Illustration of stressed jaw joint cartilage leading to bone destruction.

Jaw Osteoarthritis: Can Mechanical Stress Cause Bone Loss?

"New research reveals how mechanical stress on jaw cartilage can trigger bone loss, offering insights into TMJ disorders and potential treatments."


Temporomandibular joint osteoarthritis (TMJ-OA) stands out as a particularly challenging subtype of temporomandibular disorders (TMD). It's characterized by the breakdown of cartilage and changes in the underlying bone. While both cartilage degeneration and bone remodeling are hallmarks of TMJ-OA, the exact sequence of these events has been a subject of debate among researchers.

During skeletal development, chondrocytes—the cells found in cartilage—secrete various cytokines that influence bone formation and remodeling. However, the mechanisms through which chondrocyte signals prompt bone resorption (the breakdown of bone tissue) remain unclear. Understanding this process could unlock new therapeutic strategies for managing TMJ-OA.

Recent research has explored whether biomechanical stimulation of chondrocytes can promote osteoclastic bone resorption in the mandibular condyle, a key area affected by TMJ-OA. By understanding how mechanical forces influence these cells, we can pave the way for more targeted interventions.

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Prevalence and Patient Impact

Temporomandibular joint osteoarthritis (TMJOA) is a chronic degenerative disease and one of the most severe forms of temporomandibular disorder, with an estimated global prevalence of approximately 2% to 16%. The National Institute of Dental and Craniofacial Research states that temporomandibular disorders can cause ongoing or repeated pain and difficulty moving the jaw. In the United States, 21.6% of adults aged 18 and older had diagnosed arthritis in 2022, and osteoarthritis was the primary diagnosis in 9.9 million office-based physician visits in the cited national data.

Current Treatment Approach

TMDs include myofascial pain, internal derangement, and degenerative joint diseases such as osteoarthritis; common symptoms include jaw pain, clicking, restricted movement, and headaches. One review describes TMJ osteoarthritis as associated with disc dislocation, trauma, functional overburden, and developmental anomalies. In a three-month study of patients with symptoms in one TMJ, arthrocentesis combined with a splint produced a good outcome in 80% of patients, although this evidence represents a limited treatment period and patient group.

A Long-Recognized Joint Disorder

The TMJ consists of matching hinges on the right and left sides of the jaw that provide rotational and sliding movements for chewing and speech. Historical accounts cited by one source trace TMJ-related problems to ancient civilizations, where skeletal remains showed jaw abnormalities and dental wear. Ancient Egyptian and Greek medical texts also reportedly described remedies for jaw pain, indicating that jaw-related ailments have been recognized for millennia.

The Link Between Mechanical Stress and Bone Resorption

Illustration of stressed jaw joint cartilage leading to bone destruction.

A new study published in the Archives of Oral Biology (Kuang, Zeng, & Qin, 2019) aimed to determine whether biomechanically stimulated chondrocytes promote osteoclastic bone resorption in the mandibular condyle. The researchers subjected primary chondrocytes isolated from rat condylar cartilage to fluid flow shear stress (FSS) at varying intensities and durations. They then assessed the levels of pro-osteoclastic factors and the overall osteoclastic function.

The study also examined rats with abnormal molar occlusion to assess the relationship between cartilage degeneration and osteoclastogenesis (the formation of osteoclasts, which are responsible for bone resorption) in the subchondral bone of the mandibular condyle. Additionally, they evaluated the expression of pro-osteoclastic factors in condylar cartilage.

  • Increased Pro-Osteoclastic Factors: The study found that the mRNA and protein levels of SDF-1 and TGFβ-1 significantly increased in all FSS-treated groups. RANKL levels and the RANKL:OPG ratio also increased across all intensities and in longer durations of FSS (60 and 120 minutes). Wnt5A levels increased at all time points and in groups treated with higher FSS intensities (20 and 30 dynes/cm²).
  • Correlation with Cartilage Degeneration: The percent area of degenerative cartilage changes was positively correlated with osteoclast number and osteoclast surface/bone surface in the mandibular condyles of rats with abnormal occlusion.
  • Increased Expression in Abnormal Occlusion: Abnormal occlusion led to increased immune-positive areas and elevated mRNA expression levels of Sdf1, Tgfb1, Rankl, Wnt5a, and the RANKL:OPG ratio in rat condylar cartilage.
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Mechanical Stress and Bone Loss

Recent research reports that mechanical stimulation of condylar chondrocytes can increase expression of pro-osteoclastic factors. These factors may encourage osteoclastogenesis and contribute to resorption of the condylar subchondral bone. The same research context notes that interleukin-1 beta in subchondral bone can promote catabolism of the overlying cartilage, while a separate study investigated whether low fluid shear stress of 2 dyn/cm² or less protects chondrocytes from IL-1β-induced apoptosis.

Imaging Osteoclast Activity

A mouse-model study evaluated 64Cu-RGD and microPET/CT as imaging biomarkers for osteoclast number. Its analysis found that 64Cu-RGD bone uptake correlated with osteoclast number and could be quantified as standardized uptake values in leg bones. The finding supports comparison of osteoclast regulation through a measurable imaging signal, although the reported analysis concerned mouse leg bones rather than the human TMJ.

These results indicate that chondrocytes under mechanical stimulation can express higher levels of pro-osteoclastic factors, inducing condylar subchondral bone resorption by promoting osteoclastogenesis.

