorp LP, College Station, TX, USA) on average pupil size, computed on 30 seconds of recording. Ratio between pupil size in FHO and RP (referred to as FHO/RP ratio in the following) and yellow-green and infrared (light/darkness ratio) lighting were carried out. Shapiro-Wilk test revealed normal distribution of data. Within group differences of pupil size and of “ratio” were analyzed using a paired t test, while differences of pupil size between groups were tested using an unpaired t test. The level of significance was set at p<0.01 for all tests. Results are expressed as mean and standard deviation.

Results

Statistical comparisons between groups showed no significant differences of absolute values of pupil dimension in RP and FHO, both in yellow-green and in infrared lighting. In addition, there were no significant differences within groups comparing RP and FHO in yellow-green light.

In within group comparison of pupil size, differences between RP and FHO were significant in infrared conditions. In particular, in Control Group, pupil had significantly larger size (p = 0.005) in FHO compared to RP, while in TMD group the size of pupil was significantly lower (p = 0.009) in FHO compared to RP (Table 1).

Table 1

Pupil size (pixels) and statistical comparisons in different conditions in two groups.

	RP in yellow–greenlight condition	FHO in yellow-greenlight condition	RP in infrared lightcondition	FHO in infrared light condition
Control Group	4835.38 (1858.24)	4712.69 (1637.35)	7680.72 (2051.01)	8225.91* (1938.80)
TMD Group	4289.51 (1543.59)	4258.83 (1583.17)	8412.75 (1956.50)	8199.52** (1956.51)
t Test	0.21	0.24	0.18	0.48

In brackets the standard deviation. * Comparison between RP and FHO condition in infrared light within Control Group: p = 0.005. ** Comparison between RP and infrared light in FHO condition within TMD Group: p = 0.009.

FHO/RP ratio did not present significant differences in yellow-green light conditions in between groups comparison, whereas in infrared light condition the comparison between groups showed a highly significant difference (p = 0.0006) with a larger ratio in Control Group (1.055) compared to TMD Group (0.967) (Table 2).

Table 2

FHO and RP ratio in Control and TMD Group.

	Yellow-green light	Infrared light
FHO/RP ratio Control Group	0.996 (0.149)	1.055 (0.073)
FHO/RP ratio TMD Group	1.002 (0.169)	0.967 (0.037)
t Test	0.46	0.0006

Statistical comparison between the two groups. Significance level at p = 0.01. In brackets the standard deviation.

Light/darkness ratio showed a high significance (p = 0.0008) in the comparison between Control Group (0.662) and TMD Group (0.486) at RP, while there was no significant difference between the two groups at FHO (Table 3).

Table 3

Light/darkness ratio at RP and FHO.

	RP	FHO
Light/Darkness ratio Control Group	0.662 (.099)	0.545 (0.345)
Light/Darkness ratio TMD Group	0.486 (0.137)	0.510 (0.375)
t Test	0.0008	0.24

Comparison between Groups. Significance level at p = 0.01. In brackets the standard deviation.

Figures 1 and and22 show box plots of the distribution of FHO/RP ratio in infrared light and light/darkness ratio at RP.

Figure 1

Box plot of FHO/RP ratio in infrared light condition.

Figure 2

Box plot of Light/Darkness ratio in rest mandible position.

Discussion

The present study provides preliminary pupillometric data confirming ANS dysregulation in TMD patients.

In particular it should be noted that: a) TMD patients show values of pupil size greater in RP infrared and lower in RP light condition than control subjects, although not statistically significant; b) under stress condition (light-FHO) TMD subjects behave differently compared to control subjects: FHO/RP ratio in darkness and light/darkness ratio in RP have significantly different behavior in the two groups. Control subjects increased, whereas TMD patients decreased pupil size at FHO in infrared lightening. In infrared conditions FHO/RP ratio is significantly greater in Control Group as well as light/darkness ratio at RP.

Pupil size in RP infrared is greater in control than in TMD group. The comparison between groups does not indicate statistical significance, probably because of dispersion of values.

On the other hand, comparison within group at infrared lighting shows that FHO pupil size of the control subjects increases significantly compared to RP, while FHO pupil size of TMD subjects decreases significantly.

Difference of pupil behavior between groups, highlighted by the ratio between the two different conditions (FHO/RP), becomes significant because in control group it is directed toward a ratio greater than 1 (1.055) for the increase of the size in FHO respect to RP, while in the TMD group it is directed toward a ratio less than 1 (0.967) for the reduction of the size in FHO compared to RP.

Homogeneous behavior of FHO/RP ratio within group was highlighted by the low standard deviation, especially in FHO infrared condition (0.0734 in control group and 0,037 in TMD group).

Similar argument can be made for RP light/darkness ratio higher in control than TMD subjects. In RP infrared, as above discussed, the pupil size is lower, although not significantly, in control compared to TMD subject (7680.72 vs 8412.75), while in RP yellow-green light the pupil size is greater in control than in TMD subjects (4835.38 vs 4289.51).

As a speculative, it can be suggested that TMD subjects show a greater activation or less inhibition of iris muscles contraction under conditions of specific stimulation (presence or absence of light) and less activation or greater inhibition of the contraction under generic stimulation (FHO).

In any case, certain degree of dysregulation would occur between the two branches of ANS, suggesting that TMD subjects could suffer from impairment to be activated under stress.

Pupil size is controlled by complex interaction between sympathetic and parasympathetic branches of ANS: the first uses mainly adrenergic, the second cholinergic pathway.

Both muscles of iris (sphincter and dilator) receive reciprocal innervations from the 2 branches of ANS providing contraction and inhibition (or relaxation).

Parasympathetic cholinergic fibers, coming from Edinger-Wesphal Nucleus, supply the iris sphincter acting for contraction of the muscle and the consequent reduction of the pupil size. At the same time, the sphincter receives beta-adrenergic innervations able to reduce the contraction inducing relaxation of the muscle [43], [44]. In humans pupil dilation obtained by beta-adrenergic inhibition of sphincter can be equal to 1/3 of the maximum physiological dilation [45].

On the other hand, iris dilator muscle receives a predominant adrenergic sympathetic motor innervation (Budge’s Cilio Spinal Center) causing contraction and the consequent increase in pupil size. Dilator muscle contraction is mediated by alpha-adrenergic receptors and inhibition or relaxation may be exercised by muscarinic receptors and, although not yet fully documented, by beta-adrenergic innervations [46], [47], [48], [49], [50].

The consequence of dysregutated balance of reciprocal innervations may lead to a deficit of inhibitory effect. Defect in beta-adrenergic or muscarinic inhibition that counteracts the action of alpha-adrenergic contraction of the dilator may result in increased pupil size in darkness; at the same time, reduction of beta-adrenergic inhibition on cholinergic system of sphincter muscle could lead to increase of miosis.

Etiology of TMD remains somewhat uncertain. Some authors have shifted the focus away from stomatognathic system and occlusion suggesting that ANS could play a crucial role in generating the main signs and symptoms of this disorder [1], [2], [3], [51].

Dysregulation of ANS and the phenomena associated with chronic cortisol secretion [25], [26] would be crucial in the pathogenesis of TMD. Causes of TMD related to type of occlusion or masticatory muscle hyperactivity did not give conclusive results. Beyond some partial results, occlusion or muscular activity cannot be surely assumed at the base of TMD. Muscles, however, could be called into question secondarily by presence of ANS dysregulation with regard to coordination of simple and complex functions [6], [7], [8], [9], [10].

On the other hand, some TMD symptoms can be reduced significantly by pharmacological therapies aimed at improving the sympathetic-adrenergic regulation. Beta-adrenergic system seems to be particularly involved. TMD patients showed lower plasma epinephrine (EPI) and norepinephrine (NE) levels than healthy subjects [5]. Moreover, several studies have demonstrated the effect of propranolol (sympatholytic non-selective beta blocker) on clinical pain severity showing linear relationship between beta-adrenergic dysregulation and pain reduction after propranolol administration in genetic subgroup of TMD patients [27], [28], [52], [53].

Taken together, these works suggest that beta-adrenergic system could be one of the key dysfunction associated with TMD pain and its therapy.

As mentioned above, beta-adrenergic receptors could have an inhibitory role on dilator and sphincter muscle. In dilator muscle beta-adrenergic and muscarinic receptors could cooperate to mediate relaxation counterbalancing pupil dilation; in sphincter muscle beta-adrenergic receptors could counterbalance pupil constriction.

Our data seem in agreement with above observations about ANS dysregulation in TMD.

Beta-adrenergic system of iris muscles in TMD patients could result in reduction or inhibition of the counterbalancing action on alpha-adrenergic pupil dilation system; the effect could be the increase of pupil size in darkness, whereas beta-adrenergic defect on cholinergic sphincter contraction, determining reduction of inhibitory effect, could result in greater miosis in yellow-green lighting. The light/darkness ratio smaller in TMD subjects compared with control group could be explained in the same way.

In control healthy group and in conditions of darkness, during which the tonus of sympathetic system prevails, occlusal stress produces a further increase of pupil size, whereas in TMD subjects occlusal “stress” fails to obtain the same sympathetic activation. TMD subjects showed within group significant reduction in pupil size. It could be interpreted as a failure of the sympathetic response to stress.

FHO can be compared to muscle exercise involving activation of the sympathetic system and a simultaneous variation of the pupil size [29], [30]. Clenching, in fact, produces sympathetic activation, partly via an increase of blood flow and pressure of the head [31], [32], [33].

Accordingly, in our work the size of pupil increases during clenching in control group showing ANS response to the increase of the demand. In subjects with TMD this phenomenon is not present. In these subjects, the size of pupil decreases. Effect of type of dental occlusion on results could be excluded by strict inclusion criteria.

On the other hand, in RP yellow-green lighting TMD subjects show more accentuated reaction compared to control subjects. TMD subjects’ pupil is smaller in light condition and is greater in darkness than controls’ one. Consequently, the RP light/darkness ratio is lower in TMD compared to control subjects. This could also be in accordance with the above-discussed deficit of beta-adrenergic inhibitory control of the iris sphincter muscle.

In general, pupil size reduction can be determined by light, parasympathomimetics substances, relaxation and convergence of the eyes. All mentioned phenomena have been checked through the experimental set up and no substances (sympathetic or parasympathomimetic) were taken by the subjects during the experimental session.

