The Adolescent TMJ: How Bruxism Leads to Disc Displacement

Temporomandibular joint (TMJ) disorders affect millions worldwide, with disc displacement causing clicking and locking being one of the most common pathologies. While these disorders can affect people of all ages, there’s a notable spike in incidence during adolescence. But why? As a TMJ specialist who has studied this phenomenon for years, I’d like to share a compelling biomechanical explanation supported by decades of research.

The Perfect Storm: Adolescent Bruxism and Vulnerable Ligaments

Adolescence represents a perfect storm for TMJ disorders. The exact mechanism underlying bruxism is yet to elucidated other than it occurs during micro arousals from deeper sleep to lighter sleep. Each arousal triggers motor activity and unfortunately adolescents have more deep sleep than adults and exhibit far more bruxism and clenching of teeth.

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Sleep and Bruxism:

Recent sleep studies have shown that adolescents with bruxism may experience on average 8-10 grinding events per hour during sleep with about a 40% maximum voluntary contraction effort. When we do the math, this equates to:

• 8-10 events × 8 hours of sleep = 64-80 events per night
• 64-80 events × 365 days = 23,360-29,200 events per year
• Over 3 years = approximately 70,000-87,600 bruxism events
• Over 6 years = approximately 140,000-175,200 bruxism events

In some patients, but not all, this repetitive strain creates a cumulative effect on the TMJ structures, particularly on the lateral collateral ligament and lateral pole of the condyle.

The Science of Ligament Deformation

Ligaments, while incredibly strong, possess viscoelastic properties that make them susceptible to what biomechanists call “creep deformation” under repetitive loading (Provenzano et al., 2001). This means that when subjected to repeated stress—even below the threshold for acute injury—ligaments gradually elongate and don’t fully return to their original length.

Solomonow’s landmark research (2004) demonstrated how this process unfolds. It begins with repetitive loading triggers an inflammatory response which then disrupts the normal collagen matrix. This trauma, if it continues, causes microstructural changes  in the ligament to accumulate and eventually, permanent laxity develops. This phenomenon has been well-documented in other joints. For instance, Panjabi’s work (2006) on spinal ligaments showed that repetitive subfailure strains lead to ligament laxity and eventual joint instability.

Critical Evidence from Imaging and Modeling Studies

The landmark work of Solberg et al. (1985) provided some of the first clear evidence identifying the lateral anterior surface of the TMJ as the primary site of damage. Their cadaver studies showed that tissue change, which they called deviation in form predominantly affected the lateral portion of the joint.

Twenty-one years later, Pérez del Palomar et al. (2006) confirmed these findings through sophisticated 3D Finite Element Model (FEM) analysis. Their groundbreaking study, “3D Finite Element Simulation of the Opening Movement of the Mandible in Healthy and Pathologic Situations,” demonstrated that:

1. In healthy TMJs, the highest stresses were located at the “lateral intermediate zone of the disc”
2. The collateral ligaments were subject to the highest loads
3. During lateral jaw movements, the ipsilateral condyle showed significantly higher stress concentrations at the lateral pole than does the contralateral condyle

Their research conclusively showed that the lateral collateral ligament experiences disproportionate stress during lateral jaw movements.

The Lateral Collateral Ligament: The Weak Link

Both Finite Element Model (FEM) analyses and cadaveric studies have confirmed that this lateral pole experiences disproportionate stress during lateral jaw movements. When repeated thousands of times, as occurs in adolescent bruxism, the lateral collateral ligament undergoes the creep deformation process described above. As this ligament gradually becomes lax, it can no longer perform its critical function: maintaining the proper relationship between the condyle and disc during movement. The disc begins to displace, typically anteriorly and medially, setting the stage for further joint degeneration.

Parallels with Other Adolescent Joint Disorders

Interestingly, this pattern of repetitive stress leading to ligament damage in adolescents is not unique to the TMJ. Osgood-Schlatter disease, which affects the knee joint in adolescents, shows remarkable similarities:

• Both conditions primarily affect adolescents during growth periods
• Both typically affect one side predominantly, though bilateral involvement is possible
• Both are associated with repetitive loading (bruxism in TMJ, running/jumping in Osgood-Schlatter)
• Both respond to similar conservative treatments (activity modification, anti-inflammatories)
• Surgical intervention is rarely needed for either condition

Clinical Implications

Understanding this pathophysiological process has important clinical implications:

• Early intervention is crucial: Identifying and managing bruxism in adolescents before ligament deformation becomes irreversible could prevent disc displacement.
• Conservative approaches matter: Night guards and biofeedback techniques to reduce bruxism can limit the repetitive loading on the lateral collateral ligament.
• Consider the biomechanics: Treatment approaches should account for the specific loading patterns and structural vulnerabilities of the adolescent TMJ.
• By recognizing the connection between adolescent bruxism and ligament deformation, especially in light of the groundbreaking research by Solberg and Pérez del Palomar, we can develop more effective strategies for preventing and treating TMJ disc displacement in this vulnerable population.

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References

• Provenzano P, et al. (2001). Nonlinear ligament viscoelasticity. Annals of Biomedical Engineering, 29(10), 908-914.
• Solomonow M. (2004). Ligaments: a source of work-related musculoskeletal disorders. Journal of Electromyography and Kinesiology, 14(1), 49-60.
• Panjabi MM. (2006). A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction. European Spine Journal, 15(5), 668-676.
• Solberg WK, et al. (1985). Temporomandibular joint pain and dysfunction: A clinical study of emotional and occlusal components. Journal of Prosthetic Dentistry, 54(8), 134-149.
• Pérez del Palomar A, et al. (2006). 3D finite element simulation of the opening movement of the mandible in healthy and pathologic situations. Journal of Biomechanical Engineering, 128(2), 242-249.
• Pérez del Palomar A, et al. (2006). Finite element analysis of the temporomandibular joint during lateral excursions of the mandible. Journal of Biomechanics, 39(12), 2153-2163.