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Ankylosis

Ankylosis is a pathological condition involving the abnormal stiffening and immobilization of a due to of its bony components or by fibrous , resulting in significant or complete of mobility. This condition can affect any in the body, most commonly the (TMJ), hip, knee, or spine, and manifests as pain, restricted movement, and potential deformity if untreated. Common causes include (such as fractures or dislocations), infections (local or systemic like ), inflammatory arthritides (e.g., or ), congenital anomalies, or iatrogenic factors like radiotherapy or prior surgery. Ankylosis is classified into two primary types: fibrous ankylosis, characterized by the formation of dense fibrous bridging the joint surfaces without complete bony union, often allowing minimal movement; and bony (or osseous) ankylosis, involving direct of the articular bones, leading to complete rigidity. Subtypes may further distinguish intra-articular (within the ) from extra-articular (involving surrounding structures) involvement, with severity ranging from partial limitation to total fixation. In clinical practice, diagnosis relies on clinical , (e.g., X-rays or scans showing space obliteration), and history of predisposing factors. is tailored to the type, extent, and affected , beginning with conservative measures like , anti-inflammatory medications, or splinting to prevent progression; however, advanced cases often require surgical intervention, such as gap arthroplasty, interposition grafts (e.g., costochondral), or , followed by prolonged to restore function and prevent recurrence. Early intervention is crucial to mitigate complications like facial asymmetry, (in TMJ cases), or .

Overview

Definition

Ankylosis is a medical condition characterized by the abnormal or fusion of bones within a , resulting in partial or complete immobility due to structural changes in the articular surfaces. This fusion can be fibrous or bony, distinguishing it from mere stiffness, which involves temporary or reversible limitation without permanent structural alteration such as bone-to-bone or . Unlike synostosis, which refers to a congenital or developmental osseous between bones that are normally separate, ankylosis typically arises postnatally from pathological processes and specifically affects structures. In orthopedic contexts, ankylosis primarily involves synovial joints, such as the , , or (TMJ), where the mandibular condyle may fuse with the via bony or fibrous tissue, severely restricting jaw movement. In dental contexts, it manifests as the fusion of a —through or —to the surrounding alveolar bone, leading to loss of the periodontal ligament space and impaired or eruption. The physiological impact of ankylosis includes a profound loss of in the affected , which can necessitate compensatory mechanisms, such as altered or adjacent hypermobility, potentially leading to secondary deformities over time. This immobility disrupts normal biomechanical function, though types like fibrous or bony variants are explored further in discussions.

Classification

Ankylosis is classified based on the nature of the fusion, distinguishing between true and false types. True ankylosis involves intra-articular fusion directly affecting the space, resulting from either fibrous or bony between the articular surfaces. In contrast, false ankylosis is extra-articular, arising from conditions outside the , such as muscle contractures, scarring, or coronoid process , which mimic restricted motion without actual involvement. This distinction aids in differentiating pathological changes from secondary restrictions. Within true ankylosis, further subclassification occurs by type: fibrous, bony, or mixed. Fibrous ankylosis features through soft fibrous within the , preserving some architecture while limiting mobility. Bony ankylosis, however, entails direct osseous union across the space, often leading to complete immobilization and . Mixed ankylosis combines elements of both, with partial fibrous progressing to bony fusion. These categories reflect the underlying response and influence approaches. Classification by location highlights the joint or structure affected, including general synovial like the and , the (TMJ), and dental structures. In general joints, ankylosis may involve the (e.g., leading to fixed flexion ) or (e.g., vertebral in inflammatory conditions). TMJ ankylosis is specified as unilateral (affecting one side, often causing ) or bilateral (impairing jaw opening bilaterally). Dental ankylosis occurs when the tooth root fuses with alveolar bone, more commonly affecting primary molars (leading to infraocclusion) than , where first molars are frequently involved. By extent, ankylosis is categorized as partial or complete. Partial ankylosis restricts motion to a limited range without total fixation, allowing some functional movement. Complete ankylosis, conversely, results in total immobilization of the , severely impacting . classifications include congenital versus acquired forms. Congenital ankylosis is rare and present at birth, often linked to developmental anomalies such as congenital (TMJ) ankylosis. Acquired ankylosis develops postnatally, typically from external factors like or .