The degree of relaxation could be different in control and TMD subjects, in particular the latter may have difficulty to adapt to experimental conditions in relation to psychological characteristics described in literature [34], [35], [36].

Mood disorders, frequently related to TMD, involve dysregulation of the sympathetic system [37], [38], [39], [40], [41]. Some evidences stated that pupil diameter in the dark is not affected by anxiety but responses to light stimuli in the anxious patient had consistently lower amplitudes [42], suggesting a greater supranuclear inhibition of the parasympathetic oculomotor reflex arc in the anxious patients.

In our work we studied tonic pupil behavior in constant lightening (yellow-green and infrared) and we don’t have any direct information about pupil reflex. For this reason it’s impossible to compare our results (lower light/darkness ratio, lower FHO/RP ratio in infrared light, lower pupil size in yellow-green light, greater pupil size in darkness of TMD group) apparently in disagreement with above cited [42], [50] using light reflex. Moreover, we didn’t use psychometric scales to measure mood and psychological characteristics of subjects. We can’t exclude psychological influence on our TMD and control sample.

Our data show altered tonic adjustments of ANS in TMD patients. On the other hand, since the sequence of tests was randomized it is unlikely that the effects observed in the study are strictly related to environmental or emotional adaptation.

Of course, the interpretation of our results need more data, the sample is too small to draw definitive conclusions. Our study used pupillometry to monitor the activity of ANS without comparing pupillometric data to other data coming from signals already used in literature to study ANS (HRV, electrodermal activity, etc.). Probably, this is one reason why we can only suggest a speculative interpretation of data. Next work will be devoted to confirm what suggested interfacing various signals and sampling specific population, for example comparing TMD patients treated with beta blockade drugs with untreated.

This work can be considered a pilot study. If confirmed, it could provide a useful, rapid and noninvasive tool to test ANS behavior in TMD patients, and to monitor the response to therapy quickly and directly in dental office.

Funding Statement

These authors have no support or funding to report.

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Does orthodontic treatment provide a real functional improvement? a case control study

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2013 Oct 24

Chiara Masci, Irma Ciarrocchi, Alessandro Spadaro, Stefano Necozione, Maria Chiara Marci, and Annalisa Monaco

Abstract

Background

Electromyographic analysis of the masticatory muscles provides useful data on the behavior of these muscles during stomatognathic system functioning and allows a functional assessment of orthodontic treatments. This study was undertaken to verify if achieving an Angle Class I bite through orthodontic treatment can lead to neuromuscular balance.

Methods

This study enrolled 30 patients (20 females, 10 males, mean age: 15.78 years) with an Angle Class II, division 1 malocclusion that was orthodontically treated. A group of 30 subjects (19 females, 11 males; mean age: 16.15 years), randomly selected among subjects with an Angle Class II, division 1 malocclusion that had not been orthodontically treated served as the Control group. Both groups were subjected to electromyography to study their neuromuscular characteristics. The Shapiro-Wilk’s test revealed a non normal distribution, therefore we used a Friedman two way ANOVA by ranks test to compare differences of surface electromyography values between treated and untreated subjects at closed and open eyes condition.

Results

A statistically significant interaction between orthodontic treatment and open eyes conditions was detected for anterior temporal muscles. A significant imbalance of the anterior temporal muscles, which is indicative of an asymmetric electromyographic pattern, was also found.

Conclusions

The present data indicate that achieving a correct occlusal target does not necessarily correspond to a neuromuscular balance.

Background

The primary objective of orthodontic treatment is to achieve ideal positional relationships among the teeth within and between the arches [1–3]. Positional corrections can be made by moving the teeth and by modifying the skeletal structures and growth of the cranial and facial skeleton. An Angle’s Class I occlusion between canines and molars is considered to be the orthodontic target, in terms of both aesthetics and functionality, for patients presenting with substantial maloccusion [1,2]. The achievement of muscle balance at the end of orthodontic treatment is another very important objective often overlooked. In fact, the lack of a muscle balance could compromise the stability of the result achieved by orthodontic treatment and could require an endless use of retainers for retention [4].

In literature, several studies have investigated the achievement of a neuromuscular balance after orthodontic treatment. According to Hirata et al. [5] orthodontic treatment does not always lead to the achievement of a muscular balance, indeed they show that there is an equal prevalence of dysfunctions in patients treated orthodontically and untreated controls. Other studies have shown that patients who have undergone orthodontic treatment present more evident signs and symptoms of temporomandibular joint disorder (TMD) than subjects with malocclusion who have not been orthodontically treated [6]. Besides, recent studies suggest that it is difficult to establish a relationship between a certain type of malocclusion and TMD [7–11]. In light of the most recent literature, for the characterization of the functional aspects of the stomatognathic system, it is not sufficient to rely on the classic structural and aesthetic parameters used in orthodontics, based on cephalometric and dental class evaluations. Hence, orthodontists have in recent years started to use diagnostic instruments, such as surface electromyography (sEMG), in functional studies of the stomatognathic system [12,13]. In clinical orthodontics, electromyography has been used to evaluate the influence of occlusal conditions on the neuromuscular balance of the stomatognathic system [14–17] and to evaluate, from a functional point of view, the efficacy of orthodontic treatments [12,18–22] De Rossi et al. [12] analyzed the electromyographic activity of the masseter and temporal muscles in 27 pediatric patients (average age, 8.6 years) who were subjected to rapid maxillary expansion and found that the electromyographic activity of the examined muscles increased significantly after orthodontic treatment.

Saccucci et al. suggested that the use of a preformed functional device in subjects with Class II, division 1 malocclusion, deep bite, and labial incompetence, treated with interceptive orthodontics, induces a significant increase of the sEMG activity of the lower orbicular oris (OO) muscle at rest and of the upper OO muscle during mandibular protrusion [22].

Bothelho et al. [21] recorded the electromyographic activity of masseter and temporalis anterior muscle with the aim of assessing neuromuscular changes following orthodontic treatment, establishing that there were no statistically significant differences between the treated and no-treated subjects. Castroflorio et al. [19] assessed the effects of orthodontic functional appliance (FGB-D) on the masticatory muscles by performing sEMG in 33 young adults; they concluded that the functional appliance were effective in correcting mandibular lateral displacement. Ferrario et al. [18] attempted to quantify the influence of masticatory muscles on post-orthodontic-treatment relapses with the goal of excluding unnecessary procedures. Kecik et al. [20] compared stomatognathic changes before and after maxillary expansion treatment using a quad-helix appliance in a group of patients with a posterior cross-bite in mixed dentition, employing radiographic, clinical, and electromyographic exams. They demonstrated that diagnosis of malocclusion and assessment of results of orthodontic treatment should not be limited to clinical and cephalometric evaluations, but should also involve sEMG. sEMG allows one to formulate adequate diagnoses and prognoses and also to monitor the functional impact of orthodontic therapies over various treatment phases. There is heated discussion about the usefulness of sEMG in the study of stomatognathic system, but most reviews suggest some cautions. Indeed, sEMG’s diagnostic reliability and validity, as well as its therapeutic value, have been questioned. It is generally thought that the physiological variables that may affect the validity of sEMG are age, sex, skeletal morphology and psychological factors [23–25].

It is also important to consider the influence of the visual system on the stomatognathic system when sEMG is performed. Infact visual input play an important role in the multisensory process of postural stabilization. Ocular nuclei send fibres to the nuclei that control neck and head movements and receive afferent input from vestibular nuclei. A modification of ocular proprioception modifies head and body posture. In a study by Monaco et al. [26], electromyographic comparison between eyes closed and eyes open conditions with the mandibular in a rest position were used to show a state of neuromuscular unbalance that can affect the occlusal state of patients.

Despite the usefulness of electromyographic analyses, the neuromuscular characteristics associated with a class II, division 1 malocclusion have not been investigated using this method. Therefore, the purpose of this study was to assess the neuromuscular balance of a group of individuals with Angle class II, division 1 malocclusion who have been orthodontically treated to reach a class I molar/canine positions and overjet resolution, relative to a group of non-orthodontically-treated age- and sex-matched subjects with the same diagnosis and similar dental-skeletal characteristics as the treated group. In so doing, we sought to determine whether achievement of Angle Class I leads to a neuromuscular balance that can be verified by sEMG.

Methods

Study design

The aim of this study was to investigate if there were significant differences in sEMG values between II class malocclusion treated and untreated patients.

Setting and subjects

This study was carried out at the Dentistry Center of University of L’Aquila. This study was conducted in accordance with the declaration of Helsinki. The committee on ethics in science of the University of L’Aquila approved the study with the number 0018365/12. Participation in the study was voluntary and a written consent was obtained from the parents or guardians. From a total of 76 patients who had completed orthodontic treatment at least one year prior to the study 30 (males, n = 10; females, n = 20 mean age: 15.78 years) who met the following clinical and cephalometric criteria, based on clinical evaluation and cranial radiography (latero-lateral projection) were selected. Patients were selected according to the following inclusion criteria: molar and canine class I, 0 < overjet <4 mm, absence of facial-skeletal asymmetry, absence of tooth rotation and ANB angle within 0–4° with Fh^1 = 110° ± 4, FMA = 25 ± 10, and IMPA = 90 ± 4 (Figure 1). The exclusion criteria applied to both groups were: (1) presence of carious teeth; (2) presence of dental restorations that might alter dimensions, shape, and position of the mid-point of the clinical crown; (3) presence of prosthetic crowns or gingival defects; (4) missing teeth; (5) periodontal disease; (6) presence of marked crowding or spacing; (7) presence of a unilateral or bilateral cross-bite; (8) clinical signs or symptoms of temporomandibular clinical dysfunction; (9) trauma in the dental-facial region; (10) skeletal asymmetry; (11) genetic or congenital anomalies; (11) systemic diseases that may negatively affect growth; and (12) current or previous use of systemic drugs such as steroids. Our protocol requires the analysis of subjects with absence of visual defects [26,27].

