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Enthesitis

Enthesitis is an inflammatory condition that affects the entheses, the specialized anatomical sites where tendons, ligaments, or joint capsules insert into bone, leading to pain, swelling, and potential structural damage at these attachment points.^[1] It represents a hallmark feature of spondyloarthritis (SpA), a group of chronic inflammatory rheumatic diseases including psoriatic arthritis (PsA), ankylosing spondylitis (AS), and reactive arthritis, where it often manifests early and contributes to significant morbidity.^[2] Enthesitis can also occur in isolation or secondary to mechanical stress, overuse injuries, or metabolic conditions, though it is most prominently associated with autoimmune-driven inflammation in SpA.^[3] Enthesitis affects approximately 10-60% of patients with SpA and up to 35% of those with PsA, with higher rates of subclinical involvement detected by imaging. Prevalence varies by population and diagnostic method, being more common in individuals with genetic predispositions like HLA-B27 positivity.^[4] The pathogenesis of enthesitis involves a complex interplay of mechanical, genetic, and immunological factors, where repetitive biomechanical stress causes microdamage at the enthesis, triggering an innate immune response that evolves into chronic inflammation in susceptible individuals.^[2] Key inflammatory mediators include cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-17 (IL-17), IL-22, and IL-23, which promote immune cell infiltration and tissue remodeling, often extending beyond the enthesis to involve adjacent bone marrow and soft tissues as part of an "enthesis organ" complex.^[3] Genetic predisposition, particularly the HLA-B27 allele, increases risk in SpA-related cases, while environmental triggers like infections or gut dysbiosis may initiate autoimmunity against entheseal components such as versican or aggrecan.^[2] Clinically, enthesitis presents with localized tenderness, stiffness, and reduced function at common sites like the Achilles tendon insertion, plantar fascia, or iliac crest, sometimes accompanied by systemic symptoms such as fatigue or entheseal nail changes in PsA.^[1] Diagnosis relies on clinical examination using indices like the Maastricht Ankylosing Spondylitis Enthesitis Score (MASES) or Mander's Enthesitis Index, supplemented by imaging: ultrasonography detects soft tissue inflammation with high sensitivity (up to 60% in subclinical cases), while MRI identifies bone marrow edema for early detection.^[2] Blood tests may reveal elevated inflammatory markers, but no specific biomarker exists.^[1] Treatment focuses on symptom relief and addressing underlying inflammation, starting with nonsteroidal anti-inflammatory drugs (NSAIDs) for mild cases, which can slow progression and resolve acute episodes.^[2] For refractory or SpA-associated enthesitis, biologic therapies targeting TNF (e.g., adalimumab, etanercept) or IL-17/IL-23 pathways (e.g., secukinumab, ustekinumab) demonstrate high efficacy, while disease-modifying antirheumatic drugs like methotrexate show limited benefit.^[2] Physical therapy, rest, and local corticosteroid injections provide adjunctive support, with recent advances emphasizing early intervention to prevent chronic entheseal damage like bone spurs or ankylosis.^[1]

Introduction

Definition

Enthesitis refers to the inflammation specifically occurring at the enthesis, defined as the anatomical site where tendons, ligaments, or joint capsules insert into bone.^[5] This process involves localized inflammatory changes, often characterized by immune cell infiltration, edema, and potential erosion at the bone-tendon interface.^[6] Enthesopathy, in contrast, serves as a broader umbrella term encompassing any disorder affecting the entheses, including degenerative, traumatic, metabolic, or inflammatory etiologies, whereas enthesitis is restricted to the inflammatory variant.^[3] This distinction is crucial in clinical contexts, as enthesitis is a hallmark feature of seronegative spondyloarthropathies, guiding targeted diagnostic and therapeutic approaches.^[4] The recognition of enthesitis emerged in the mid-20th century within the framework of spondyloarthropathies, with the related concept of enthesopathy first articulated by Niepel in 1966 to describe insertion-site pathologies in these conditions. By the 1970s and 1980s, the enthesitis hypothesis expanded to unify inflammatory processes across spondyloarthropathies, including ankylosing spondylitis and psoriatic arthritis, as detailed in seminal works by Moll and Wright.^[3] In psoriatic arthritis, enthesitis is now acknowledged as an early and prevalent manifestation, often preceding joint involvement.^[7] Entheses are structurally classified into two main types: fibrous, where connective tissue directly attaches to the periosteum (e.g., deltoid insertion on the humerus), and fibrocartilaginous, featuring an intervening fibrocartilage layer at the bone interface (e.g., Achilles tendon or plantar fascia insertions).^[4] In inflammatory conditions like spondyloarthropathies, enthesitis predominantly targets fibrocartilaginous entheses due to their susceptibility to biomechanical stress and vascular changes that facilitate immune-mediated inflammation.^[3]