Causes

Trauma

Trauma represents a primary cause of ankylosis, particularly through direct mechanical injury to joints that disrupts normal architecture and initiates aberrant processes. Common types include fractures, such as condylar fractures in the (TMJ), dislocations, and blunt force that induces formation, which can organize into fibrous or bony bridging the joint space. In the TMJ, condylar fractures are the predominant traumatic etiology, often resulting from high-impact injuries like motor vehicle accidents or falls. Trauma accounts for the majority of TMJ ankylosis cases, with studies reporting incidences ranging from 70% to 82% attributable to injury-related events. This form of ankylosis is also observed in other joints, including long bones like the and , where post-traumatic fusion can occur following severe fractures, though it is less frequent than in the TMJ. Representative examples include post-traumatic ankylosis developing after a fracture, often due to complications like non-union or leading to heterotopic bone formation. In the dental context, ankylosis frequently arises from traumatic avulsion of , where can result in fusion of the root to the alveolar bone if the periodontal is severely damaged. Excessive orthodontic force applied to teeth with prior trauma or infraocclusion can also induce iatrogenic ankylosis by causing undue pressure and resorption. Key risk factors unique to traumatic ankylosis include delayed of fractures, which allows for prolonged and hematoma organization, and inadequate , potentially leading to excessive fibrous tissue formation or . These elements exacerbate the likelihood of , particularly in pediatric patients where growth disturbances can the issue.

Infection

Infectious ankylosis arises primarily from microbial invasion of joint spaces, most commonly through , where pathogens trigger acute purulent inflammation that can progress to irreversible joint fusion. Bacterial agents predominate, with accounting for over 50% of cases in both adults and children, followed by streptococcal species and gram-negative bacilli such as . Less frequently, viral pathogens like or , and rarely fungal or mycobacterial agents, contribute, particularly in immunocompromised individuals where opportunistic infections elevate risk. The advent of antibiotics in the mid-20th century has markedly reduced the incidence of infection-related ankylosis, especially in (TMJ) cases, which were once common due to untreated infections or . The pathophysiological process begins with pathogen entry via hematogenous spread, direct inoculation, or contiguous extension from adjacent , leading to synovial invasion and rapid proliferation. This elicits an intense response, releasing cytokines, proteases, and bacterial toxins that erode articular cartilage within hours, often causing irreversible damage by 8 hours post-onset. Prolonged results in purulent , subchondral , and subsequent reparative ; in severe or untreated cases, heterotopic forms bony bridges across the , culminating in complete ankylosis. This sequence is exacerbated in children, where growth plates may contribute to more extensive . Specific manifestations include of the or , where delayed treatment can lead to fibrous or bony ankylosis, severely limiting mobility and causing . In pediatric populations, or neonatal —often due to S. aureus from umbilical infections—frequently involves the TMJ, resulting in unilateral fusion, facial asymmetry, and , as seen in cases diagnosed as early as 15 months of age. Dental ankylosis, a localized form, can stem from chronic infections like untreated periodontitis, where persistent bacterial invasion disrupts the periodontal ligament, fusing the tooth root directly to alveolar bone and impeding eruption or exfoliation. Epidemiologically, infectious ankylosis remains more prevalent in developing regions, where limited access to antibiotics and higher burdens of diseases like sustain infection rates, accounting for up to 16.8% of TMJ cases in some cohorts. Immunocompromised patients, including those with , , or on immunosuppressive therapy, face amplified susceptibility due to impaired host defenses, with fungal or atypical pathogens complicating outcomes. Overall incidence of septic arthritis precursor conditions is 2-6 per 100,000 annually, but progression to ankylosis varies with promptness of intervention.

