Effect of multiple injections of botulinum toxin into painful masticatory muscles on bone density in the temporomandibular complex.

BACKGROUND: Adverse effects of masticatory muscle injections of Botulinum Toxin (Btx) have been noted in animal and, less dramatically, human studies. OBJECTIVE: Among women treated in multiple community-based private practices, to compare TMJ bone density and mandibular condylar volume between patients with myofascial TMJD receiving multiple masticatory muscle Btx treatments and similarly diagnosed women not receiving such treatment. METHODS: Cohorts consisted of women whose treatment charts indicated a diagnosis of myofascial TMJD: 35 received at least 2 Btx treatment cycles; 44 received none. Bone density at pre-specified regions of interest (ROI) was defined by grey scale values from Cone Beam CT, adjusting for a fixed density phantom included in each scan. Mean bone density and mandibular condyle volume were compared between groups. Dose-response effects were tested within the Btx-exposed group. RESULTS: The mean density of primary and secondary ROIs was similar between exposure groups, as was condylar volume. Among Btx-exposed women, increasing dose of Btx to the temporalis muscle was inversely proportional to the density of the trabecular area of the mandible body. Many Btx-exposed women received smaller doses of Btx to the masseter muscles than in most TMJD Btx clinical trials. CONCLUSION: Masticatory muscle injections of Btx failed to produce clinically significant TMJ bone-related changes. Should Btx receive regulatory approval for treatment of myofascial TMJD, a phase IV study is recommended to evaluate potential adverse effects of Btx on bone and muscle when administered at higher doses and/or for more treatment cycles.

Thermal temporal summation and decay of after-sensations in temporomandibular myofascial pain patients with and without comorbid fibromyalgia.

INTRODUCTION: Chronic myofascial temporomandibular disorders (TMD) may have multiple etiological and maintenance factors. One potential factor, central pain sensitization, was quantified here as the response to the temporal summation (TS) paradigm, and that response was compared between case and control groups. OBJECTIVES: As previous research has shown that fibromyalgia (FM) is diagnosed iñ20% of TMD patients, Aim 1 determined whether central sensitization is found preferentially in myofascial TMD cases that have orofacial pain as a regional manifestation of FM. Aim 2 determined if the report of after-sensations (AS) following TS varied depending on whether repeated stimuli were rated as increasingly painful. METHODS: One hundred sixty-eight women, 43 controls, 100 myofascial TMD-only cases, and 25 myofascial TMD + FM cases, were compared on thermal warmth and pain thresholds, thermal TS, and decay of thermal AS. All cases met Research Diagnostic Criteria for TMD; comorbid cases also met the 1990 American College of Rheumatology criteria for FM. RESULTS: Pain thresholds and TS were similar in all groups. When TS was achieved (~60%), significantly higher levels of AS were reported in the first poststimulus interval, and AS decayed more slowly over time, in myofascial TMD cases than controls. By contrast, groups showed similar AS decay patterns following steady state or decreasing responses to repetitive stimulation. CONCLUSION: In this case-control study, all myofascial TMD cases were characterized by a similar delay in the decay of AS. Thus, this indicator of central sensitization failed to suggest different pain maintenance factors in myofascial TMD cases with and without FM.

Polysomnographic investigation of sleep and respiratory parameters in women with temporomandibular pain disorders.

STUDY OBJECTIVES: Temporomandibular pain disorders (TMD) and myofascial pain were linked to increased prevalence of insomnia and obstructive sleep apnea (OSA) on clinical grounds. However, the literature lacks an accurate polysomnographic (PSG) characterization of sleep abnormalities associated with TMD, given that prior studies included small or uncontrolled samples of TMD patients. The present investigation aims to objectively evaluate measures of sleep and respiratory disturbance in a large representative sample of TMD cases in comparison with matched controls. METHODS: Sleep, respiration, and limb movements were measured using a 2-night attended PSG protocol in 170 women-124 TMD cases with myofascial pain and 46 demographically matched controls. The second night data were compared between the groups using ANCOVAs. In TMD cases, the relationship between pain ratings and sleep parameters was analyzed using multiple regressions. RESULTS: In comparison to healthy controls, TMD cased evidenced a significant increase in stage N1 sleep (12.2% ± 7.6% vs. 9.2% ± 5.0%, p = 0.03), which was only mild relative to normative values. TMD cases also demonstrated mild but significant elevations in arousals associated with all types of respiratory events (6.0/h ± 6.1 vs. 3.5/h ± 3.3 p = 0.02) and in respiratory effort related arousals (RERAs, 4.3/h ± 4.3 vs. 2.6/h ± 2.7, p = 0.02). Myofascial pain predicted a lower sleep efficiency (p = 0.01), more frequent awakenings (p = 0.04), and higher RERA index (p = 0.04) among TMD cases. CONCLUSIONS: Myofascial pain in TMD is associated with mild elevation in sleep fragmentation and increased frequency of RERA events. Further research is required to evaluate the clinical significance of these findings.

Effect of contingent electrical stimulation on masticatory muscle activity and pain in patients with a myofascial temporomandibular disorder and sleep bruxism.