Epidemiology

Enthesitis is a common manifestation in patients with spondyloarthropathies (SpA), affecting an estimated 10-60% of individuals with these conditions depending on the diagnostic method and population studied.^[8] Within specific subtypes, prevalence is notably higher in psoriatic arthritis (PsA), where clinical enthesitis occurs in 30-50% of cases, with some studies reporting rates up to 65.7% in Western populations.^[8]^[9] In ankylosing spondylitis (AS), a form of axial SpA, enthesitis is observed in 25-74% of patients, often involving axial and peripheral sites.^[10] Demographically, enthesitis predominantly affects adults in their third and fourth decades of life, aligning with the typical onset age of 20-40 years for inflammatory SpA.^[11] Inflammatory forms show a slight male predominance, with males comprising 57-61% of affected cohorts and exhibiting higher rates of sonographic enthesitis compared to females in PsA.^[12]^[13] In pediatric populations, enthesitis manifests as enthesitis-related arthritis (ERA), a subtype of juvenile idiopathic arthritis (JIA) accounting for 10-15% of JIA cases, particularly in non-Western regions where it may represent up to 37% of diagnoses.^[14]^[15] Key risk factors for enthesitis include genetic predispositions, such as HLA-B27 positivity, which is present in 50-90% of SpA-related cases and strongly associates with ERA in children.^[16] Environmental triggers, including infections and mechanical stress at entheseal sites, further contribute to its development in susceptible individuals.^[17] Recent data through 2025 highlight increasing recognition of enthesitis in inflammatory bowel disease (IBD) cohorts, with prevalence ranging from 20-33% among patients with Crohn's disease or ulcerative colitis, even without axial skeletal involvement.^[18]^[19]

Pathophysiology and Causes

Anatomy of Entheses

Entheses represent the specialized interfaces where tendons or ligaments attach to bone, facilitating the transmission of mechanical forces from soft connective tissues to the skeletal system. These structures are essential for maintaining musculoskeletal integrity during movement and load-bearing activities.^[20] Entheses are classified into two primary structural types based on their tissue composition and attachment mechanism: fibrous and fibrocartilaginous. Fibrous entheses involve a direct insertion of the tendon or ligament into the bone via Sharpey's fibers, which are collagenous bundles that penetrate the periosteum and anchor into the cortical bone, often occurring at diaphyseal sites. In contrast, fibrocartilaginous entheses feature an indirect attachment through a transitional zone of fibrocartilage, which helps dissipate stress and accommodate varying biomechanical demands, typically at epiphyseal or apophyseal locations.^[21]^[22] Functionally, entheses serve as biomechanical interfaces that absorb and distribute tensile forces generated by muscle contractions, thereby preventing stress concentrations at the bone-tendon junction and minimizing the risk of injury under dynamic loading. This role is particularly critical in areas subjected to high mechanical stress, where the graded tissue organization optimizes force transfer while protecting adjacent bone and soft tissues.^[20]^[23] Microscopically, fibrocartilaginous entheses exhibit a zoned architecture that transitions smoothly from tendon to bone: beginning with the dense fibrous connective tissue of the tendon proper, followed by uncalcified fibrocartilage rich in type II collagen and proteoglycans, then calcified fibrocartilage where mineralization occurs, and finally merging into the subchondral bone. This zonal arrangement, often spanning several millimeters, includes a vascular supply primarily from perforating vessels in the bone and adjacent soft tissues, as well as neural elements such as free nerve endings and mechanoreceptors that contribute to proprioception and pain signaling. Fibrous entheses, while lacking this fibrocartilaginous layering, rely on the penetration of Sharpey's fibers for anchorage, with similar but less pronounced vascular and neural components.^[22]^[21]^[23] Representative examples illustrate these distinctions: the Achilles tendon insertion at the calcaneus exemplifies a fibrocartilaginous enthesis, with its multi-zoned structure adapted to withstand propulsive forces during gait, whereas the deltoid tendon insertion at the humerus represents a fibrous enthesis, featuring direct Sharpey's fiber integration suited to the action of the deltoid muscle.^[22]