Inflammatory and autoimmune conditions

Inflammatory and autoimmune conditions represent a major category of causes for ankylosis, where chronic immune-mediated inflammation progressively damages joint structures, leading to fibrous or bony fusion. These disorders primarily affect synovial joints through sustained synovitis, distinguishing them from acute infectious or traumatic etiologies. Ankylosing spondylitis (AS), a prototypical spondyloarthropathy, predominantly causes ankylosis in the axial skeleton, including the spine and sacroiliac joints, through enthesitis and osteoproliferation driven by chronic inflammation. In AS, the human leukocyte antigen (HLA)-B27 gene variant is strongly associated, present in up to 90% of patients in certain populations, contributing approximately 20% to disease heritability via mechanisms involving misfolded protein handling and immune dysregulation. Sacroiliac joint fusion is a hallmark, occurring in over 50% of untreated cases after 10 years, exemplifying how persistent inflammation promotes syndesmophyte formation and vertebral bridging. Rheumatoid arthritis (RA), a systemic targeting peripheral joints, leads to ankylosis less commonly than erosions, typically in small joints like the or hand due to aggressive . Chronic synovial inflammation in RA fosters formation—a hyperplastic, invasive tissue mass—that releases proteases and cytokines, eroding and subchondral , which in severe, longstanding cases (over 8-10 years) results in spontaneous bony fusion in about 2% of patients. Genetic factors, including HLA-DRB1 alleles, heighten susceptibility in autoimmune-prone individuals, with prevalence of joint damage correlating to early onset and inadequate . Psoriatic arthritis (PsA), often linked to , can induce ankylosis in both peripheral and axial joints, mimicking AS in up to 25-70% of cases with spinal involvement. Mechanisms involve T-cell driven and new bone formation alongside erosions, with pannus-like synovial proliferation contributing to , particularly in the sacroiliac joints where ankylosis can develop over time, though less frequently and severely than in AS. Like AS, PsA shows elevated prevalence in HLA-B27-positive individuals for axial disease, though skin involvement differentiates it clinically. Juvenile idiopathic arthritis (JIA), particularly the extended oligoarticular or polyarticular subtypes, frequently involves the (TMJ), with arthritis affecting 40-96% of JIA patients overall; in severe pediatric cases with chronic untreated , this can lead to and subsequent fibrous or bony ankylosis, disrupting craniofacial growth. While rare in adults (under 5% progressing to full fusion), it occurs more in autoimmune-prone youth with prolonged untreated inflammation. Across these conditions, ankylosis prevalence is higher in populations with genetic predispositions like HLA associations, emphasizing early intervention to mitigate fusion risk.

Congenital and iatrogenic causes

Congenital ankylosis is rare and typically affects the TMJ, arising from developmental anomalies such as or idiopathic intrauterine factors that result in fibrous or bony fusion at birth or early infancy, leading to restricted mouth opening and facial asymmetry if untreated. Iatrogenic causes include complications from medical interventions, such as radiotherapy for head and neck cancers, which can induce and in the TMJ; prior surgical procedures on the joint or adjacent structures; or prolonged use of cytotoxic medications that promote aberrant healing. These factors are less common but significant in patients with a treatment or multiple joint surgeries.

Pathophysiology

Mechanisms of fusion

The development of ankylosis involves a progressive biological cascade that typically begins with an acute inflammatory phase following joint insult, such as , characterized by formation, immune cell infiltration, and release of proinflammatory mediators. This initial organizes into , promoting vascularization and cellular recruitment essential for subsequent repair processes. As inflammation subsides, a fibrotic stage ensues, where fibroblasts proliferate and deposit , leading to adhesions that restrict mobility and bridge opposing articular surfaces. Transitioning from to marks the critical phase of permanent fusion, driven by where mesenchymal cells differentiate into chondrocytes and then , forming new matrix within the space. Cytokines play pivotal roles in this progression; for instance, transforming growth factor-beta (TGF-β) enhances proliferation and while suppressing osteoclastogenesis, creating an imbalance that favors net accumulation over resorption. This osteoclast- dysregulation, often with reduced osteoclast activity in later stages, perpetuates excessive mineralization and inhibits normal remodeling. In synovial joints, mechanisms include , which fills the articular cavity with fibrous or fibrocartilaginous tissue, alongside progressive degeneration that exposes subchondral to osteogenic influences. This culminates in heterotopic , where ectopic forms continuously with adjacent skeletal elements, effectively immobilizing the . These processes underscore the shift from repair to pathological bony bridging. In dental ankylosis, arises from reparative cementogenesis, where damage to the periodontal prompts cementoblast activity to deposit mineralized tissue bridging the to alveolar . The progressive ankylosis protein (), a key regulator of inorganic —a mineralization inhibitor—modulates this by transporting into the ; deficiency disrupts this balance, accelerating overgrowth and direct root-bone adhesion. Progression of these mechanisms is modulated by factors such as , with children exhibiting faster due to heightened osteogenic potential and regenerative vigor, and joint immobility, which fosters unchecked adhesions by minimizing mechanical shear that could otherwise disrupt forming tissues.