AIMS: To determine whether an intervention reduces oromotor activity and masticatory muscle pain in myofascial temporomandibular disorder (M/TMD) patients with high levels of masticatory muscle activity associated with sleep bruxism. METHODS: Fourteen women with M/TMD and prior polysomnographic evidence consistent with sleep bruxism participated in a 10-week single-group pre-test/ post-test mechanistic clinical trial. A 2-week period of baseline monitoring of individually biocalibrated electromyographic (EMG) events associated with sleep bruxism was followed by 6 weeks of EMG-event-contingent treatment via an innocuous electrical pulse to the skin overlying the temporalis muscle. Treatment was discontinued during 2-week follow-up monitoring. Each night before sleep, subjects recorded their average daily pain. RESULTS: Mixed-model analysis of variance showed a reliable reduction of EMG events during contingent stimulation treatment periods, but frequency of EMG events returned to baseline levels during follow-up (linear term, P = .002; quadratic term, P = .001). In contrast, nightly pain reports failed to show any systematic changes during treatment (linear and quadratic trends, both P > .10). CONCLUSION: Spontaneous pain severity and nighttime oromotor activity vary independently over nights, even in M/TMD patients selected for relatively high levels of both characteristics.

Sleep bruxism and myofascial temporomandibular disorders: a laboratory-based polysomnographic investigation.

BACKGROUND: Many dentists believe that sleep bruxism (SB) is a pathogenic factor in myofascial temporomandibular disorder (TMD), but almost all supportive data rely on patients' self-reports rather than on direct observation. METHODS: The authors administered a structured self-report interview to determine whether a large and well-characterized sample of patients with myofascial TMD (124 women) experienced SB more often than did matched control participants (46 women). The authors then used data from a two-night laboratory-based polysomnographic (PSG) study to determine whether the case participants exhibited more SB than the control participants. RESULTS: The results of independent sample t tests and χ(2) analyses showed that, although self-reported rates of SB were significantly higher in case participants (55.3 percent) than in control participants (15.2 percent), PSG-based measures showed much lower and statistically similar rates of SB in the two groups (9.7 percent and 10.9 percent, respectively). Grinding noises were common in both case participants (59.7 percent) and control participants (78.3 percent). CONCLUSIONS: Most case participants did not exhibit SB, and the common belief that SB is a sufficient explanation for myofascial TMD should be abandoned. CLINICAL IMPLICATIONS: Although other reasons to consider treating SB may exist, misplaced concern about SB's sustaining or exacerbating a chronic myofascial TMD condition should not be used to justify SB treatment.

Dental care of patients with autoimmune vesiculobullous diseases: case reports and literature review.

Dental management of patients with autoimmune vesiculobullous disorders is complicated because of prominent involvement of oral mucosa, increased risk of oral disease, and difficulty in rendering dental care. Although these diseases are relatively uncommon, dental practitioners should be familiar with the oral sequelae of these conditions and their management. Pemphigus vulgaris, cicatricial pemphigoid, and epidermolysis bullosa represent the most common autoimmune oral vesiculobullous diseases. This case-illustrated review summarizes the pathogenesis, diagnostic features, and natural history of oral vesiculobullous disorders, placing an emphasis on the treatment and prevention of associated oral disease aimed at maintaining a healthy, functional dentition.

Cytotoxicity of liposomal alpha-tocopheryl succinate towards hamster cheek pouch carcinoma (HCPC-1) cells in culture.

There is compelling evidence for the cancer chemopreventive effects of vitamin E and related compounds. Of all the vitamin E derivatives that have been investigated to date, vitamin E acid succinate is the most effective anti-cancer agent. This report describes the preparation and testing of liposomal formulation of mono alpha-tocopheryl ester of succinic acid (alpha-TOS) for cytotoxicity against hamster cheek pouch carcinoma cell line (HCPC-1). Small unilamellar vesicles (SUV) of phosphatidylcholine incorporating 70 microM alpha-TOS were superior to alpha-TOS alone or SUV without incorporated alpha-TOS, as inducers of apoptosis in HCPC-1 cells. Liposomal alpha-TOS perturbed the lipid structure in cells, promoted apoptosis, and decreased cell viability. The mechanism of action of alpha-TOS appears to involve membrane damage and induction of ceramide mediated apoptosis.

Structural and functional injury in minipig salivary glands following fractionated exposure to 70 Gy of ionizing radiation: an animal model for human radiation-induced salivary gland injury.

This study explored the feasibility of developing an animal model for radiation-induced salivary gland injury with a radiation protocol identical to current clinical practice. Three male Hanford minipigs were subjected to fractionated daily irradiation with a total dose of 70 Gy; structural and functional measures were compared with those of a control group of minipigs. We found that irradiated submandibular and parotid glands were one-third to one-half the gross size of control glands. Whereas no pathologic changes were noted in control glands, irradiated glands consistently demonstrated significant parenchymal loss with extensive acinar atrophy and interstitial fibrosis, enlarged nuclei in remaining acinar cells, and ductal dilatation and proliferation. Stimulated salivary flow was reduced by 81% in irradiated animals compared with preirradiation flow (P <.001); salivary flow in the control group increased by 30% during the same period (P <.001). The observed radiation-induced structural and functional salivary gland changes are comparable in every respect to those observed following irradiation of human salivary glands.

Multiple intraoral melanoacanthomas: a case report with unusual findings.

Melanoacanthoma is a rare, benign, mucocutaneous pigmented lesion characterized by colonization of acanthotic epithelium by dendritic melanocytes.(1,2) The most common intraoral sites are the buccal(3,4) and masticatory mucosa subject to chronic irritation.(1,5) The pathogenesis of oral melanoacanthoma remains uncertain, although its clinical behavior is suggestive of a reactive cause.(3,4,6,7) The clinical appearance of melanoacanthoma is nondiagnostic, and biopsy is mandatory.(2,3,5,6,8) The lesion, however, requires no treatment(5) and elimination of local irritants as well as periodic observation are the recommended interventions.(1,8) We describe a 39-year-old black patient with a recently reported palatal melanoacanthoma who developed additional lesions in other intraoral sites approximately 3 months after the initial lesion was biopsied. This article also documents the reactive and reversible nature of intraoral melanoacanthoma in a rare case of multiple lesions.