Etiological Factors

Enthesitis is predominantly associated with inflammatory etiologies, particularly autoimmune conditions within the spectrum of spondyloarthropathies (SpA). These include psoriatic arthritis (PsA), where enthesitis occurs in approximately 35% of cases, and ankylosing spondylitis (AS), with prevalence ranging from 10% to 60% in SpA overall.^[4] Genetic predisposition plays a key role, with the HLA-B27 allele strongly linked to enthesitis in AS and related juvenile idiopathic arthritis-enthesitis-related arthritis (JIA-ERA), mirroring its association in adult AS.^[24] Mechanical and overuse factors contribute to enthesitis through repetitive stress and microtrauma at entheseal sites, commonly observed in athletes and laborers. For instance, Achilles enthesitis frequently arises from chronic overload in runners or sports involving explosive movements, leading to partial damage that initiates secondary inflammation.^[4]^[25] Infectious triggers often manifest as reactive enthesitis following bacterial infections, particularly in the context of post-infectious SpA. Gastrointestinal or urogenital pathogens, such as Chlamydia or Yersinia enterocolitica, can precipitate sterile inflammation at entheses weeks after the initial infection, with gut microbiota perturbations implicated in sustaining the response.^[26]^[27] Other etiological factors encompass metabolic, iatrogenic, and idiopathic causes. Metabolic enthesitis is linked to hyperuricemia in gout, where urate crystal deposition affects sites like the quadriceps tendon insertion at the patella, correlating with age and inflammatory markers.^[28] Iatrogenic cases include fluoroquinolone-induced tendinopathy extending to entheseal involvement, most notably at the Achilles tendon.^[29] Isolated enthesitis may present idiopathically without systemic disease. Emerging research as of 2024 highlights microbiome dysbiosis in inflammatory bowel disease (IBD)-associated enthesitis within SpA, where alterations in intestinal flora influence immune responses, potentially modulated by therapies like anti-TNF agents.^[30]

Pathogenic Mechanisms

Enthesitis develops through a complex interplay of immune-mediated inflammation and biomechanical stress at the entheseal sites, where tendon or ligament insertions into bone occur. Entheseal cells, including fibroblasts and chondrocytes, express mechanosensitive molecules such as integrins and connexins, which respond to physical forces by activating signaling pathways like MAPK, leading to the production of proinflammatory cytokines. In spondyloarthritis (SpA), this process triggers the IL-23/IL-17 axis, where IL-23 produced by resident macrophages or stromal cells stimulates innate lymphoid cells (ILC3s) and double-negative T cells (CD3+CD4−CD8−) to secrete IL-17A, IL-22, and TNF-α, promoting neutrophil infiltration and further amplification of inflammation via IL-6 release.^[2]^[31]^[3] Biomechanical stress plays a pivotal role in initiating and perpetuating enthesitis, as repetitive mechanical loading induces microdamage at the fibrocartilage interface, activating toll-like receptors (TLRs) through damage-associated molecular patterns (DAMPs) and recruiting enthesis-resident immune cells. These cells, including γδ T cells and ILC3s, respond to the stress by upregulating adhesion molecules such as ICAM-1 on endothelial cells, facilitating leukocyte adhesion and transmigration into the tissue. This mechanical-immune crosstalk results in localized inflammation, with studies in animal models demonstrating that entheseal stress alone can drive IL-23-dependent pathology even in the absence of systemic infection.^[2]^[31]^[3] At the tissue level, acute enthesitis manifests as edema in soft tissues and bone marrow, driven by vascular permeability from cytokine release, progressing to fibrosis through collagen deposition and matrix metalloproteinase activity that degrades fibrocartilage. Chronic inflammation leads to osteoclast activation via RANKL signaling, causing erosions at the entheseal margins, followed by reparative ossification and formation of enthesophytes through BMP and Hedgehog pathway-mediated mesenchymal progenitor cell differentiation into osteoblasts. These changes highlight a shift from inflammatory to structural damage, with IL-22 promoting new bone formation in persistent cases. Genetic factors like HLA-B27 may enhance susceptibility by altering immune responses to these stressors.^[2]^[31]^[32]