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Figure 1

Hard-tissue landmarks used in lateral cephalometric radiographs: nasion (Na); orbitale (Or); sella (S); porion (Po); A-point (A); B-point (B); menton (Me); gonion (Go). Skeletal angular and linear measurements of lateral cephalograms: ANB = angle that provides information on the ralative positions of the jaws to each other and provides a genaral idea of the anteroposterior discrepancy of the maxillary to the mandibular apical bases. Fh^1 = angle that measures the inclination of the upper incisors with respect to the maxilla. FMA = angle that shows the type of facial growth of the subject. IMPA = angle that measures the inclination of lower incisors with respect to the jaw.

A group of 30 sex- and age-matched subjects (males, n = 11; females, n = 19 mean age: 16.15 years) with Angle class II, division 1 malocclusion who had received no orthodontic treatment acted as Control group. The mean age and sex ratios between the Control group and the Study group did not differ significantly. The two groups before treatment were statistically homogeneous in terms of their clinical and cephalometric values.

Orthodontic treatment

Study group patients included were subjected to orthopedic therapy during the growth peak to obtain a skeletal balance in the sagittal and transversal planes and to promote mandibular advancement in the sagittal plane because, in second class, this bone structure is usually retropositioned.

They were subsequently subjected to finalization with non-extraction orthodontic treatment with fixed appliances multibrackets and use of Class II elastics to achieve good alignment of the teeth and to reach Andrews’ six occlusion keys [2].

sEMG

Two electromyographic recordings were obtained for each subject while in a rest position (teeth not in contact), seated on a wooden chair with a straight back in a comfortable room. During the first recording, each subject was asked to keep his/her eyes closed. During the second recording, each subject was asked to open his/her eyes and to look straight forward, maintaining light contact between his/her lips. The participants received these instructions before commencement of recordings. The ambient light was a standard hospital illumination. The windows were obscured. A researcher observed the patient’s face to control if the children had unwanted motion, and eventually repeated the examination. The recording duration for each sEMG test was 15 seconds. Electromyographic activity was recorded with an eight-channel K7 system (Myotronic Inc.; Seattle, WA) using pre-gelled adhesive surface bipolar electrodes with an inter-electrode distance of 20 mm. The skin surface where the electrodes were applied was cleaned before placement of electrodes. Electrodes were positioned on the left and right masseter muscles (LMM, RMM) and the left and right anterior temporal muscles (LTA, RTA), as described by Castroflorio et al. [28,29], as well as on the left and right anterior digastric muscles (RDA, LDA) [30] and the left and right sternocleidomastoid muscle (LSC, RSC) bilaterally parallel to the muscular fibers and over the lower portion of the muscle according to Falla et. al [31] to avoid innervations point. A template was used to enabled the electrodes to be re-positioned in the same position when the measurements were repeated at different times or if an electrode had to be removed because of a malfunction.

Electrical signals were amplified, recorded, and digitized using software designed for clinical purposes (K7, Myotronics Inc., Seattle, WA). Root mean square (RMS) values (in μV) were used as indices of the signal amplitude.

An expert examiner, who was not informed of the purpose of the study, carried out the sEMG recordings. The data were analyzed by a second investigator, who was also uninformed about the reasons for the analysis and was blind to the group designations of the subjects.

The repeatability of the recording protocol was investigated for the test conditions, by asking the selected subjects to repeat the sEMG recording two times, with a gap of 15 min between the two recordings. The results of the first and second set of experiments showed a repeatability of measurements.

To ensure anonymity, each subject was randomly assigned an alphanumeric code. To reduce the possibility of bias, groups assignments were not revealed until the data were compared.

Statistical analysis

The average values of root mean square (RMS) of the tracks performed with closed eyes were compared with the averages of EMG performed with open eyes. Repeatability of assessments had been previously tested on a set of 30 patients with the Intraclass Correlation Coefficient (ICC), which had reported values ranging from 0.9668 (CI = 0.9404-0.9829) and 0.9886 (CI = 0.9792-0.9941). The ICC values obtained for the examined muscles shows an excellent repeatability [32].

The distribution of the electromyographic data was analysed by Shapiro-Wilk test that revealed that data were not normally distribuited. For this reason data were analyzed with a Friedman two way ANOVA by ranks test to compare differences of sEMG values between treated and untreated subjects at closed and open eyes condition. The level of significance was assumed at the value of p ≤ 0.05.

From the electromyographic data, symmetry index (SI) values were calculated as described by Humsi et al. [33], according to the formula (a – b)/(a + b), where a and b represent the values of the homologous muscles of each muscle in the compared conditions. Shapiro-Wilk test revealed that the symmetry index (SI) values were normally distributed. Therefore, a paired t-test for dependent samples was used to compare SI values in the eyes closed versus the eyes open conditions, and paired t-tests for independent samples were carried out to compare SI data within each condition (open or closed eyes). The first null hypothesis posited that pattern would not differ between the two conditions. If there were significant differences between open and closed eyes condition in SI data the null hypothesis was rejected and the alternative hypothesis that visual input affect SI would be supported.

Subsequently, we conducted paired t-tests for independent samples to compare closed and open eyes conditions between the two groups. Thus, the second null hypothesis posited that the two groups would not differ from each other in either condition, such that the SI values of the Control and Study groups behave in homogeneous way within one or in both conditions. Alternatively, if the groups’ SI values do differ from each other in one or in both conditions, the null hypothesis would be rejected, and the alternative hypothesis that orthodontic treatment affects SI would be supported. P values less than or equal to 0.05 were considered significant and indicated that the null hypotheses should be rejected in favor of the alternate predictions.

Statistical analyses were performed with SAS version 9.2 (2008; SAS Institute Inc.).

Results

Study cohort demographics

As shown in Table 1, of the mean age and sex ratios did not differ significantly between the Control and Study groups.

Table 1

Group comparisons of means (standard deviations) of demographic data

Parameter	Control group	Study group post-tx	P
Age (years)	16.15 (1.26)	15.78 (1.03)	NS
Sex	19 females, 11 males	20 females, 10 males	NS

NS, not significant (p > .05); tx, treatment.

Cephalometric data

The mean values of the cephalometric data of the two groups are compared in Table 2. The cephalometric data for the Study group before treatment were similar to the Control group data. However, significant differences were found for all parameters between the Study group after treatment dataset versus the Control group and the Study group before treatment datasets, with the exception of the comparison between pre-treatment Study group versus post-treatment Study group for overbite.

Table 2

Analysis of the effects of treatment on cephalometric data, means (standard deviations)

Parameter	V.N.	Study group pre-tx	Control group	P value: pre-tx vs. Control	Study group post-tx	P: control vs. post-tx	P: pre-tx vs. post-tx
ANB	0–4°	6.6 (1.3)	6.4 (1.2)	0.19	3.7 (0.69)	0.001	0.001
Fh^1	106–114°	115.9 (2.8)	115.2 (2.4)	0.33	108.3 (2.3)	0.001	0.001
FMA	15–35°	25.5 (2.0)	25.4 (2.5)	0.44	28.5 (2.3)	0.001	0.001
IMPA	86–94°	88.4 (2.06)	89.4 (2.34)	0.10	91.5 (1.9)	0.001	0.001
Overjet	0–4 mm	6.6 (1.3)	6.5 (1.3)	0.45	3.05 (0.91)	0.001	0.001
Overbite	0–4 mm	2.6 (1.0)	2.5 (1.1)	0.38	3.2 (1.1)	0.04	0.06

Significant p values in bold.

sEMG and SI

Friedman’s analysis showed a significant difference between orthodontic treatment and open eyes conditions for variables LTA (p = 0.0398) and RTA (p = 0.0246), while for the other variables has not been demonstrated any interaction between treatment and eyes conditions. (Table 3) (Figures 2, ,3,3, ,44 and and55).

Table 3

Significance levels of differences in sEMG values between study and control groups in investigated muscles at open eyes condition (Friedman’s test)

Muscles	Mean values control group	Mean values study group	P VALUE
LTA	3.01 ± 1.91	1.95 ± 1.4	0.0398
RTA	2.59 ± 1.39	2.05 ± 1.28	0.0246
LMM	1.48 ± 0.94	1.29 ± 0.84	0.8085
RMM	1.24 ± 0.6	1.12 ± 0.61	0.1358
LDA	1.91 ± 0.97	2.03 ± 1.14	0.2305
RDA	2.08 ± 1.22	1.9 ± 1.04	0.1956
LSC	2.18 ± 1.51	1.6 ± 1.04	0.9226
RSC	2.07 ± 1.28	1.71 ± 1.15	0.2119

Significant p values in bold.

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Figure 2

SEMG track for a patient of the treated group. RTA and LTA have an higher activation in the opening and the open eyes condition than closed eyes.See text for abbraviations. The numbers on the right of the tracks represent the RMS in microvolts for each muscle.

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Figure 3

SEMG track for a patient of the control group. No differences in sEMG activity of the muscles between open and closed condition. See text for abbraviations. The numbers on the right of the tracks represent the RMS in microvolts for each muscle.

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Figure 4

Differences of EMG value of LTA muscles between study and control groups in closed and open eyes conditions.

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Figure 5

Differences of EMG value of RTA muscles between study and control groups in closed and open eyes conditions.

None of the SI values of homologous muscles differed between the open eyes versus closed eyes conditions (Table 4) within each group. Meanwhile, only comparison between groups revealed a significant difference. That is, in the open eyes condition, the anterior temporal muscles had a higher SI value in the Study group after treatment than in the Control group. All other SI values in both conditions did not differ significantly between the groups.

Table 4

Muscle SI (standard deviation) comparisons between conditions and between groups

Group	TAMs		P	DAMs		P	SCMs		P	MMs		P
	Closed eyes	Open eyes		Closed eyes	Open eyes		Closed eyes	Open eyes		Closed eyes	Open eyes
Study, post-tx	0.18 (0.15)	0.20 (0.13)	NS	0.11(0.10)	0.12 (0.09)	NS	0.16 (0.13)	0.15 (0.14)	NS	0.17 (0.16)	0.17 (0.15)	NS
Control	0.17 (0.15)	0.14 (0.12)	NS	0.11 (0.09)	0.10 (0.08)	NS	0.17 (0.15)	0.14 (0.13)	NS	0.14 (0.11)	0.12 (0.11)	NS
P	NS	<.01	–	NS	NS	–	NS	NS	–	NS	NS	–

TAMs, Anterior temporal muscles; DAMs, Anterior digastric muscles; SCMs, Sternocleidomastoid muscles; MMs Masseter muscles.