Implications and Future Directions

This research highlights the critical role of chondrocyte signaling in osteoclastic bone resorption within the mandibular condyle. The finding that mechanical stimulation can induce the expression of pro-osteoclastic factors by chondrocytes opens new avenues for therapeutic intervention in TMJ-OA. Future studies could focus on developing targeted therapies to modulate chondrocyte activity and prevent excessive bone resorption, ultimately improving outcomes for individuals suffering from this debilitating condition.

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An Unresolved Disease Mechanism

A narrative review of TMJ osteoarthritis summarized current and recent knowledge through a literature review. It reported that many signaling pathways have been investigated, but the etiopathogenesis of TMJOA remains unclear. This uncertainty means that observed associations between mechanical stress, cartilage changes, and subchondral bone loss do not yet establish a single complete disease mechanism.

Toward More Durable TMJ Care

One recent overview reports that degenerative TMJ arthritis involves physical breakdown of cartilage and bone, and that current treatments cannot fully reverse this structural change. Emerging care discussions emphasize disorders involving the jaw joint and its muscles, with symptoms such as pain, chewing difficulty, clicking or popping, and limited movement. These sources identify treatment advances and improved understanding as ongoing priorities, while market reports describe increasing awareness and advancing treatment methodologies.

Cartilage, Bone, and Joint Dysfunction

TMJ osteoarthritis is described as a degenerative disorder characterized by progressive cartilage breakdown, subchondral bone remodeling, and joint dysfunction. These structural changes distinguish the condition from symptoms alone and link tissue degradation with impaired joint performance. Separately, infection of the TMJ may result from direct spread from a neighboring infection or from bloodborne organisms, causing inflammation and painful, limited jaw movement.

Pain and Restricted Function

A reported advanced case of TMJ osteoarthritis illustrates the clinical challenge posed by pain, restricted jaw movement, and degenerative changes visible on imaging. Another case-study source presents TMJ arthroscopy as an approach associated with relief from jaw clicking and pain. Together, these reports show how TMJ osteoarthritis can affect both comfort and everyday jaw function, while also reflecting the difference between a clinical case report and a promotional treatment account.

About this Article -

Written with AI assistance from published research, and reviewed by the Mystum team. See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1016/j.archoralbio.2018.12.002, Alternate LINK

Title: Biomechanically Stimulated Chondrocytes Promote Osteoclastic Bone Resorption In The Mandibular Condyle

Subject: Cell Biology

Journal: Archives of Oral Biology

Publisher: Elsevier BV

Authors: Bin Kuang, Zhaobin Zeng, Qing Qin

Published: 2019-02-01

Everything You Need To Know

1

What is Temporomandibular joint osteoarthritis (TMJ-OA)?

Temporomandibular joint osteoarthritis (TMJ-OA) is a specific type of temporomandibular disorder (TMD) that involves the deterioration of cartilage and changes in the underlying bone structure within the temporomandibular joint. This condition is particularly challenging because the exact sequence of events leading to cartilage degeneration and bone remodeling has been a subject of debate. The condition is significant because it can cause pain and affect jaw function. Understanding this process can help develop new therapeutic strategies for managing TMJ-OA.

2

What role does mechanical stress play in jaw osteoarthritis?

Mechanical stress refers to the forces and pressures exerted on the cells and tissues within the jaw joint, specifically the chondrocytes in the cartilage. The research shows that biomechanical stimulation of chondrocytes, such as that caused by fluid flow shear stress (FSS), can lead to increased expression of pro-osteoclastic factors. This is important because it initiates the process of osteoclastic bone resorption, which contributes to bone loss in the mandibular condyle, a key area affected by TMJ-OA. The implications of this are that mechanical stress can directly contribute to the progression of TMJ-OA by stimulating processes that degrade bone.

3

What are chondrocytes, and how do they contribute to bone loss?

Chondrocytes are the cells found in cartilage, which secrete various cytokines that influence bone formation and remodeling. The recent research suggests that when chondrocytes are exposed to mechanical stress, they release pro-osteoclastic factors, which then promote osteoclastogenesis. These factors include SDF-1, TGFβ-1, RANKL, and Wnt5A. The significance here is that these chondrocyte signals prompt bone resorption, thus causing the bone breakdown that is a hallmark of TMJ-OA. This understanding is crucial as it shows how these cells can be targeted in future therapies to prevent bone loss.

4

What are osteoclasts, and how does osteoclastogenesis relate to jaw osteoarthritis?

Osteoclasts are cells responsible for breaking down and resorbing bone tissue. Osteoclastogenesis is the formation of these osteoclasts. The research indicates that mechanical stimulation of chondrocytes promotes osteoclastogenesis in the subchondral bone of the mandibular condyle, contributing to bone loss. The implications of this process is that bone resorption and remodeling is directly influenced by mechanical forces. This means that factors affecting chondrocytes can have a profound effect on bone health within the jaw joint, making this process a key target for therapeutic intervention.

5

What are the key findings and implications of this research?

The findings of the study are that mechanical stimulation of chondrocytes, such as via fluid flow shear stress (FSS), leads to increased expression of pro-osteoclastic factors, which then promote bone resorption in the mandibular condyle. This means that mechanical stress on the cartilage cells directly impacts the underlying bone. Future directions include developing therapies to modulate chondrocyte activity. The implications of this research are that mechanical forces play a critical role in TMJ-OA. Thus, new therapies that address chondrocyte activity could prevent bone loss and improve outcomes for individuals suffering from this debilitating condition.

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