Clinical Features

Signs and Symptoms

Enthesitis manifests primarily as localized pain at the site of tendon, ligament, or joint capsule insertion into bone, which is often exacerbated by movement or direct pressure on the affected area.^[4] Tenderness upon palpation is a hallmark feature, frequently eliciting significant discomfort during physical examination.^[33] Morning stiffness lasting more than 30 minutes is commonly reported, particularly in inflammatory forms associated with spondyloarthritis.^[34] Associated features include swelling and warmth at the enthesis, reflecting local inflammation, along with reduced range of motion in the adjacent joint.^[4] In systemic conditions such as psoriatic arthritis or ankylosing spondylitis, patients may experience accompanying fatigue.^[34] The condition can present in acute or chronic patterns; acute enthesitis often has a sudden onset following injury or mechanical stress, while chronic forms develop insidiously with fluctuating symptoms over time.^[4] A characteristic examination finding is marked tenderness on palpation, sometimes described as eliciting a reflexive withdrawal response due to the intensity of pain.^[33] In pediatric patients with enthesitis-related arthritis (ERA), a subtype of juvenile idiopathic arthritis, symptoms frequently include hip or groin pain alongside enthesitis, often accompanied by asymmetric oligoarthritis affecting a limited number of joints, predominantly in the lower extremities.^[34]^[35]

Common Entheseal Sites

Enthesitis most commonly affects sites in the lower extremities, where mechanical stress from weight-bearing activities contributes to inflammation at tendon and ligament insertions. The Achilles tendon insertion at the posterior calcaneus is frequently involved in spondyloarthritis (SpA) patients.^[36] The plantar fascia attachment at the medial calcaneus is another prevalent lower extremity site, particularly in seronegative SpA, where it manifests as heel pain and is associated with up to 18.5% tenderness in active psoriatic arthritis (PsA) cohorts.^[37] The patellar tendon insertion at the inferior pole of the patella also represents a common lower limb location, often linked to knee discomfort in inflammatory conditions.^[38] In the upper extremities, enthesitis typically targets sites exposed to repetitive motion. The common extensor origin at the lateral epicondyle of the humerus is a key area, presenting as a variant of "tennis elbow" in inflammatory enthesopathies in PsA cases via clinical indices.^[11] Rotator cuff insertions at the humeral head, including the supraspinatus tendon, are also commonly affected, contributing to shoulder pain in axial SpA patients with peripheral involvement.^[39] Axial sites are particularly prominent in ankylosing spondylitis (AS), a subset of SpA. The iliac crest and ischial tuberosity serve as frequent attachment points for ligaments and muscles, with involvement detected in registries of axial SpA patients. Spinal ligament attachments, such as those at the lumbar and thoracic spinous processes, are common in AS.^[11] The Achilles tendon and plantar fascia are among the most common sites of enthesitis in PsA, often alongside dactylitis-like involvement of toe entheses that mimics sausage digits.^[37] Fibrocartilaginous entheses, characterized by a transitional zone of fibrocartilage at the bone-tendon interface, are more prone to inflammatory enthesitis in SpA compared to fibrous types, due to their role in stress dissipation and susceptibility to immune-mediated damage.^[40] These sites often present with localized pain and swelling, as detailed in clinical symptom profiles.