Fibrous versus bony ankylosis

Ankylosis manifests in two primary forms: fibrous and bony, distinguished by the nature of tissue involvement and the extent of joint restriction. Fibrous ankylosis involves the formation of dense or fibrous adhesions within the space, without osseous union, leading to partial limitation of movement. This type typically arises in the early or milder stages of , where scarring predominates, allowing for some preserved function compared to more severe cases. In contrast, bony ankylosis results from complete of the surfaces through new formation, often via , rendering the joint immobile and structurally rigid. This form is associated with advanced pathological processes, such as prolonged or severe , where degeneration progresses to heterotopic across the joint. Pathophysiologically, fibrous ankylosis features irregular fibrous with thickened but non-ossified , intruding into the without bridging the gap. Bony ankylosis, however, involves hypertrophic masses, osteophytes, and continuous trabecular patterns, often with a radiolucent zone in intermediate stages indicating ongoing fusion. In inflammatory conditions like , bony ankylosis may develop in advanced stages due to chronic and formation leading to erosion and subsequent fusion, whereas rarely progresses to true bony union, more commonly resulting in fibrous stiffness.

Signs and symptoms

Joint involvement

Ankylosis of synovial manifests primarily through progressive and restricted , often accompanied by during attempted movement. This arises as the surfaces fuse either fibrosely or osseously, leading to a gradual loss of joint function over time. In the early stages, patients may experience intermittent and swelling, but as fusion advances, the typically diminishes while immobility persists, severely limiting daily activities. For instance, in hip ankylosis resulting from or , patients may develop an inability to walk independently, relying on assistive devices or facing complete dependency for mobility. In inflammatory conditions like , is prominent and leads to —a forward curvature of the thoracic that impairs and . Hips and knees are also frequent locations, especially following post-traumatic or septic events, resulting in flexed deformities that hinder weight-bearing and gait. Other peripheral joints, such as shoulders and elbows, may similarly exhibit stiffness and functional loss. Compensatory mechanisms, such as in the region, may develop to offset the primary , further complicating and overall . These site-specific effects underscore the variable presentation depending on the underlying , with peripheral joints like the hips often showing more rapid functional decline than axial involvement. Complications from ankylosed synovial joints include due to prolonged disuse, as surrounding musculature weakens without regular contraction, exacerbating instability in adjacent areas. frequently occurs from immobility, increasing risk in the fused and nearby bones, particularly in the where vertebral fragility heightens the chance of traumatic injury. In cases of severe immobilization, such as ankylosed hips or knees in non-functional positions, pressure sores can form over bony prominences from constant contact and reduced circulation. These secondary issues compound the primary , leading to broader skeletal and deterioration. The overall impact on patients involves a marked reduction in , with persistent functional limitations fostering dependency in , , and participation. Daily tasks like dressing, bending, or ambulating become challenging, often necessitating adaptations or support, which can contribute to psychological distress and . In chronic cases, such as spinal ankylosis, the cumulative effects of , , and significantly impair physical and emotional well-being, highlighting the need for multidisciplinary management to mitigate long-term .

