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Managua, Nicaragua
Sunday 7th December 2014

In this series of articles, I am investigating the impact that temporomandibular joint dysfunction (TMJD) can have on the physical & physiological wellbeing of an athlete as well as how we can manage TMJD & I am really pleased with the feedback so far & the interest that has been shown in the ideas I have been sharing.


What I will discuss in this post & the next post, is whether or not TMJD could impact the physiological ability of joints, tendons, ligaments & other collagenous structures to respond to load & recover from injury.


In the first instance, I am going to establish that a link exists between TMJD & the composition of connective tissue, which was illustrated in several studies during the early 1990’s as part of the thesis submitted by a PhD dental candidate from Sweden.


Westling (1992) investigated the collagen distribution & mitral valve function in patients with TMJD alongside a control group of normal subjects.  


Westling, L.  Temporomandibular joint dysfunction & systemic joint laxity.  Swed Dent J Suppl, 1992; 81: pp 1-79


Measuring the general joint mobility in 360 subjects, Westling compared 74 patients with craniomandibular dysfunction to 73 age/sex matched control subjects & found that there were significantly more individuals screening positive for joint hyper-mobility in the patient group than in the control group.


In those patients with craniomandibular dysfunction that did not have hyper-mobile joint scores, trauma to the head & jaw significantly correlated to the dysfunction but this was not the case for those TMJD patients who demonstrated positive scores for joint hyper-mobility.


Furthermore, the study highlighted that the patients with TMJD had significantly more musculoskeletal disorders than the other craniomandibular dysfunction patients and the control subjects.


Westling et al (1992) then compared 10 women with TMJD and general joint hyper-mobility to a group of 10 women who had no symptoms & did not demonstrate systemic laxity.


Westling, L. et al.  Temporomandibular joint dysfunction, connective tissue variations in skin biopsy & mitral valve function.  Oral Surg Oral Med Oral Pathol, 1992; 74(6): pp 709-718


The authors harvested connective tissue biopsies from the subjects’ arms & discovered that the collagen concentrations were lower, whilst the proteoglycan values were higher in the patient group compared to the control subjects.


Once again, Westling et al noted that the subjects in the patient group reported a significantly greater number of musculoskeletal complaints than the subjects in the control group.


These studies suggest that there is an association between joint hyper-mobility, abnormal skin & connective tissue characteristics (related to collagen composition) & an increased incidence of musculoskeletal disorders in various populations of subjects with TMJD.


These studies provided credence to a study conducted a few years earlier by Harinstein et al (1988), who had evaluated 40 patients with TMJD (37 admitted for TMJ reconstructive surgery & 3 outpatients) for rheumatic disease or other etiological factor that might account for the condition.


Harinstein, D. et al.  Systemic joint laxity (the hypermobile joint syndrome) is associated with temporomandibular joint dysfunction.  Arthritis Rheum, 1988; 31(10): pp 1259-1264


During the screening process, the authors noticed that many of the patients had generalised joint laxity, with 18 of the 40 satisfying the criteria for hyper-mobile joint syndrome & another 3 found to have Ehlers-Danlos syndrome or a related disorder.


Furthermore, no patient in the group demonstrated any signs of systemic inflammatory disorder or indeed any other apparent etiological factor that could be related to the TMJD.


So what these studies do suggest, is an apparent cause & effect relationship between joint laxity & TMJD.  What they do not answer is what the potential causes may be & what effects they then precipitate.


Before I delve further into the research in an attempt to establish more answers in this relationship, I want to illustrate the effects such a relationship may have on the work of performance professionals, such as physical therapists, conditioning coaches & sports medics operating in elite sport.


Without getting into the specifics of injury pathogenesis & just conducting a quick Medline search for joint hyper-mobility related to the incidence of sports-related injury, there are a few recent papers that have made a connection.


Pacey et al (2010) conducted a systematic review & meta-analysis which found a positive correlation between generalised joint hyper-mobility & the risk of lower limb joint injury, whilst Konopinski et al (2012) conducted a cohort study highlighting the subsequent increased risk of injury in a team of professional soccer players.


Pacey, V. et al.  Generalized joint hypermobility & risk of lower limb joint injury during sport:  A systematic review with meta-analysis.  Am J Sports Med, 2010; 38(7): pp 1487-1497


Konopinski, M.D. et al.  The effect of hypermobility on the incidence of injuries in elite-level professional soccer players:  A cohort study.  Am J Sports Med, 2012; 40(4):  pp 763-769


Collinge & Simmonds also looked at injury rates in a professional soccer team, comparing players with positive hyper-mobility scores with those screened as normal in relation to joint hyper-mobility.  


Whereas Kopopinski et al (2012) had found an increased incidence of injury in the players demonstrating joint hyper-mobility in comparison to those with normal joint ranges, Collinge & Simmonds reported similar injury rates between the two populations (6.2 vs 6.3 injury episodes per 1,000 hours exposure).  However, Collinge & Simmonds discovered that once injured, the subjects with joint hyper-mobility demonstrated a tendency towards missing both more competitive first team games than their “joint-normal” counterparts (12 as opposed to 5 games per season) & more training days (71 vs 31 days/season).


It must be noted that the results that Collinge & Simmonds reported were not found to be statistically significant but the trends do suggest further studies in this area are necessary.


I would also note from my experience of working with the FA Audit of Injury databases (both senior & academy cohorts) that this type of data is notoriously difficult to draw strong conclusions from given the varied exposure & number of confounding variables at play.


However, the conclusions that both Konopinski et al & Collinge & Simmonds draw in relation to introducing routine joint mobility screens & being cognisant of the potential increased time taken for players with joint hyper-mobility to satisfy progression criteria in return to play rehabilitation programmes, do stand up.


It is also worth noting, that whilst there is a place for guided screening software programmes, even the best products on the market only highlight joint hypo-mobility as an issue requiring intervention, whereas (at least when I last looked in late 2014) joint hyper-mobility is not flagged as warranting intervention.  It is worth testing this yourself if you use such systems, by inputting pathologically high joint ranges as data points & seeing how the software responds.


So now that we have highlight a cause & effect relationship between connective tissue composition, joint laxity & TMJD & then quickly underlined the fact that this is obviously an issue that sports performance professionals need to understand, in my next post, I will start to shed some light on some possible mechanisms that we need to be aware of, which will help us understand what is the root cause of the problem that needs addressing.



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