Connective Tissue Diseases Codexery

Fibrous ankylosis

Fibrous ankylosis limits joint motion, often after trauma or infection.

Fibrous ankylosis, also called false ankylosis, is a condition of fibrous connective tissue that restricts joint movement. It most often results from physical trauma, though diseases such as tubercular arthritis or septic arthritis can also cause it. The condition was once thought to be a precursor to bony ankylosis, where bone fusion further reduces mobility.

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Signs and symptoms

Symptoms include limited motion of the affected joint, joint stiffness, and joint pain. Inflammation is also reported when the condition arises from viral diseases such as tuberculosis or from arthritis. Fibrous ankylosis can occur in the jawbone, limbs, and any other joints. Ankylosis spondylitis, which affects the spine, may lead to enthesitis (inflammation of the entheses) and, in severe cases, paralysis. Complications from inflammation can affect cardiovascular, pulmonary, or neurological health, with secondary conditions such as aortitis and breathing dysfunction reported. Temporomandibular joint (TMJ) ankylosis, a rare form, involves fusion of the mandibular condyle and the temporal bone; it can be bilateral or unilateral and reduces the ability to eat, speak, and maintain dental hygiene, potentially causing starvation and malnutrition.

Cause

Physical trauma is a prominent cause of fibrous ankylosis. After severe injury, mesenchymal stromal cells (MSCs) are activated to differentiate into osteoblasts or other cells for healing, but altered MSC function leads to improper restoration and blood leakage from the wound, forming a hematoma that stiffens the joint. Systemic diseases such as tubercular arthritis, septic arthritis, and non-infective inflammatory arthritis can also cause the condition by damaging blood vessels; MSCs then release growth factors like FGF or VEGF to induce angiogenesis, and blood escaping from capillaries creates a hematoma. Hematomas may also form after improperly performed surgery or poor wound healing. Genetic factors play a role: for ankylosing spondylitis, the HLA allele B27 increases risk. Prolonged immobilization causes blood to pool in capillaries and form hematomas.

Pathophysiology or mechanisms

The disease begins with the formation of an intra-articular hematoma, which develops gradually over months or years after physical trauma or infection. When the body attempts to heal damaged blood vessels, mesenchymal stromal cells (MSCs) differentiate into forms such as osteoblasts for bone repair or into cells that induce growth factors for capillary repair. However, due to incorrect signaling or other issues, MSCs target the area improperly, redirecting blood outside the capillaries to form a hematoma. Normally, the hematoma resolves with exercise or other methods, but if it persists, fibrous ankylosis can develop. The direct cause of MSC dysfunction remains unknown. Studies in animal models (sheep) suggest that growth factors and mechanical factors influence hematoma development through gene expression. For example, hypoxia, caused by the gene hypoxia inducing factor 1α (HIF-1α), increases hematoma severity when expression is low; it also promotes osteogenesis and suppresses adipogenesis of MSCs. Growth factors such as vascular endothelial growth factor and bone morphogenetic protein 7 help regulate MSC differentiation, and the type of ankylosis depends on which MSCs are sent and in what quantity.

Treatment or management

Early detection is necessary to avoid major complications. For inflammatory and autoimmune arthritis, NSAIDs such as aspirin, ibuprofen, Lodine, or naproxen can reduce inflammation and pain. Disease-modifying antirheumatic drugs like methotrexate, hydroxychloroquine, or sulfasalazine are recommended to slow arthritis progression before it becomes ankylosis. If symptoms progress to bony ankylosis, non-surgical treatment—including medication and exercise to strengthen joints—is optimal. For serious conditions like temporomandibular ankylosis, surgery is recommended. Options include condylectomy (removal of the condyle with jaw readjustment using pins or wires), high condylectomy (reshaping the condyle), arthroplasty (bone replacement or removal for structural improvement), and brisement force surgery (forcing the mouth open with a mouth gag, followed by jaw exercises). Brisement force is advised as soon as TMJ ankylosis is recognized.

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