Diagnosis

History and Physical Examination

The clinical assessment of enthesitis begins with a detailed history taking to identify symptoms suggestive of entheseal inflammation. Patients are queried about the onset and duration of pain, typically described as localized tenderness at tendon or ligament insertion sites, often exacerbated by physical activity or prolonged rest. Aggravating factors such as repetitive movements or weight-bearing activities are explored, alongside associated symptoms including inflammatory back pain, peripheral joint involvement, skin lesions characteristic of psoriatic arthritis (PsA), or extra-articular manifestations like uveitis. Family history of autoimmune conditions, particularly spondyloarthritis (SpA), is elicited to assess genetic predisposition. This approach has demonstrated a sensitivity of 72% and specificity of 63% for detecting chronic enthesitic pain when correlated with imaging findings.^[41]^[42] Physical examination focuses on direct palpation of entheseal sites to elicit tenderness, applying firm pressure (approximately 4 kg, sufficient to blanch the examiner's fingernail) while distinguishing entheseal pain from adjacent joint or soft tissue involvement. Provocative maneuvers, such as heel compression for plantar enthesitis or resisted movements for Achilles involvement, help localize inflammation. In cases associated with axial SpA, spinal mobility is assessed through tests like the Schober's test or occiput-to-wall distance to evaluate for related stiffness. Standardized scoring systems enhance reliability: the Leeds Enthesitis Index (LEI) evaluates six bilateral sites—lateral epicondyles, medial femoral condyles, and Achilles insertions—scoring tenderness as present (1) or absent (0), with a total range of 0-6, originally validated in PsA cohorts for its feasibility and reproducibility. The Spondyloarthritis Research Consortium of Canada (SPARCC) enthesitis index assesses 18 sites (scored as 0-16, combining proximal patellar and tibial tuberosity), including Achilles, plantar fascia, and greater trochanter, showing strong interobserver reliability (ICC 0.96) and responsiveness to treatment in ankylosing spondylitis (AS). The Maastricht Ankylosing Spondylitis Enthesitis Score (MASES) targets 13 sites, such as the posterior and anterior superior iliac spines, iliac crests, and Achilles/plantar regions, with a 0-13 range based on binary tenderness scoring, offering improved feasibility over broader indices like the Mander Enthesis Index while correlating well (Spearman 0.90). These tools are recommended for initial screening in SpA, with clinical examination sensitivity around 68% for acute enthesitis.^[43]^[44]^[45]^[46]^[47]^[48]^[49]^[41]^[42] Red flags warranting urgent evaluation include systemic symptoms such as unexplained fever, significant weight loss, night sweats, or progressive neurological deficits, which may indicate underlying infection (e.g., septic enthesitis) or malignancy (e.g., metastatic disease mimicking enthesopathy). In the absence of these, the history and examination guide toward inflammatory etiologies, but persistent atypical features necessitate exclusion of differentials like trauma or crystal arthropathy.^[8]^[1]

Imaging Modalities

Ultrasound serves as the first-line imaging modality for the dynamic assessment of enthesitis due to its accessibility, real-time capabilities, and ability to evaluate superficial entheseal sites.^[50] It detects key elementary lesions as defined by the Outcome Measures in Rheumatology (OMERACT) ultrasound group, including entheseal hypoechogenicity, thickening, erosions, enthesophytes, and calcifications, with power Doppler signal indicating increased vascularity and active inflammation.^[51] These features allow for the identification of both inflammatory and structural changes, with high inter-reader reliability for power Doppler positivity in spondyloarthritis (SpA)-related enthesitis.^[52] Magnetic resonance imaging (MRI) is considered the gold standard for visualizing deep entheseal structures and associated pathologies, particularly in axial SpA and psoriatic arthritis (PsA).^[53] It excels at detecting bone marrow edema, a hallmark of early inflammation, as well as enthesophyte formation and soft tissue involvement, often using short tau inversion recovery (STIR) sequences to highlight active inflammatory processes.^[54] MRI's multiplanar imaging and superior soft tissue contrast enable comprehensive evaluation of enthesitis extent, including capsulitis and retroenthesial bursitis, outperforming other modalities for hidden sites like the sacroiliac joints.^[55] Conventional radiography (X-ray) is primarily useful for identifying chronic entheseal changes, such as erosions, calcifications, and enthesophytes, which reflect long-standing disease progression.^[56] However, it lacks sensitivity for early inflammatory alterations, often appearing normal in acute enthesitis due to its inability to visualize soft tissue edema or vascularity.^[41] Computed tomography (CT) is employed in rare cases for detailed bony assessment, particularly when evaluating complex structural abnormalities like osteoproliferation or subtle erosions not well visualized on X-ray.^[57] Recent advances, including integrated scoring systems like the DEUS Enthesitis Index (DEI) introduced in 2025, enhance ultrasound's role in SpA trials by combining sonographic inflammation with clinical findings for more reliable enthesitis quantification.^[58] Diagnosis of enthesitis on imaging typically requires evidence of both structural damage (e.g., erosions or enthesophytes) and active inflammation (e.g., power Doppler signal or bone marrow edema) to distinguish it from degenerative changes.^[59] While clinical tenderness at entheseal sites may prompt imaging, objective confirmation relies on these multimodal findings.^[60]