Dental and TMJ manifestations

Dental ankylosis refers to the fusion of a tooth to the surrounding alveolar bone, preventing normal eruption and mobility. This condition commonly manifests as infraocclusion, where the affected tooth submerges below the occlusal plane relative to adjacent teeth, often to a mild degree (less than 1 mm) or moderate (greater than 1 mm but without severe cases in primary molars). The lack of eruption results from the ankylosed tooth's inability to undergo post-eruptive movements, leading to progressive submergence as the alveolar bone continues to grow vertically around it. Early stages are typically painless, with the primary clinical sign being a high-pitched sound on percussion due to reduced mobility. Adjacent teeth may experience tilting or migration toward the ankylosed site due to disrupted transseptal fibers, though this occurs in only a minority of cases (around 17%) when infraocclusion is mild. Root resorption, particularly replacement resorption where substitutes for lost root structure, is a frequent complication, accelerating in growing patients and potentially leading to late exfoliation (observed in 20% of primary molar cases). In severe instances, extensive resorption renders the tooth unrestorable, often necessitating to prevent further complications like alveolar loss or interference with permanent . Temporomandibular joint (TMJ) ankylosis involves fibrous or bony fusion of the joint, resulting in severe restriction of mouth opening, with maximum interincisal opening typically ranging from 0 to 30 mm and correlating negatively with ankylosis severity. In severe cases, opening may be limited to less than 5 mm, profoundly impacting daily functions. Common manifestations include facial asymmetry, particularly in unilateral cases, and due to altered mandibular , often leading to mandibular retrusion or retrognathia in bilateral involvement. These changes contribute to difficulties in speech, mastication, and eating, with children experiencing additional psychosocial effects such as feeding challenges and retardation. While TMJ ankylosis is generally painless, chronic jaw pain and headaches can arise from compensatory muscle hyperactivity and strain on surrounding structures. In pediatric cases, the progressive nature exacerbates burdens, including aesthetic concerns from asymmetry and functional limitations that hinder and social development. Unique complications include syndrome in severe cases, stemming from retrognathic airway obstruction.

Diagnosis

Clinical assessment

The clinical assessment of ankylosis commences with a comprehensive history-taking to elucidate the and progression of joint fusion. Key elements include the onset of symptoms, which may be acute following direct such as condylar fractures or gradual in cases of chronic inflammation or . Patients are routinely questioned regarding prior traumatic events, local or systemic infections (e.g., leading to involvement), and associated conditions like autoimmune disorders such as or . Family history of inflammatory arthropathies is also probed, as genetic factors like positivity can influence susceptibility in axial forms. Physical examination focuses on evaluating joint function and integrity through targeted maneuvers. is systematically tested using goniometry to quantify restrictions in flexion, extension, , and adduction, revealing characteristic or complete immobility indicative of fibrous or bony . Palpation of the affected joint assesses for , tenderness, or , while functional tests—such as jaw protrusion, lateral deviation, or spinal flexion (e.g., for lumbar involvement)—help localize the extent of impairment. In cases, maximal interincisal opening is measured, often reduced to less than 20 mm in advanced ankylosis. Red flags warranting urgent evaluation include systemic symptoms like persistent fever, unexplained weight loss, or night pain suggesting an underlying inflammatory or infectious process, as well as growth disturbances such as mandibular or facial asymmetry in pediatric patients. These features may signal progression to extra-articular complications or the need for multidisciplinary input. Differential diagnosis encompasses conditions mimicking ankylosis, including degenerative with secondary stiffness, post-traumatic contractures from , and neoplastic processes like synovial sarcomas that cause obliteration. Clinical findings of limited mobility often overlap with those described in , guiding the need for confirmatory in subsequent evaluation.

Imaging and laboratory tests

Imaging plays a central role in diagnosing ankylosis by visualizing structural changes in affected , distinguishing between fibrous and bony , and assessing the extent of involvement. Conventional , such as X-rays, is often the initial , revealing bony ankylosis through features like loss of joint space, subchondral sclerosis, and bridging osteophytes across the joint. In cases of (TMJ) ankylosis, panoramic radiographs are particularly useful, showing irregularities of the TMJ surfaces, suspected condylar fractures, and associated alveolar changes. Computed tomography (CT) provides detailed three-dimensional assessment of joint architecture and is considered the gold standard for TMJ ankylosis, delineating the ankylotic mass, its proximity to vital structures like the skull base, and secondary bony deformities. Multidetector or cone-beam enhances preoperative planning by quantifying the extent of fusion and evaluating alterations. (MRI) excels in detecting involvement and early fibrous ankylosis, highlighting synovial , disc displacement, and not visible on plain films. serves as a non-invasive initial screening tool for peripheral joints, identifying , , or early fibrous adhesions in accessible areas like the or . Laboratory tests support the of ankylosis by identifying underlying etiologies such as , , or . Elevated (ESR) and (CRP) levels indicate active inflammatory processes, commonly seen in autoimmune-related ankylosis like that in . B27 (HLA-B27) testing is recommended when is suspected, as positivity supports the diagnosis in the context of radiographic changes, though it is not specific. For suspected infectious causes, such as leading to ankylosis, microbial cultures from or blood are essential to identify pathogens like . Interpretation of imaging findings focuses on confirming ankylosis type and severity; for instance, complete obliteration of the joint space with continuous bony bridging signifies advanced bony ankylosis, while preserved space with signal changes on MRI suggests fibrous ankylosis. These objective features complement clinical by providing verifiable evidence of progression.