Discussion

This study evaluated the functional balance of subjects without visual defects with class II division 1 malocclusion who had or had not been subjected to orthognatodontic treatment aimed at achieving a molar and canine Angle class I. For this aim, sEMG was conducted on four pairs of muscles (Anterior Temporalis, Masseter, Anterior Digastric, and Sternocleidomastoid) at rest. Various authors have underscored the need for functional evaluation of the stomatognathic system [12,34,35]. Conventional orthodontic treatment aims to achieve morphological and aesthetical norms based on static assessments. However, the functioning of the cranial-mandibular muscles and of the joints involved with occlusion occurs through interactions with the nervous system. Hence, it would be desirable to employ an approach that assesses functional aspects of the occlusion, unlike conventional malocclusion diagnosis techniques [36].

Several recent studies have verified the muscular features of patients subjected to orthodontic treatment and orthognatic surgery. In particular, using sEMG, Botelho et al. [21] in their cross-sectional study analyzed the neuro-muscular changes in maximum voluntary clench (MVC) that take place following orthodontic treatment comparing subjects who were undergoing orthodontic intervention with subjects who had no orthodontic intervention. In the cross-sectional study of Tartaglia et al. [37] the effects of functional orthodontic devices on muscular function was evaluated in MVC comparing orthodontic patients with healthy subjects who were not orthodontically treated. A longitudinal study of Nuño-Licona et al. [38] analyzed the electromyographic muscular patterns in MVC of 10 children with a class III malocclusion before, during, and after treatment with myofunctional appliance (the monobloc). The authors demonstrated that sEMG is a non-invasive method, extremely useful for studying functional effects of the orthodontic treatment. The longitudinal study of Van den Braber et al. [39] demonstrated that electromyography can be used to study the effects of orthognatic surgery on masticatory function in patients with mandibular retrognathism. In this study the electromyographic activity (EMG) was performed during isometric clenching and during chewing. These studies concluded that the treatments did not significantly affect electromyographic values, indicating that the treatments did not significantly alter, positively or negatively, the neuromuscular condition of the patients.

The aforementioned studies compared treated versus non-treated groups without specifying whether the subjects eyes were open or closed during testing, and thus without any analysis on the influence of visual stimulation on electromyographic data [40].

The influence of visual input on stomatognatic muscles is well known [40]. However, only a recent study [27] have shown that in healthy subjects there are no differences in the sEMG activity of anterior temporal muscles at open and closed eyes condition, while in disfunctional subjects, the sEMG activity of anterior temporal muscles is higher in open eyes condition than in closed eyes one, suggesting that sEMG testing could be employed to reveal or confirm a dysfunctional condition [26].

Furthermore, there have been a small number of studies that have used the SI [19,33,41], suggesting that symmetry in electromyographic values should be considered as an index of normal muscular function.

Therefore, this study considers the effects of visual input on the stomatognathic system (open and closed eyes conditions) and it evaluates symmetry index (SI) for testing symmetry between homologous muscles. Our results show that, treated subjects showed an increase in electromyographic values of the RTA and LTA when they transitioned from closed eyes to open eyes. Furthermore, the present data also suggest an exacerbation of asymmetry when the eyes are opened that is indicative of a worsening of neuromuscular function, at least under a rest condition [42]. Hence, we can deduce that although orthodontic treatment in subjects with class II division 1 malocclusion toward an Angle class I bite (meeting all 6 Andrews’ keys) [2] can bring an aesthetic occlusal result, it is not necessarily accompanied by a neuromuscular balance at rest. Meanwhile, these phenomena were not observed in the Control group, suggesting that the impairment in the neuromuscular balance observed in the Study group may not be strictly associated with the presence of a class II, division 1 malocclusion [43].

Our observation that subjects at rest who had been treated orthodontically for a class II, division 1 bite did not have neuromuscular balance that was on par with Control subjects supports prior suggestions that there are a large number of patients in the orthodontically treated population that continue to have neuromuscular dysfunction [44,45]. Hence, more attention should be paid to neuromuscular diagnosis in subjects who are being prepared for orthodontic treatment so that orthodontists might better understand the reasons underlying failures and relapses [46]. This suggestion is in agreement with Wang et al. [6] that patients subjected to orthodontic treatment show more signs and symptoms of TMD than untreated individuals, but is in contrast to various other studies that do not support a causative relationship between orthodontics and TMJ problems [47].

For this reason longitudinal studies are needed to clarify these issues.

The present work has limitations related to sampling and analysis in that electromyographic data were not available for Study group subjects before or during the treatment. Ideally, a study should be conducted that follows patients over several years starting from the original diagnosis, ultimately comparing data between those that received orthodontic treatment and those that did not. This type of longitudinal study is in progress in our clinic, but the results will not be available for several more years. A further limitation is related to the ongoing debate over the value of sEMG at rest. Although some authors have claimed such data do not have a sufficient signal-to-noise gain to be considered reliable, sEMG remains the only instrument available that can monitor variations in the muscles electric tone. Furthermore, previous works [48,49] have demonstrated that sEMG can be useful in the assessment of neuromuscular patterns.

Conclusion

At present, the effects of orthodontic treatment on stomatognathic system function are not well understood. sEMG allows one to delineate the neuromuscular patterns of patients, which can be used to define an appropriate orthodontic therapy that takes into consideration the balance of the stomatognathic system. Here, the sEMG activity of anterior temporalis muscles was found to be significantly higher in treated patients than untreated patients. Hence, it is our view that further studies, employing a correct research methodology, more detailed design and larger number of samples are needed to examine the effects that orthodontic treatment, by way of changing occlusion, might have on muscular and articular function. To do so, it will be necessary to use valid diagnostic instruments such as sEMG, which, through the study of patients’ electromyographic parameters, allow the effects of dental changes on the neuromuscular system to be monitored.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

All authors contributed towards the conception and design of the study and critical revision for important intellectual content. CM, IC and AS contributed with the acquisition, analysis and interpretation of data, AS and MCM contributed scientifically to the paper by performing literature searches, CM, IC and AM contributed with drafting of the manuscript. SN provided statistical support. AM contributed with the design, interpretation of data and revision of the manuscript. All authors read and approved the final manuscript.

Pre-publication history

The pre-publication history for this paper can be accessed here:

http://www.biomedcentral.com/1472-6831/13/57/prepub

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Periodontal probing of an impacted tooth recovered through a surgical-orthodontic approach: a case report

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2014 Jan 27

Maria Teresa Dinoi, Mariano Lacarbonara, Salvatore DiMartino, Annalisa Monaco, and Giuseppe Marzo

Abstract

Introduction

The aim of this work was to assess the periodontal support of a central upper incisor recovered through a surgical-orthodontic approach compared to the spontaneously erupted contralateral incisor.

Case presentation

This case study describes an 8-year-old Caucasian female with an impacted upper right central incisor. Surgical-orthodontic treatment was performed to reset the impacted dental element in the arch. Periodontal probing was performed of all sites (mesio-buccal, central-buccal, disto-buccal, mesio-palatal, central-palatal and disto-palatal) of the recovered impacted tooth and the contralateral tooth. The results were compared to determine whether the treated element showed signs of periodontal injury.

Conclusions

Most of the probing results on both her right and left incisors gave values of approximately 3mm, which were not considered pathological. Both dental elements had adequate and physiological osseous attachments.

Introduction

The eruption of permanent teeth in the arch is regulated by strict genetic control, which guides the correct formation of the various dental gems and their eruption in the arch in the expected position. Under certain anatomical conditions, trauma or infective processes involving the corresponding deciduous teeth may cause alterations of the eruptive process, preventing the tooth from appearing in the oral cavity within the physiological eruption time frame and in an ectopic position. A tooth is considered to be “impacted” when it has not appeared in the arch within the maximum time limit of its physiological eruption, its root apices are closed and, consequently, it lacks eruption ability. The incidence of dental impactions has been reported to vary between 5.6% and 18.8%, with a higher frequency in women [1]. The teeth that are most frequently impacted are the lower and upper third molars (20 to 30%), followed by the upper canines (85% with palatal dislocation), lower second premolars (0.3%), and central upper incisors (0.1%) [2–4].

Several classifications can be used to evaluate the degree of the impaction of the dental elements. These classifications are based on different factors, such as the degree of impaction (that is, total versus partial) [5], number of impacted teeth (that is, single versus multiple) [5], duration of impacted (that is, temporary versus permanent), and cause of impaction (that is, primitive versus secondary). In particular, primitive impaction is caused by intrinsic factors, such as the anatomy and tilt of the tooth, whereas secondary impaction is caused by external factors, such as cystic pathologies, supernumerary teeth, and neoformations [5]. The etiopathogenesis of dental impactions is vast. Causes of dental impaction can be divided into general, local, and structural. General causes include genetics, hypofunction or hyperfunction of the endocrine system, metabolic dysfunction, and infectious diseases [6]. Local causes may be connected to the deciduous tooth (ankylosis, premature loss, and periapical chronic phlogosis) or to the permanent tooth (radicular ankylosis, corono-radicular morphological alterations, and positional anomalies) [6]. Structural causes include maxillary hypoplasia, serious hyperdivergence, skeletal open-bite, and congenital pathologies of the maxillofacial system [6].

Several therapies are possible, including classic orthodontic treatment, combined surgical-orthodontic treatments, conservative surgery, and radical surgical treatment [6]. In the simplest cases of tooth retention, a classical orthodontic treatment should be chosen. When the impacted tooth shows location and inclination anomalies or a particular corono-radicular morphology, a combined surgical-orthodontic treatment should be chosen. When the tooth eruption is hampered by a pathological condition (a cyst or odontoma) and its position in the arch is conditioned by the removal of the obstacle, conservative surgical treatment should be selected. In the case of serious anomalies in the tooth anatomy or location, or at the patient’s request, radical surgical treatment (extraction) may be chosen. Recovering the teeth in the arch is important, to ensure that the patient will have adequate functionality and good aesthetics. It is especially important at a young age, to ensure trophism in adjacent tissues and to maintain space for aesthetic and functional reasons.