Laboratory Investigations

Laboratory investigations play a key role in supporting the diagnosis of enthesitis by assessing systemic inflammation, identifying associated autoimmune conditions, and ruling out alternative etiologies such as infection or crystal arthropathies.^[2] Common tests include evaluation of inflammatory markers and serologic studies, which help differentiate enthesitis from other forms of arthritis. Inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are often elevated in cases of active enthesitis associated with spondyloarthritis (SpA), reflecting underlying systemic inflammation; these markers are raised in approximately 60-80% of patients with active disease, though they may remain normal in isolated mechanical enthesitis without systemic involvement.^[61]^[3] Normal ESR and CRP levels do not exclude enthesitis but suggest a lower likelihood of inflammatory SpA-related pathology.^[62] Autoimmune serology includes testing for human leukocyte antigen B27 (HLA-B27), which is positive in about 70% of cases of ankylosing spondylitis (AS)-related enthesitis, aiding in the identification of SpA spectrum disorders.^[63]^[16] Rheumatoid factor (RF) and antinuclear antibody (ANA) are typically negative in enthesitis, helping to distinguish it from rheumatoid arthritis (RA).^[64]^[65] Additional tests target potential underlying causes. Serum uric acid levels are measured to evaluate for gout as a mimic of enthesitis, particularly in cases with crystal deposition at tendon insertions.^[66] Stool calprotectin is useful for detecting subclinical inflammatory bowel disease (IBD), which is linked to enthesitis in up to 10-20% of SpA cases.^[67]^[68] For suspected infectious etiology, such as in reactive arthritis, cultures from synovial fluid or relevant sites are performed to identify pathogens.^[69] Entheseal biopsy is rarely performed due to its invasiveness but, when done, reveals inflammatory infiltrates, fibrocartilage destruction, and macrophage invasion in early lesions.^[2] Synovial fluid analysis, if joint effusion is present, may show inflammatory cells or crystals, correlating with adjacent entheseal involvement observed on imaging.^[70] Recent advancements include emerging biomarkers like serum interleukin-23 (IL-23), which shows elevated levels in AS patients and correlates with disease activity, offering potential for SpA-specific enthesitis prediction.^[71]

Treatment and Management

Conservative Measures

Conservative measures form the cornerstone of initial management for enthesitis, focusing on alleviating pain, reducing inflammation, and minimizing mechanical stress at tendon insertion sites without relying on medications. These approaches are particularly effective for overuse-related cases and can promote long-term recovery by addressing biomechanical contributors to symptoms.^[4] Rest and activity modification are essential first steps, involving temporary immobilization to offload the affected enthesis and avoidance of provocative movements such as repetitive jumping or running. For Achilles enthesitis, heel lifts or wedges inserted into footwear can reduce tensile forces on the insertion, while for plantar enthesitis, supportive taping or short-term non-weight-bearing periods help mitigate heel strike impact. These strategies typically yield symptom relief within 7-10 days in acute overuse enthesopathies by allowing tissue repair.^[4]^[72] Physical therapy is a widely recommended intervention, emphasizing targeted stretching and strengthening to improve flexibility, strength, and function around the enthesis. Stretching protocols for the Achilles tendon and plantar fascia, performed twice daily for 30 seconds per repetition, have demonstrated significant pain reduction in plantar enthesitis, with one randomized controlled trial (RCT) reporting a 71.8% response rate after 8 weeks. Eccentric exercises, such as modified heel-lowering protocols adapted from the Alfredson regimen for insertional sites, enhance tendon loading tolerance; in an RCT on insertional Achilles tendinopathy, conventional physical therapy including stretches and eccentric strengthening resulted in 86.7% of patients achieving clinically significant pain improvement (mean 41.3% VAS reduction) and 93.3% functional gains over 12 weeks. Ultrasound therapy may provide adjunctive pain relief through thermal effects in some protocols, though evidence is primarily from case series for calcaneal enthesitis. Overall, RCTs indicate 50-90% improvement rates in pain and function with physical therapy for entheseal overuse conditions.^[73]^[74]^[75] Orthotics and supportive devices offer biomechanical correction tailored to specific sites, reducing repetitive strain and promoting alignment. Custom insoles for plantar enthesitis distribute pressure away from the heel insertion, with RCTs showing 64-95% of patients experiencing good to excellent pain relief at 8-12 weeks. For elbow enthesitis (e.g., lateral epicondyle), counterforce braces limit forearm muscle excursion, while knee braces stabilize patellar tendon insertions during activity; these supports are most effective when combined with activity modification, achieving up to 80% symptom reduction in observational studies of overuse enthesopathies.^[73]^[4]^[76] Lifestyle modifications further support conservative management by addressing modifiable risk factors that exacerbate entheseal load. Weight management is crucial, as excess body weight increases mechanical stress on lower limb entheses; in patients with psoriatic arthritis, a very low-energy diet leading to 5-10% weight loss over 16 weeks improved enthesitis scores by reducing inflammation and disease activity. Ice application (10-15 minutes several times daily) provides acute pain relief via vasoconstriction for inflammatory flares, while heat therapy aids chronic stiffness by enhancing blood flow. Patients are advised to incorporate gradual return-to-activity principles to prevent recurrence.^[77]^[1]^[4]

