Systemic joint laxity (the hypermobile joint syndrome) is associated with temporomandibular joint dysfunction

Abstract

A consecutive series of 37 individuals admitted to the hospital for elective temporomandibular joint (TMJ) reconstructive surgery and 3 seen as outpatients with TMJ disease were evaluated for rheumatic disease or for another etiologic factor that might account for this problem. These 40 patients were screened by history, physical examination, and laboratory study. We soon noticed that many patients had generalized joint laxity. Eighteen of the first 40 individuals satisfied established criteria for the hypermobile joint syndrome. An additional 3 were found to have Ehlers‐Danlos syndrome or a forme fruste of this disorder. Many were markedly hypermobile and could perform a number of flexible maneuvers. Although excessive joint laxity is known to be associated with a variety of rheumatic conditions, TMJ disease has not been recognized as one of them. No patient in this series had a systemic inflammatory disorder or any other apparent etiologic factor for TMJ disease. We suggest that there is a cause‐and‐effect relationship between generalized joint laxity and TMJ disease.

Ehlers–Danlos Syndrome (EDS) focusing on oral symptoms: a questionnaire study

“…A further clinical study is needed in the future to find whether there is a general predisposition among persons with EDS to develop periodontitis without having the type VIII diagnosis. Dental problems, many as case reports, have previously been reported in the literature (7)(8)(9)(10)(11)(12)(13)(14)(15)(16). A quite common dental problem that was reported in the present study was the spontaneous fractures of the teeth.…”

Oral and mandibular manifestations in the Ehlers–Danlos syndromes

“…TMJ hypermobility and TMD have been linked to systemic joint hypermobility in several studies [Harinstein et al, ; Buckingham et al, ; Westling and Mattiasson, ; Westling, ; De Coster et al, ; Kavuncu et al, ; Hirsch et al, ] with fewer linking to hEDS [Diep et al, ]. Much like any joint in EDS, the TMJ often is hypermobile, subluxes and can dislocate [Norton and Assael, ; Wincour et al, ; Pasinato et al, ].…”

Trauma modifies strength and composition of retrodiscal tissues of the goat temporomandibular joint

“…Gage, Westling and colleagues have suggested that the level of type III collagen, the level of type I trimer, and/or the ratios of type III/type I collagen in female joint tissue create conditions of risk for the development of chronic TM pain. It is known that increased type III/type I ratios are associated with joint laxity (Westling and Mattiasson, 1991;Gage et al, 1995) and that joint laxity/hypermobility is linked to the development of osteroarthritis (Scott et al, 1979;Child, 1986) and increased risk for TM pain (Bennish and Tilds, 1979;Harinstein et al, 1988;Westling and Mattiasson, 1991;. Moreover, Gage has shown that in at least one instance, a woman with anterior displacement and pain had an elevated level of type III collagen in retrodiscal tissue (Gage et al, 1995).…”

“…It has been proposed that genetic or acute micro and/or macrotraumatic events increase 'joint laxity' due to shifts in the proportion of type III collagen, type I collagen or type I trimer within TM tissues (Gage, 1989;Gage et al, 1990Gage et al, , 1995. In some instances, joint laxity or hypermobility can be a manifestation of a form of connective tissue disease that is characterized by increased ratios of type III to type I collagen (as assessed in skin biopsy); such individuals have increased susceptibility to joint injury, osteoarthrosis (Scott et al, 1979;Child, 1986) and temporomandibular joint pain (Bennish and Tilds, 1979;Harinstein et al, 1988;Westling and Mattiasson, 1991;. In the latter group, there is anterior displacement of the intracapsular disc (Westling, 1989;Westling and Mattiasson, 1992).…”