Management

Conservative approaches

Conservative approaches to managing ankylosis focus on alleviating symptoms such as and , preserving any remaining function, and halting disease progression in early or mild cases, particularly those involving fibrous rather than complete bony . These strategies are typically indicated for initial or as adjuncts following surgical intervention, targeting autoimmune-related conditions like (AS) or (TMJ) disorders before resorting to more invasive options. Physiotherapy plays a central role in , emphasizing stretching and mobilization exercises to maintain residual motion, especially in fibrous ankylosis where some pliability persists. In AS, supervised programs incorporating range-of-motion exercises, strengthening of back and abdominal muscles, and posture training have been shown to reduce , enhance flexibility, and improve overall function compared to no intervention. For TMJ ankylosis, jaw-opening exercises, often started early and continued intensively for up to a year, help prevent re-fusion and restore mobility when combined with rest and reassurance. Medications target and without addressing the underlying . Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, serve as first-line for AS-related ankylosis, effectively reducing and inflammatory symptoms in most patients, though long-term use requires monitoring for gastrointestinal risks. For autoimmune-driven cases unresponsive to NSAIDs, disease-modifying antirheumatic drugs (DMARDs) like or may be employed to manage peripheral joint involvement, while biologic agents such as (TNF) inhibitors (e.g., or ), interleukin-17 (IL-17) inhibitors (e.g., ), and (JAK) inhibitors (e.g., ) inhibit inflammatory pathways to slow axial progression as of 2025. In TMJ manifestations, muscle relaxants and low-dose antidepressants can alleviate associated muscle tension and discomfort. Orthotic devices provide supportive care to prevent contractures and redistribute stresses. In TMJ ankylosis, custom oral splints or mouth guards worn at night reposition the , reduce loading on the , and mitigate symptoms like clicking or , often as part of a broader regimen including heat or ice application. For larger ankylosis, such as in AS-affected hips or knees, dynamic braces or splints may be used adjunctively with physiotherapy to maintain alignment and limit progression, though rigid bracing is generally avoided to promote active movement. Dental management of ankylosed teeth emphasizes monitoring and non-extractive interventions to address infraocclusion and guide eruption. Regular radiographic surveillance tracks and tooth position, while orthodontic adjustments, such as segmental mechanics or space maintenance appliances, attempt to upright submerged teeth in growing patients without disrupting adjacent . These approaches are particularly suitable for mild cases in children, where spontaneous resolution or minimal intervention can suffice until permanent successors erupt.

Surgical treatments

Surgical treatments for ankylosis aim to restore mobility, alleviate , and prevent secondary deformities by excising the fused or fibrous and reconstructing the space. These interventions are typically reserved for cases where conservative measures fail, guided by preoperative to delineate the extent of fusion. Common approaches include techniques that remove the ankylotic mass, with or without interpositional materials to maintain the gap and reduce re-fusion risk. In peripheral joints such as the , affected by conditions like , total hip arthroplasty is a standard procedure that replaces the fused joint with a prosthetic implant, improving and function. For general joint ankylosis, gap arthroplasty involves resecting the ankylotic bridge without reconstruction, suitable for smaller joints but carrying higher re-ankylosis risk. Interposition arthroplasty enhances outcomes by placing grafts—such as autogenous fat, muscle flaps, or dermal matrices—into the created gap to prevent bone re-contact and promote interposition. Temporomandibular joint (TMJ) ankylosis requires specialized procedures due to its impact on facial growth and . Condylectomy removes the ankylosed condylar head to release the fusion, often combined with aggressive resection of the entire ankylotic mass. Coronoidectomy, the excision of the coronoid process, addresses associated muscle contractures and improves opening. frequently employs costochondral grafts, which provide a growing neocondyle in pediatric cases, typically harvested from the 5th to 7th and fixed to the mandibular ramus for functional restoration. Alloplastic total joint replacement has emerged as an , particularly for adults, recurrent cases, or when autologous grafts are unsuitable, using prostheses for durable functional and esthetic outcomes as of 2025. In dental ankylosis, where a permanent fuses to alveolar , surgical extraction is indicated for severely infrapositioned or impacted teeth to allow eruption of adjacent and prevent alveolar distortion. For submerged primary teeth in children, decoronation—surgical removal of the crown while retaining the root—preserves alveolar height for future placement, avoiding premature loss of vertical dimension. Complications of ankylosis surgery include re-ankylosis, with reported rates of 10-20% in TMJ cases, higher in children (up to 19%) and first-time gap (around 15%) compared to interpositional methods (5%). Other risks encompass postoperative infection, facial nerve injury leading to temporary or permanent weakness (3-5% incidence), and hematoma formation, necessitating vigilant perioperative antibiotic use and monitoring. Timing of surgery is critical, particularly in pediatric patients, where early before age 10-12 mitigates mandibular growth retardation, facial asymmetry, and impacts from restricted mouth opening. Delaying beyond skeletal maturity increases surgical complexity and recurrence likelihood due to denser bone fusion.