Case presentation

Here, we describe the case of an 8-year-old Caucasian girl, in the mixed dentition period. An extraoral examination did not reveal facial asymmetry. Intraoral examination showed that her dental development was age-appropriate, except for the absence of her central upper right incisor. The probable cause of the lack of eruption of her incisor was connected to a traumatic event that occurred during her childhood. As reported in her anamnesis, she fell at approximately 2 years of age. This trauma caused the impaction of her deciduous upper central right incisor, producing a delay in the formation of the corresponding permanent tooth and subsequent impaction. No pathologies or situations that may cause eruption anomalies were noted from her family or medical history.

To determine an adequate treatment plan, a panoramic radiograph of her arches and a projection teleradiograph of her cranium in the latero-lateral position were needed for cephalometric evaluations. The panoramic radiograph confirmed the suspected diagnosis; her upper right central incisor was impacted, the incisor radicular apex was closed, and the tooth was unable to erupt (Figure 1). A combined surgical-orthodontic treatment was selected, which included surgical exposure in the proximity of the impacted incisor, traction of her impacted incisor into the dental arch using an anchorage device, and a period of functional orthodontics to improve the shape of her arches.

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Figure 1

Initial panoramic radiography.

During the first session, an impression was taken with a band on her upper sixth to create a splint with an eyelet in zone 11, which was used later to apply traction to her impacted tooth. The splint was cemented (Figures 2 and and3).3). After 15 days, the upper arch was banded with pre-torque and pre-angled brackets. The first arch utilized was a 36mm (0.014-inch) nickel-titanium (Ni-Ti) round arch. Banding was performed using her deciduous teeth to ensure a better anchorage (Figure 4). Approximately 20 days after banding, surgical exposure was performed. A button was placed at her crown level and tied with an elastic wire to the eyelet of the auxiliary device to start traction, which was applied slowly, replacing the elastic wire approximately every 15 days. During the next session (15 days after surgical exposure), her stitches were removed, and the arch was replaced with a 0.016″ × 0.022″ rectangular Ni-Ti wire. In the same session, an expansion spring was fixed between her left central incisor and her lateral right incisor to make space for the settling of her central incisor (Figure 5). Approximately 60 days after exposure surgery, her tooth was visible in the arch. The contralateral tooth was correctly positioned at the start of treatment to allow a correct progression of her right incisor.

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Figure 2

Splint being cemented. Intraoral photo.

Figure 3

Splint being cemented. Occlusal intraoral photo.

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Figure 4

Banding of the upper arch.

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Figure 5

Expansion spring being positioned.

Once her incisor reached the proximity of the correct eruption position, the splint eyelet was removed, and the button was replaced with a bracket that was later directly tied to the arch (Figure 6). About 3 months after banding, the internal device was removed, and her tooth had reached its normal position (Figure 7). Once the established objectives were met, the bands were removed. The fixed treatment lasted a total of 7 months.

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Figure 6

Tooth has almost reached the correct eruption zone.

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Figure 7

Tooth has reached its physiological position.

We continued with orthodontic treatment via two Schwarz’s plates, to obtain a slow expansion of the arches and improve their shape, postponing the final alignment of dental elements to a later stage when dental development was completed (Figure 8). After treatment, a defect was visible in her smile at the gingival attachment level of her right central incisor, which was clearly more apical when compared to the contralateral tooth (Figure 9).

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Figure 8

Functional orthodontics.

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Figure 9

Final intraoral photo.

To check if there had been a loss of tooth osseous support, periodontal probing of her two central upper incisors was performed. We compared the measurements to establish whether her right incisor had received any periodontal damage during traction. With a healthy periodontium, the distance between the gingival margin and the underlying bone should not exceed 3mm. When periodontal disease develops, there is a loss in the tooth bony support that partially or totally involves the root. The resulting “periodontal pocket”, or deepening of the gingival sulcus, is defined as pathological when the loss of attachment exceeds 4 to 5mm. A graduated periodontal probe, with a 0.5mm-diameter rounded tip and a colored area extending from 3.5 to 5.5mm, was used for probing. All her teeth and all levels (mesio-buccal, center-buccal, disto-buccal, mesio-palatal, center-palatal, disto-palatal) were probed. The probe was gently inserted in the tooth-gingival sulcus, with a force of about 25 to 30g, held parallel to the apical surface, and moved along the tooth surface until resistance was encountered. The probing depth was read on the probe, using the height of the colored area with respect to the gingival margin as a reference [7–9].

The results of the probing are shown in Table 1. The probing results for her right incisor were very similar to those of her left incisor. The mesio-buccal, mesio-palatal, and center-palatal probing results were identical (3 and 4mm). The center-buccal and disto-buccal probing results of the recovered incisor were 1mm less than those of the contralateral probing. Finally, the disto-palatal probing result of the recovered tooth was 1mm greater than that of the contralateral tooth. We concluded that most of the probing values of her right and left incisors were around 3mm and were not indicated as pathological. Both dental elements had suitable and physiological osseous attachments.

Table 1

Results of periodontal probing after surgical-orthodontic treatment

	Right incisor	Left incisor
Mesio-buccal	3	3
Center-buccal	2	3
Disto-buccal	2	3
Mesio-palatal	3	3
Center-palatal	4	4
Disto-palatal	4	3

Conclusions

The aim of this work was to assess the level of osseous attachment of an impacted tooth recovered through a surgical-orthodontic approach, compared to its spontaneously erupted contralateral counterpart. After recovering the included tooth through a fixed orthodontics treatment approach, periodontal probing of the recovered and contralateral incisors was performed to determine whether the treatment had caused serious osseous damage. The orthodontically recovered tooth had adequate periodontal support that was very similar to that of the contralateral tooth. The probing results were physiological and demonstrated that no loss of osseous support had occurred. This result was due to a good surgical exposure, which was achieved as conservatively as possible. The periodontal tissues were respected throughout the treatment. Finally, the orthodontic treatment used anchorages and light and constant forces, without damaging the tractioned tooth or the adjacent teeth.

Consent

Written informed consent was obtained from the patient’s guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

MTD conceived of the study, and participated in its design and coordination and helped to draft the manuscript. ML conceived of the study, and participated in its design and coordination and helped to draft the manuscript. SDM conceived of the study, and participated in its design and coordination and helped to draft the manuscript. AM conceived of the study, and participated in its design and coordination and helped to draft the manuscript. GM conceived of the study, and participated in its design and coordination and helped to draft the manuscript. MTD, ML and SDM were involved in the writing of the manuscript, GM had the idea for the manuscript, and AM reviewed the manuscript. All authors read and approved the final manuscript.

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Unusual symptomatic inclusion cysts in a newborn: a case report

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2014 Sep 21

Roberta Marini, Nicolae Chipaila, Annalisa Monaco, Domenico Vitolo, and Gian Luca Sfasciotti

Abstract

Introduction

Dental lamina cysts are cysts that occur as white or pink small nodules, often multiple, approximately 1 to 3mm in diameter. They are typically located on the midpalatine raphe and less frequently on the maxillary and mandibular alveolar mucosa; in the latter case these can be appear to be neonatal teeth.

On microscopic examination, these lesions show a stratified squamous epithelium (two to three cell layers); it is possible to find protein, keratin and/or exfoliated epithelial cells in the lumen of the lesions.

Neonatal cysts usually show no particular symptoms. They are associated with an excellent prognosis because they regress spontaneously within a few weeks and are not associated to any complications. However, if pain, bleeding or other symptoms occur, a surgical excision is required.

Case presentation

In this paper, we present an anomalous case of symptomatic dental lamina cyst which affected a 60-day-old male Caucasian newborn. The surgical treatment was elective in this case and 6-month follow-ups were mandatory.

Conclusions

We can underline the successful predictability of the surgical approach; however, we consider that the treatment choice should take place in the light of medical history and clinical considerations, and always be evaluated on a case-by-case basis. Further studies and reviews in this field should be performed in order to suggest guidelines for clinicians, although these cases are rare.

Introduction

Many features of a baby’s mouth are unique and peculiar to this development period, such as gingival cysts, inclusion cysts and natal teeth [1–4].

In 1967, according to histogenesis and location in the oral cavity, Fromm [5] classified oral cysts as Epstein’s pearls, Bohn’s nodules and dental lamina cysts. This classification was based on their location and histology: all neonatal cysts are keratin-filled nodules but Epstein’s pearls are predominantly located along the midpalatine raphe and probably derive from residual epithelial cells arising from embryonic palatine processes. Bohn’s nodules derive from palatal salivary glands’ structures and their most common site is the palate. Dental lamina cysts occur as white or pink small nodules, often multiple, approximately 1 to 3mm in diameter. Dental lamina cysts are typically located on the midpalatine raphe and less frequently on the maxillary and mandibular alveolar mucosa; in the latter case these can appear to be neonatal teeth. It is probable that these lesions originate from remnants of the dental lamina.

This case report describes the unusual clinical presentation and management of multiple oral cysts in a newborn baby.

Case presentation

A Caucasian 60-day-old male newborn baby came to our observation. His parents complained that he had bleeding gums in his lower and upper jaws, pain in sucking and consequent difficulties in feeding. He was full-term born and his weight at birth was 2900g. His past medical history was not significant.No noticeable findings were recorded during an extraoral examination. The intraoral examination revealed multiple whitish small masses localized on the alveolar ridge of his maxilla and mandible. His mandibular alveolar ridge showed small nodular lesions in the region of the right deciduous canine and left deciduous canine and first molar (Figure 1). The size of these masses varied from 3 to 4mm in diameter.

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Figure 1

Intraoral examination of mandible.

A surgical removal of the lesions was planned in order to solve feeding problems and bleeding.

The excisions were performed in different sessions in order to limit the postoperative discomfort to the baby. All oral surgeries were performed under local anesthesia (mepivacaine 3% without adrenalin) with a 15C scalpel blade. After excision of the cysts a sponge of fibrin was used and the wounds were sutured with resorbable polyglactin suture (Vicryl 4-0; Ethicon, Johnson & Johnson, New Brunswick, New Jersey, USA) that was removed after 10 days.The first surgery involved the excision of two lesions on his left mandibular gum (Figure 2).The second surgical session was made after 15 days. The excision of his right mandibular lesions revealed a neonatal tooth. In this step the surgeon decided not to remove it because the tooth incisal margin was below the gingival level and it would not create feeding problems (Figure 3). A follow-up visit 30 days after the surgery showed the neonatal tooth eruption and a new maxillary lesion in the deciduous first molar region. A new surgical cyst excision was necessary and, in the same session, the neonatal tooth extraction was performed in order to allow the baby breastfeeding without hurting the mother (Figure 4).