Pharmacotherapy

Pharmacotherapy for enthesitis primarily targets inflammation and the underlying spondyloarthropathy, with treatment escalating from non-steroidal anti-inflammatory drugs (NSAIDs) to disease-modifying antirheumatic drugs (DMARDs) and biologics based on disease severity and response.^[78] In mild cases, NSAIDs such as ibuprofen at doses of 400-800 mg three times daily provide symptomatic relief for pain and inflammation, achieving response rates of approximately 60-70% in peripheral enthesitis associated with psoriatic arthritis (PsA) or axial spondyloarthritis (axSpA).^[79] These agents are recommended as first-line therapy for up to 4 weeks, with continuous use if effective, while balancing cardiovascular and gastrointestinal risks.^[80] For patients with persistent enthesitis despite NSAIDs, conventional synthetic DMARDs like sulfasalazine or methotrexate are considered, particularly in peripheral SpA manifestations, though their efficacy specifically for enthesitis is limited and supported only by conditional recommendations.^[79] Sulfasalazine may be used at 2-3 g daily for peripheral involvement, but it is not routinely advised for axial disease alone.^[80] Methotrexate, dosed at 15-25 mg weekly, shows modest benefits in PsA but lacks robust enthesitis-specific data from randomized trials.^[78] Biologic DMARDs serve as second-line options for refractory enthesitis, with tumor necrosis factor (TNF) inhibitors such as etanercept (50 mg subcutaneous weekly) or adalimumab (40 mg subcutaneous every two weeks) demonstrating significant reductions in enthesitis scores by 40-60% in clinical trials, including resolution rates exceeding 50% at 12 months in axSpA cohorts.^[81] Interleukin-17 inhibitors like secukinumab (150-300 mg subcutaneous monthly) are particularly effective in PsA-related enthesitis, with similar resolution rates and preference in cases with prominent skin involvement.^[79] Local corticosteroid injections, such as 40 mg triamcinolone acetonide directly at the entheseal site, offer rapid relief as an adjunct but carry risks including tendon rupture, especially with repeated use near load-bearing tendons like the Achilles.^[82] Emerging targeted synthetic DMARDs, including Janus kinase (JAK) inhibitors like tofacitinib (5-10 mg orally twice daily), are recommended in recent guidelines, such as the EULAR 2023 recommendations (published 2024) and the 2025 British Society for Rheumatology guideline for axSpA, for the management of enthesitis in PsA and axSpA unresponsive to biologics, showing improvements in enthesitis resolution comparable to TNF inhibitors in phase III trials.^[78]^[83]^[84] Response to pharmacotherapy is monitored using validated indices such as the Ankylosing Spondylitis Disease Activity Score (ASDAS) for axSpA or Disease Activity Score 28 (DAS28) for peripheral involvement, targeting low disease activity or remission within 3-6 months.^[80]