Prognosis and epidemiology

Clinical outcomes

The prognosis of ankylosis varies significantly depending on the type and location of fusion, as well as the timing of . Early and , particularly in cases of leading to spinal ankylosis, can substantially improve joint mobility and prevent progression to severe structural damage by reducing inflammation and maintaining function. In (TMJ) ankylosis, bony fusion generally carries a poorer than fibrous ankylosis, as it involves complete osseous bridging that restricts mandibular movement more severely and increases the risk of recurrence after , often necessitating more invasive surgical approaches. Surgical outcomes for TMJ ankylosis demonstrate moderate success in restoring function, with studies reporting success rates of 50-70% for procedures such as or interpositional , defined by improved maximal interincisal opening and low recurrence. In contrast, untreated spinal ankylosis in frequently results in chronic and progressive stiffness, impairing daily activities and leading to long-term in advanced cases. Long-term complications of ankylosis, especially in , include spinal deformities such as and the "bamboo spine" appearance due to , which compromise posture and mobility. Additionally, patients face elevated cardiovascular risks, including and increased mortality from heart disease, driven by chronic . These issues highlight the importance of ongoing monitoring to mitigate secondary effects. Quality of life in ankylosis patients is highly variable, influenced by disease severity and access to care, but multidisciplinary approaches involving , , and surgical expertise have been shown to enhance functional outcomes and reduce symptom burden.

Prevalence and risk factors

Ankylosis is a rare condition overall, occurring as a complication in approximately 1-2% of patients with chronic arthritis such as , particularly in longstanding severe cases involving small joints. In the context of (TMJ) ankylosis, the prevalence is notably higher among children; a population-based study in rural estimated it at 0.46 per 1,000 children aged 3-15 years (roughly 1 in 2,200). For dental ankylosis, it affects infrequently overall (less than 1% in the general population), but following traumatic injuries like avulsion and , reported incidences range from about 17% for immediately replanted teeth to 55% for those with delayed replantation or unfavorable storage. Several risk factors contribute to the development of ankylosis, varying by type. TMJ ankylosis exhibits a predominance, with a ratio of approximately 2:1, largely attributable to higher exposure to among males. Genetic factors play a significant role in joint ankylosis associated with , where the allele is present in over 90% of affected individuals, conferring a strong hereditary risk. A history of , including condylar fractures or perinatal injuries, is the leading precipitant for both TMJ and dental ankylosis, often initiating the fusion process. Additionally, low heightens vulnerability, particularly for infection-related cases, due to limited access to timely medical care and higher infection rates in resource-poor settings. Geographically, TMJ ankylosis shows elevated prevalence in regions of and , where rates are substantially higher than in or , driven by increased incidences of and untreated infections. Over time, trends indicate a decline in infectious etiologies of TMJ ankylosis in developed areas, attributed to widespread use and improved infection management, reducing cases linked to conditions like . Concurrently, there is growing recognition of autoimmune mechanisms, particularly in HLA-B27-associated forms, leading to earlier diagnosis and intervention in inflammatory arthritides.