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Figure 2

Excision of lesions on the left mandibular gum.

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Figure 3

Excision of lesions on the right mandibular gum.

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Figure 4

Excision of lesions on the maxillary gum.

The obtained specimens were fixed in 10% formalin solution and submitted for histological examination.Periodic recall visits were advised to verify the absence of new lesions and to monitor the developing dentition (Figure 5).All three histological examinations revealed that the characteristics of the lesions were compatible with the diagnosis of dental lamina cysts: they were lined with keratinizing, stratified squamous epithelium, developing from islands of basophilic epithelium, which were interpreted as remnants of the dental lamina (Figure 6).

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Figure 5

A clinical examination of the patient at the age of 2 years showing normal dentition.

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Figure 6

Biopsy specimen of first removed cysts: histological examination showed small islands of odontogenic epithelium (remnants of dental lamina). Hematoxylin and eosin, ×200.

Discussion

The dental lamina cyst, also known as gingival cyst of newborn, is considered a true cyst because it is lined by thin epithelium with a lumen usually filled with desquamated keratin and occasionally inflammatory cells [6,7]. These cysts can easily be wrongly diagnosed as natal teeth, especially if they are located in the newborn’s mandibular anterior ridge. They typically appear as multiple nodules along the alveolar ridge in babies. It is believed that fragments of dental lamina remain within the alveolar ridge mucosa after tooth formation and then proliferate to develop these small, keratinized cysts. However, many of them degenerate, reduce in size or are broken spontaneously in the oral cavity within 2 weeks to 5 months of postnatal life [8–11].

It is more difficult to elucidate the method of their disappearance. In a study of 32 human fetal heads from 8 to 22 weeks of fetal age, not more than 20 midpalatal raphe cysts were found in any fetus by week 14, and they did not increase in frequency with time [12]. The authors suggested that as the cysts developed, the epithelium differentiated, fused with the oral epithelium and the contents discharged. Some cysts may produce keratin, enlarge, extend to the surface and rupture during the first few months after birth [12–14].

As regards the prevalence of oral cysts in newborns, George et al. [6] in a study of 1038 newborn Indian babies, found that gingival cysts were present in 143 neonates (13.8%): 112 (10.8%) on the alveolar region, 19 (1.8%) palatally and 12 (1.2%) on both regions; moreover, in 5 cases, gingival cysts were present on the mandibular ridge. Epstein’s pearls were present in 365 newborn (35.2%), and were located in the midline within the median raphae of the hard palate in the maxilla. Bohn’s nodules were present in 492 newborn (47.4%), which were located at the junction of the hard and soft palate, adjacent to the midpalatal raphae. Fromm [5] reported cysts in 75.9% of 1367 neonates less than 48-hours old and Cataldo and Berkman [1], in a study of 209 neonates between 1 and 5 days of age, reported that the most common location for the cysts was along the median palatal raphe (65.1%) and the least common site was the mandibular alveolar mucosa (9.9%). Jorgensen et al. [7] found palatal cysts in 73% of 596 White children in the USA and alveolar cysts in 53.5%. Cetinkaya et al. [2], through an oral examination of 2021 newborn Turkish children, registered that palatally located oral mucosal cysts were the most common findings (29%).

Whereas some authors reported a female predilection [10,15], others found no gender differences [7]. Moreover, in some surveys [7,11,15] an increased incidence has been noticed in Caucasian as opposed to Negro children; our patient was a Caucasian newborn.

Donley and Nelson [3] demonstrated that oral cysts are correlated with gestational age and weight at birth. They are less frequent in preterm newborns or those with weight at birth of less than 2500g. A greater frequency of submucous cysts with less clinical prevalence or greater difficulty in clinical exploration of preterm infants could explain these differences. Our patient was a full-term baby with weight at birth of 2900g.

The particularity of this case is due to two unusual features that occur in this patient: the presence of symptoms and the different onset time of the lesions. In fact, all the cysts showed spontaneous bleeding and tenderness to palpation. In addition, during the first observation only the mandibular cysts were present; after 30 days the maxillary lesion also appeared.

The treatment options have been: no treatment and follow up, marsupialization or surgical extraction. In this case the surgical treatment was mandatory because of the inability of the baby to feed properly.

The role of histopathology in establishing the final diagnosis is not essential because the treatment was required by the symptomatology of the newborn; however, it is important to prevent any misdiagnosis, such as hemangioma, melanoma, unicystic ameloblastoma, keratinizing cystic odontogenic tumor and mucocele [16–18].

Inclusion cysts may be associated to natal or neonatal teeth like in this case. When natal or neonatal teeth interfere with feeding, have high mobility, and/or are poorly developed, there is the indication to remove them [15].

Conclusions

The present case of inclusion cysts was successfully managed by the surgical excision of the lesions and the extraction of the neonatal tooth, in order to promote the baby’s natural breastfeeding, without hurting his mother. The parents were well informed about the pathology and its implications. After surgery, both the child and his mother had no complications during feeding; normal eruption of primary teeth occurred by the 6th month. Although for this patient surgical excision of the lesions was the ideal approach, in our opinion the treatment choice must be carefully evaluated on a case-by-case basis after an adequate analysis of clinical findings. Moreover, further studies (mainly randomized controlled trials) on this topic should be performed in order to draw up guidelines for clinicians and oral surgeons, although these cases are quite rare.

Consent

Written informed consent was obtained from the patient’s parents for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

RM conceived the study and drafted the manuscript, NC and AM participated in its design and coordination, DV performed the histopathological analysis and GLS performed the surgery. All authors read and approved the final manuscript.

References

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How to maintain the oral health of a child with Wolff-Parkinson-White syndrome: a case report

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2014 Sep 30

Tsampikos Petroniatis, Eleonora Ortu, Nicola Marchili, Mario Giannoni, Giuseppe Marzo, and Annalisa Monaco

Abstract

Introduction

Wolff-Parkinson-White syndrome is one of the most important disorders of the heart conduction system. It is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles.

Case presentation

In the present report, we describe the correct oral health management of a 12-year-old Caucasian girl with Wolff-Parkinson-White syndrome.

Conclusions

We successfully undertook the dental care of a girl with Wolff-Parkinson-White syndrome, which we describe here.

Introduction

Wolff-Parkinson-White syndrome (WPWS) is a disease, described for the first time in 1930, characterized by a short PR interval associated with ventricular preexcitation manifested by a delta wave. This disease can generate symptomatic or asymptomatic arrhythmias and, in the most unfortunate cases, sudden death. Cardiac electrical activity starts in the sinus node, physiologically, located in the right atrium, propagates through the atrioventricular node and through the bundle of His into the ventricles. The atrioventricular node functions as a gate, limiting the electrical activity that reaches the ventricles. Patients with WPWS have an accessory pathway that connects the atria and ventricles, in addition to the atrioventricular node. This accessory pathway is the bundle of Kent. This accessory bundle can conduct electrical impulses much faster than atrioventricular node. This event itself is unfavorable: heart rates as fast as they occur in this disease, may develop hemodynamic problems and cardiovascular shock [1–3]. The diagnosis is made by electrocardiogram (ECG) in subjects without symptoms. Typical signs of the disease are: supraventricular tachycardia (38 percent), palpitations (22 percent), chest pain (5 percent), syncope (4 percent), atrial fibrillation (0.4 percent), sudden death (0.2 percent), and incidental findings (26 percent); data were unavailable in 4 percent. Subjects can also develop lightheadedness and/or dizziness [4,5]. The treatments of the pathology are drug therapy, radiofrequency ablation, and surgical ablation. The patients who suffer from atrial fibrillation and rapid ventricular response are treated with amiodarone or procainamide to monitor always their heart rate [6]. AV node blockers should be avoided in atrial fibrillation and atrial flutter with WPW or history of it; this includes adenosine, diltiazem, verapamil, other calcium channel blockers and beta-blockers may aggravate the syndrome by blocking the normal electrical pathway of the heart. The definitive treatment of WPW is a destruction of the abnormal electrical pathway catheter ablation radiofrequence [7]. It is very important to maintain the best oral health in these patients. There is no documented evidence in the literature. Patients with this type of pathology must be kept under control and must undergo specialized controls consistently. In addition, these patients should be able to maintain a good level of oral health. Dental procedures must be kept under antibiotic cover only when it is necessary and the use of equipment that bestow pulses of electrical stimulation (transcutaneous electrical nervous stimulation (TENS), radiofrequency scalpel, piezosurgery) is banned because it may interfere with heart rhythm [8]. Regarding procedures, such as dental calculus removal, pursued by mechanical equipment, clinicians are encouraged to ask for specialist advice from the cardiologist. The aim of this manuscript is to show how to behave in the case of WPWS in a child, in order to adopt best practices without interfering with the pathology.

Case presentation

A 12-year-old Caucasian girl was presented to our dental clinic for a dental visit. An extraoral examination did not reveal facial asymmetry. Intraoral examination showed that her dental development was age-appropriate (Figures 1, ,22 and and3).3). During the anamnestic interview, the parents of our patient referred to a light unintentional activity of rubbing of the teeth by the child during the night. Our patient was also under the care of a cardiologist for the presence of WPWS with frequent episodes of supraventricular tachycardia. The ECG (Figures 4, ,55 and and6)6) performed one month before the dental visit showed the sinoatrial rhythm with alternate conduction medium atrioventricular node and the accessory conduction pathway. For this disease, our patient was treated with flecainide acetate (30mg three times a day) and propanolol 40mg once a day. Polysomnography was also performed on the child to evaluate the presence of pediatric obstructive sleep apnea (OSA) but the result was normal. Our patient was taken under the care of dentists and hygienists to achieve good oral health. In collaboration with the cardiologist, a treatment plan was created that included:

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Figure 1

Frontal intraoral photo.

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Figure 2

Buccal intraoral right photo.

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Figure 3

Buccal intraoral left photo.

Figure 4

Electrocardiogram of the patient with Wolff-Parkinson-White syndrome.

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Figure 5

Electrocardiogram of the patient- note the characteristic delta wave, the PR interval, and the QRS complex.

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Figure 6

Electrocardiogram of the patient-sinus rhythm with alternating conduction through the atrioventricular node and the bundle side.

– periodic checks to be carried out every three months;

– sessions of oral hygiene with manual and mechanical instrumentation to be carried out at least every six months under antibiotic therapy;

– oral hygiene instructions and motivation;

– sealing of the first molars and fluoride use.

If more invasive treatments are needed in the future, they will be performed under antibiotic therapy and in collaboration with the cardiologist.

Conclusions

The aim of this case report is to show how to maintain the correct oral health in a child with WPWS. There is no evidence of this problem in the scientific literature. The paroxysmal ventricular tachycardia can have different ways of presentation: WPWS is one of these. However, it is scientifically clear that the WPWS causes tachycardia, due to the disturbance of cardiac conduction. Tachycardia is an alteration of the autonomic nervous system (an increased tone of the sympathetic nervous system) [9]. The differential diagnosis with other diseases is more important. The ECG findings in people with the WPWS pattern can be similar to ECG findings seen in other cardiac conditions: myocardial infarction, ventricular premature beats or idioventricular rhythm, bundle branch block. Finally, some cases of hypertrophic cardiomyopathy may mimic WPWS [10]. Nowadays, one of the purposes to be achieved, by dentists and hygienists, is to keep the patient as relaxed as possible, explaining the procedures that will be performed each time to avoid unnecessary fears that can speed up the heartbeat. Several other issues are also discussed, such as the importance of continual collaboration with medical colleagues, the risk-benefit of using epinephrine-containing local anesthesia for dental treatment for patients with arrhythmias, the potential risk of repeated general anesthesia in a patient with a cardiac arrhythmia, and the challenges of providing comprehensive dental treatment in a high caries-risk patient with extreme dental anxiety [11]. Arrhythmias can be also induced by compression of the neck, the carotid sinus or eyes (vagal reflex). The risk is greater in older people and in patients with coronary artery disease or aortic stenosis. Arrhythmias may occur following administration of erythromycin or azole antifungal drugs in patients taking terfenadine, astemizole, or cisapride. Syncope may be the consequence of a bradycardia, a branch block or atrial tachycardia, and it may be recognized by the slowness or irregularity of the heartbeat. Such signs are important to distinguish syncope from a simple faint, although the immediate treatment is the same. Ventricular fibrillation is clinically indistinguishable from asystole and is one of the most serious emergencies that it may be necessary to treat in a dental clinic. Some antiarrhythmic drugs can cause oral lesions. Verapamil, enalapril and diltiazem can cause gingival hyperplasia; some beta blockers can, although rarely, cause lichenoid lesions; procainamide can cause lupus-like lesions [12]. If more invasive treatments are needed, the authors suggest to treat patients always under antibiotic therapy and in collaboration with the cardiologist. It is therefore very important to always check these patients even in collaboration with other medical specialists.

Consent

Written informed consent was obtained from the patient’s parent for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Abbreviations

ECG: electrocardiogram; OSA: obstructive sleep apnea; TENS: transcutaneous electrical nervous stimulation; WPWS: Wolff-Parkinson-White syndrome.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

Our patient was under the care of AM and MG; AM and GM operated on our patient. EO analyzed and interpreted the data. EO, NM and TP wrote the manuscript. All authors reviewed and approved the final manuscript.

Acknowledgements

The authors thank all the staff of the Dental Clinic of L’Aquila. The authors thank also the MD Kefalakis Eleytherios for the cardiology consult.

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Effects of intervertebral disc disorders of low back on the mandibular kinematic: kinesiographic study

7 Luglio 2020 admin1535 Articoli scientifici No comments yet

Published online 2014 Aug 26

Alessandro Spadaro, Irma Ciarrocchi, Chiara Masci, Vincenzo Cozzolino, and Annalisa Monaco

Abstract

Background

Intervertebral disc disorders are one of the most common causes of low back pain. Neuromuscular dysfunction frequently is present in patients with lumbar disc herniation.

When considering joint dysfunction, it is important to remember that the spine functions as a unit. Dysfunction on one level can trigger compensatory changes in other spinal levels or in other areas of the musculoskeleton. Findings demonstrated the relationship between stomatognathic and postural systems justifying the hypothesis that muscular-skeletal impairment in one system could affect the other one. However, evidence that a lumbar intervertebral disc herniation could influence the mandibular kinematics is still lacking. Aim of this study was to analyse the effects that intervertebral disc herniation of low back could have on the mandibular kinematics.

Findings

Kinesiographic evaluations of the mandibular dynamics of 23 adult patients suffering L4/L5 and L5/S1 lumbosacral disc hernation were compared with a non pathological control group. A statistically significant difference of maximal mouth opening (p < .05) and of maximal mouth opening velocity (p < .03) was found comparing the study patients with the control subjects.

Conclusion

Lumbosacral disc herniation appears to be associated with changes in the activity of mandibular kinematics both in rate and quality of movement. The study suggests the existence of connections between masticatory system and lumbar disk herniation.

Background

Some Authors discussed the relationship between stomatognathic and postural systems [1, 2].

Clark et al. [3] showed co-activation of sternocleidomastoid and masseter muscles. Trigeminal electrical and mechanical stimulation elicited sternocleidomastoid inhibition showing functional coupling between mandible and neck-trunk system. Ehrlich et al. [4] supported Clark’s data stating that sternocleidomastoid, trapezius, paravertebral and rectus abdomis muscles increased from 3.3 to 7.6 times their Surface Electromyography (sEMG) resting activity during clenching [5, 6].

According to Giannakopoulos et al. [6] there is a close association between the head and neck movements.

Trigeminal nerve has numerous neuroanatomical connections within the brainstem and several projections to all levels of the spinal cord. This leads a variety of neuromuscular interactions, for instance, synchronized extension–flexion movements of the head during jaw-opening/closing cycles [7].

Head position is an important factor in determining the amount of vertical mandibular opening in healthy adults. Higbie et al. [8] stated that vertical mandibular opening ranged from 44 mm to 36.2 mm changing from extended to flexed head position. In a recent work Monaco et al. compared Osteophatic Manipulative Therapy (OMT) effects on two groups of subject affected by temporomandibular disorders (TMD): study group and no-intervention group. The study group, treated with OMT of postural system, showed a significant improvement of maximal mouth opening and maximal mouth opening velocity compared with no-intervention group indicating that manipulative treatment of no-stomathognatic areas was related to changes in the kinesiographic (KNG) activity of mandible [9].

Intervertebral disc disorders (IVDs) is one of the most common causes that lead to low back pain.

The lifetime prevalence of symptomatic herniated disks is estimated at 1% to 3% [10, 11], although anatomic evidence of disk herniation has been found in 20% to 40% of imaging tests among asymptomatic people [12, 13]. Most clinically relevant herniations occur between the ages of 30 and 50 but can also occur in adolescents and older people.

Neuromuscular dysfunction frequently is present in patients with lumbar disc herniation [14]; in patients with lumbar disc herniation, muscle strength of the trunk and knees was decreased to a similar extent [15].

When considering joint dysfunction, it is important to remember that the spine functions as a unit. Dysfunction on one level can trigger compensatory changes at other spinal levels or in other areas (leg, hip, knee, ankle) of the musculoskeleton [16].

Findings demonstrated the relationship between stomatognathic and postural systems justifying the hypothesis that muscular-skeletal impairment in one system could affect the other one.

Several authors have highlighted the importance of electromyographic and kinesiografic analysis in the assessment of Stomatognathic System and mandibular kinematics [17–22].

However, evidence that a lumbar intervertebral disc herniation could influence the mandibular kinematics is still lacking. Hence the aim of this study was to investigate the mandibular kinematics by using kinesiographic instruments in adult patients with lumbosacral disc herniations to compare these data with those of the non-pathologic control subjects. This could be a great interest for the researchers, as it could contribute to clarify the nature of the relationship between body posture and stomatognathic apparatus.

Findings

Twenty three subjects, Caucasian adults (average age 35 yrs SD, i.e. Standard Deviation, 8.6 yrs) presenting L4/5 or L5/S1 disc herniations (disk protrusion according to a morphological classification of disk herniation) [23] diagnosed by clinical and radiographical evaluation at least 6 months before testing, and an equal number of voluntary control subjects (average age 36.6 yrs SD 7.9 yrs), matched for age and sex (14 male and 9 female), with no pathology of the intervertebral disc, were included into the sample.

The patients were selected from an initial group of 65 patients with intervertebral disc herniation from the Unit of Physiatry, University of L’Aquila, based on the following criteria, which were also used to select the control subjects: (a) absence of any previous orthodontic treatment; (b) presence of full natural permanent dentition (28 teeth at least) and a bilateral molar support with molar and cusp Angle class I; (c) Normal facial type (d) absence of cross-bite, (e) absence of dental restorations that might alter dimensions, shape, and position of the mid-point of the 161 clinical crown (f) no prosthetic rehabilitation (g) absence of previous surgical treatments of the affected disc; (h) no missing teeth (with the exception of the third molars) (i) absence of periodontal problems, (l) absence of low back pain (m) lack of Temporo-mandibular joint pain (n) absence of treatment for TMD.

Exclusion criteria were (a) skeletal anomalies (b) malocclusions, (c) painful dysfunction of the cranio-cervical region (d) presence of carious teeth; (e) presence of prosthetic rehabilitation; (f) presence of a unilateral or bilateral cross-bite; (g) trauma in the dental-facial region; (h) skeletal asymmetry; (i) genetic or congenital anomalies;

Ethics approval was obtained by the University’s Review Board for Health Sciences Research involving Human Subjects, and all subjects were provided of written-informed consent before testing.

Kinesiographic equipment and measurements

Mandibular movements were recorded by the kinesiograph of the K7 Diagnostic System (Myotronics Research Inc., Seattle, WA, USA). The equipment consisted of an array of sensors placed on the subject’s head that provided information about the position of the mandible. When the mandible moved, changes in the magnetic flux of the small bar magnet fixed on the mandibular incisor teeth were detected. The kinesiograph was connected to a computerized system that recorded and displaied spatial coordinates in the vertical, antero-posterior and lateral axes to the nearest 0.1 mm. For each movement the software package indicated the amount and the velocity of the movement. The measures were in millimeter for the amount of movement and in mm/sec. for the velocity (Figures 1 and and22).