History and society

Etymology and historical recognition

The term ankylosis originates from the word ankylōsis (ἀγκύλωσις), meaning "stiffening of the joints," derived from ankylos (ἀγκύλος), signifying "bent," "crooked," or "stiffened." This etymological root reflects the condition's hallmark of joint rigidity due to abnormal adhesion or fusion of bones. The word entered English medical lexicon in 1713 as an alternative spelling of anchylosis, initially describing the pathological union of two or more bones into a single rigid structure, often resulting from , , or . Early medical recognition of ankylosis dates back to the 5th century BCE, when described cases of joint stiffness and spinal inflexibility in his writings, attributing them to , , or natural progression, though without a specific term for the condition. These observations laid foundational descriptive accounts of joint immobility, distinguishing it from mere . By the , ankylosis gained clearer recognition in the context of rheumatoid conditions, emphasizing chronic leading to bony fusion in affected patients. Key advancements in classification occurred mid-century, with British surgeon Bernard Edward Brodhurst differentiating between fibrous ankylosis—characterized by adhesions causing partial restriction—and bony (osseous) ankylosis, involving complete bone fusion, in his 1857 paper on treating ankylosed joint surfaces through forcible extension. This distinction enabled more targeted surgical interventions. Further refinement came in 1897, when German neurologist Adolf Strümpell provided a modern delineation of , a specific inflammatory form of spinal ankylosis, highlighting its progressive nature and distinction from other arthritides. The understanding of ankylosis evolved significantly post-1950s with the integration of radiological techniques, shifting from purely descriptive to etiological insights; revealed characteristic features such as formation and the "bamboo spine" appearance in , facilitating earlier diagnosis and linking the condition to genetic and inflammatory mechanisms.

Paleopathological evidence

Paleopathological evidence of ankylosis provides insights into the prevalence and etiology of joint fusion in prehistoric and ancient human populations, often linked to , , or inflammatory processes. One of the earliest potential cases involves the Neanderthal skeleton, an elderly male dated to approximately 50,000 years ago, which exhibits advanced in the spinal column and hip joint, possibly resulting from a infection. This pathology highlights how infectious agents may have induced degenerative joint alterations in early hominins, though direct evidence of complete ankylosis remains interpretive due to taphonomic preservation. In ancient human remains, (TMJ) ankylosis appears frequently, particularly in contexts. A severe case of bilateral TMJ ankylosis was identified in a from the New Kingdom necropolis at , (circa 1550–1070 BCE), where osseous fusion likely stemmed from trauma or infection, as evidenced by the extent of bony overgrowth restricting jaw mobility. Similarly, mummies from Tomb in the Valley of the Kings (18th Dynasty) show bilateral TMJ pathological changes consistent with rheumatic disease, suggesting inflammatory ankylosis in elite individuals. These findings indicate that TMJ ankylosis, often trauma-related, affected ancient , potentially exacerbated by occupational or accidental injuries. Medieval skeletal assemblages reveal a broader spectrum of ankylosis types, predominantly inflammatory. In a Croatian medieval series (10th–15th centuries CE), four cases of were documented among 303 skeletons, characterized by spinal and fusions in three males and one female, pointing to genetic or environmental triggers in post-Roman . A larger sample from the Bátmonostor cemetery in southern (11th–13th centuries CE) yielded 30 ankylosis cases among 426 adult skeletons, affecting joints such as the knee (4 cases), tibiofibular (8 cases), and sternoclavicular (4 cases), with two-thirds occurring in males over 40 years old; these likely represent post-traumatic or degenerative fusions. Interpretations of these remains suggest higher ankylosis rates in populations due to elevated exposure from subsistence activities. In southern Patagonian s (circa 6,000–250 years BP), approximately 20% of individuals displayed bone , including fractures that could progress to joint ankylosis if untreated, underscoring the physical demands of mobile lifestyles. Dietary factors may have influenced dental ankylosis in some ancient groups, where excessive occlusal from abrasive foods led to tooth-to-bone , though this is less common than joint forms. Modern studies employing computed tomography () on fossils have refined these insights; for instance, imaging of Istrian remains (medieval period) confirmed knee joint ankylosis with cortical thickening, while broader analyses indicate joint pathology rates of 5–10% in select ancient populations, aiding between traumatic and inflammatory etiologies.