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Figure 1

Kinesiographic track showing the amount of opening movement (mm) of study group patient in the two traces (sagittal and frontal).

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Figure 2

Kinesiographic track showing the amount of opening-closing movement velocity (mm/s) of study group patient in the three traces (sagittal, frontal and velocity).

The sample rate was 125 Hz; during every single second 125 samples were collected by the kinesiograph regarding position of the magnet and velocity of its movement.

During the recordings the patient was comfortably seated in a wood chair with headrest, placed in a comfortable room, with eyes closed to avoid environmental information.

Patients were previously informed on the movements they had to do; the recording session started only when the patient understood the correct way to perform the kinesiographic tests.

In the first test the patients were asked to open the mouth as wide as possible starting from occlusal contact. The operator stopped them after the recording of 3 consecutive movements.

In the second test the subjects opened the mouth as fast and wide as possible, reaching the maximal opening position and, finally, to close the mouth returning to occlusal contact. After 15 successive movements the operator stopped the patients. Each kinesiographic trial was provided of two KNG recordings. This record allowed to obtain the following parameters:

Maximal Opening Velocity (MOV): it is the maximal velocity reached during the movement of opening starting from occlusal position (velocity = 0 mm/sec.) and ending in maximal opening position (velocity = 0 mm/sec.).

Maximal Closing Velocity (MCV): it is the maximal velocity reached during the second phase of the opening/closing movement staring from maximal opening position (velocity = 0 mm/sec.) and ending to occlusal position (velocity = 0 mm/sec.).

The opening movements were performed up before pain onset.

20 seconds passed between the two recordings.

The patient was accepted if kinesiographic values didn’t exceed 1 standard deviation (no missing patient was observed).

KNG tracks were examined by a second operator without knowledge of recording purpose.

Statistical analysis

We have calculated that 23 patients per group was sufficient to demonstrate a statistically significant difference (α = 0.05) of 5 mm in the mouth opening between the study group and the control group, with a statistical power (1-β) of 90%.

A Student’s t-test for independent samples was performed, using Stata statistics Package, on means and variance values of kinesiographic data to assess the significance of the differences in KNG activities between the study and the control group. People with lumbar disk herniation formed the study group, people without lumbar disk herniation represented the control group.

Differences with a value of p < .05 and < .005 were respectively regarded as significant and highly significant.

In null hypothesis no significant difference in means and variance shows that the two group have the same mandibular kinematics and the lumbar herniation probably doesn’t influence the characteristics of the mandible movement.

In alternative hypothesis significant difference could show that lumbar disk herniation could affect the mandible kinematics.

Table 1 shows Mean values and Standard Deviation (in parenthesis) of kinesiographic data of study and control group.

Table 1

Mean values and standard deviation (in parenthesis) of kinesiographic data of study and control group

PARAMETER (m.u.)	CONDITION	MEAN (S.D.)
MO (mm)	SG	34.77 (6,44)
	CG	41.94 (2,72)
	Diff.	.05*
MOV (mm x s⁻¹)	SG	244.8 (109,3)
	CG	321.3 (85,1)
	Diff.	.003**
MCV (mm x s⁻¹)	SG	290.0 (108,4)
MCV (mm x s⁻¹)	CG	320.0 (92,3)
	Diff.	NS

MO = Maximal Opening; MOV = Maximal Opening Velocity; MCV = Maximal Closing Velocity; m.u. = measure unit;

* = significant; ** = Highly significant; NS = Not Significant; SD = standard deviation.

In our study patients who suffered disc herniation showed both a lower amount of vertical mandible maximal opening (MO) and a lower maximal opening velocity (MOV) compared to control group.

Dysfunction on one level can trigger compensatory changes at other spinal levels or in other areas (leg, hip, knee, ankle) of the musculoskeleton [16].

In describing these relations, McAndrews [24] used the artful metaphor of a mobile hanging over a child’s crib. When one of the mobile’s strings is cut, all of its suspended ornaments start to bounce and shift erratically until achieving a new equilibrium. In this new state of equilibrium, however, the ornaments have shifted both in relation to the central axis and in relation to each other. The body’s musculoskeletal system works in much the same way. When equilibrium is disrupted, whether by injury, chronic postural stress, or other causes, structural patterns are altered to a greater or lesser degree depending onto the nature and intensity of the forces that threw off the old pattern of balance. Over time compensatory imbalances can embed themselves deeply as muscles, ligaments, cartilage, and even bone undergo changes in structure and function. The result could be a chronic musculoskeletal imbalance and pain. A key corollary of the principle of compensation is that the site of pain may not be the site of the pain’s cause. For instance, some cases of knee pain result from structural injury to the knee while others are compensations for mechanical joint dysfunction in the lumbar spine or sacroiliac joints.

A consequence of the longitudinal organization of central nervous system (CNS) is that a lesion in a lower district could influence upper levels of structural organization, by determining postural adjustments in relation to somatosensorial information changes [2, 25].

The recent findings of Monaco et al. [9] cited in the introduction supported the Irvin data showing that the established postural homeostasis with OMT resulted in improvement of mandible kinetics, in particularly in MO and in MOV [26].

One of the reasons asserted to explain results obtained on mandible Kinematics by OMT was that direct and indirect sympathetic control could affect some muscular-skeletal symptoms, including restricted range of active and passive movement or pain.

Various coupling and regulating mechanisms have been proposed to explain the homeostatic influence on physiologic processes responsible for maintaining restricted range of movement and pain [27–29]. Homeostasis may be altered through sympathetic, biochemical or neuroendocrine mechanisms affecting specifying structures or target receptors, or both.

Modulation of sympathetic tonus, enhancing healing rates, has been linked to improvement of visceral and, in the light of our study, somatic functions [30].

As claimed by osteopathic literature osteopathic lesion, responsible of movement restriction, is referred to impairment of sympathetic transmission [9]. According to this hypothesis manipulative treatment enhancing balance in sympathetic nervous system could improve movement restriction.

Somatomotor system and sympathetic nervous system (SNS) are intimately correlated. SNS supplies motor performance by modifying vegetative function parameters to meet the varying metabolic requirements of the active muscle [31, 32]. Increase in SNS outflow affects motor function through actions exerted at the muscle level.

Passatore et al. [31] stated that sympathetic nervous system controls both muscle blood flow and intracellular contractile mechanism and may affect motor function by modulating afferent activity from muscle spindles that are highly concentrated in jaw-closing muscles. In his study the electrical stimulation of rat sympathetic superior ganglion (SSG) cause an impairment of jaw jerk reflex.

Recent immunohistochemical data on masseter muscle confirmed the presence of non vascular sympathetic innervation on muscle spindles in close association with intrafusal muscle fibers [33]. These data support Passatore data and suggest that sympathetic nervous system could modulate the spindle afferent discharge by altering intrafusal fiber mechanics [33]. Increase in SNS outflow may act by: 1. decreasing muscle blood perfusion, which is an inseparable factor of muscle pain; 2. enhancing contractile force in fast-contracting muscle, while exerting a fatiguing action on slow-contracting ones; 3. reducing the quality of proprioceptive information. The latter action is likely to worsen different aspects of motor control increasing of co-contraction of antagonist muscles aimed at recovering movement precision by increasing joint stiffness. This effect has been studied in “in vitro” and “in vivo” and seems to be particularly powerful in jaw closing muscles [34].

Koolstra et al. [35] demonstrated in open jaw movement the passive forces produced by the jaw-closing muscles were remarkably stronger than those produced by the jaw-opening muscles in close jaw movement.

The foregoing statements could explain the findings of our study on MO and MOV. First of all the different but impaired mandible kinematics showed by people suffering IDVs compare to control group clearly confirmed the functional and the dysfunctional relationship among different part of the body quoted in literature, even when the two part aren’t contiguous like low-back and mandible are. It’s possible that only the connectivity of Nervous System could explain this relationship.

On the other end considering the stronger resistance exerted by closing jaw muscles (masseter, anterior temporalis and medial pterygoid) on opening movement it is possible that the effect of hyperactivity of Sympathetic Nervous System could be remarkably higher in these muscles. In this case the most influenced movement of the mandible would be the opening movement in which, according to co-activation of closing and opening muscles, closing muscles resist to the movement. Our data on MO and MOV, maximal opening movement and maximal velocity of opening movement, could confirm previous cited findings.

A limit of our work is that this is a cross sectional study, so it is not defined the actual timing of the problems. Ideally, a study should be conducted following patients over several years, investigating patients before low back problems and during their disease and treatment. This type of longitudinal study is in progress in our clinic, but the results will not be available for several more years.

Conclusions

This preliminary study compared Kinesiographic data of patients affected by Intervertebral disc herniation with those of control subjects. The patients showed a significant reduction of maximal mouth opening and maximal opening velocity compared with the control group.

Findings in our study allow hypothesising active and direct involvement of sympathetic nervous system on stomatognathic kinematics. Considering the close anatomical relation between sympathetic cervical system, which supplies facial and cranial districts, and cervical spine and, through it, head, neck and trunk posture, it is possible to suggest the critical role in relate stomatognathic and postural system performed by sympathetic nervous system.

Future investigation will be aimed at evaluating these variables in a longitudinal model and to evaluate them before and after the disc herniation resolution in order to clarify the mechanism at work.

Acknowledgements

We wish to acknowledge Dr. Ruggero Cattaneo for his important contribution on the study design and Dr. Stefano Necozione for the significant revision of statistical data.

Footnotes

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

All authors contributed towards the conception and design of the study and critical revision for important intellectual content. AS and VC contributed with the acquisition, analysis and interpretation of data, AS, IC and CM contributed scientifically to the paper by performing literature searches, CM, IC and AM contributed with drafting of the manuscript. AS provided statistical support. AM contributed with the design, interpretation of data and revision of the manuscript. All authors read and approved the final manuscript.

Contributor Information

Alessandro Spadaro, Email: ti.orebil@ela.radaps.

Irma Ciarrocchi, Email: ti.liamtoh@ihccorraic.amri.

Chiara Masci, Email: moc.liamtoh@icsamaraihc.

Vincenzo Cozzolino, Email: ude.toia@onilozzoc.oznecniv.

Annalisa Monaco, Email: ti.oohay@ocanomasilanna.

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