Surgical Interventions

Surgical interventions for enthesitis are reserved for severe, refractory cases where conservative measures and pharmacotherapy have failed, or when structural complications such as tendon rupture, significant enthesophyte formation, or irreversible deformity compromise function.^[4] Indications typically include persistent pain and disability lasting beyond 6-12 months despite optimal medical management, particularly in peripheral sites like the Achilles tendon or plantar fascia, or axial involvement leading to spinal fusion needs in advanced spondyloarthropathies.^[85] For instance, in insertional Achilles enthesitis, surgery is considered when imaging reveals bony spurs or partial tendon tears that impair mobility.^[72] Common procedures focus on debridement and repair to alleviate inflammation and restore anatomy, such as excision of inflamed tissue and enthesophytes at the tendon-bone interface, or tendon reattachment in cases of rupture. In Achilles insertional tendinopathy associated with enthesitis, Achilles tendonectomy involves removing the diseased insertional portion followed by reattachment, often combined with Haglund's deformity resection if present.^[85] For plantar enthesitis with equinus contracture, gastrocnemius recession lengthens the tendon to reduce tension, while axial enthesitis in spondyloarthropathies may necessitate spinal fusion to stabilize affected segments.^[86] Excision of enthesophytes is targeted at sites like the calcaneus to eliminate mechanical irritation.^[72] Techniques vary between open surgery, which provides direct visualization for extensive debridement, and minimally invasive arthroscopic approaches that reduce tissue trauma and recovery time. Open procedures, such as midline tendon-splitting for Achilles debridement, allow thorough removal of degenerative tissue but carry higher risks of wound complications.^[87] Arthroscopic methods, including suture anchor repair for central extensor tendon enthesitis, enable precise intervention with smaller incisions, particularly beneficial in inflammatory contexts to minimize flare-ups.^[88] Outcomes generally show 70-85% of patients achieving significant pain relief and functional improvement in selected cases, with Victorian Institute of Sports Assessment-Achilles (VISA-A) scores improving by 20-40 points post-debridement for insertional pathology.^[89] However, complication rates range from 10-25%, including infection, tendon weakening, and recurrence, necessitating careful patient selection.^[90] By 2025, regenerative adjuncts like platelet-rich plasma (PRP) injections prior to or during surgery have emerged to enhance healing at the enthesis, though evidence remains mixed with meta-analyses showing modest benefits in pain reduction but inconsistent tendon regeneration.^[91] Innovations such as demineralized bone fiber implants (e.g., EnFix) and gradient biomimetic scaffolds aim to promote interfacial regeneration in tendon-bone repairs, with early clinical applications reporting improved load-to-failure in rotator cuff models adaptable to enthesitis sites.^[92]^[93]

Prognosis and Complications

Long-term Outcomes

The long-term outcomes of enthesitis vary significantly depending on its etiology, with acute cases arising from overuse typically resolving more favorably than those associated with chronic inflammatory conditions like spondyloarthropathies (SpA). In acute overuse enthesitis, such as in tendinopathies, most patients achieve resolution within 3 to 6 months through rest and rehabilitation, though persistent symptoms may indicate underlying structural changes.^[94] In contrast, chronic inflammatory enthesitis in SpA often persists without disease-modifying antirheumatic drugs (DMARDs) or biologics, leading to recurrent flares and potential structural damage; for instance, Achilles enthesitis resolved in only 67.4% of patients after 2 years, with 32.6% showing ongoing persistence.^[95] With appropriate therapy, resolution rates improve substantially, reaching 80-86% complete remission within 8-9 months on average in psoriatic arthritis (PsA) cohorts treated with DMARDs.^[96] Factors influencing remission include early intervention and genetic markers; prompt treatment initiation in axial SpA enhances long-term remission rates by reducing disease progression, while HLA-B27-negative patients generally exhibit a better prognosis with less severe chronicity compared to HLA-B27-positive individuals.^[97]^[98] Enthesitis can lead to lasting functional impacts, including chronic pain and disability, particularly in PsA, where affected patients show elevated Health Assessment Questionnaire (HAQ) scores indicative of impaired physical function and greater work limitations.^[99] Ongoing follow-up with serial imaging, such as MRI or ultrasound, is recommended in SpA to monitor enthesitis resolution and detect progression toward ankylosis or fibrosis.^[100] Recent 2025 registry and trial data highlight biologics' role in sustained outcomes, with bimekizumab achieving enthesitis remission in approximately 40-53% of SpA patients over 104 weeks, depending on radiographic status.^[101]

Associated Risks

Untreated or chronic enthesitis can lead to several local complications at the affected insertion sites. One significant risk is tendon rupture following corticosteroid injections, with reported incidences around 1-2%; this risk is heightened due to the potential weakening of tendon integrity from the injected steroids, especially in the Achilles tendon where intratendinous administration is contraindicated.^[91] Additionally, persistent inflammation at the enthesis often promotes enthesophyte formation—abnormal bony outgrowths that develop as a reparative response to mechanical stress and chronic irritation—resulting in joint stiffness and reduced mobility.^[102]^[3] Systemic risks arise from the inflammatory cascade extending beyond the local site, potentially progressing to broader spondyloarthropathy (SpA) manifestations. In enthesitis-related arthritis (ERA), a subtype of juvenile idiopathic arthritis, axial involvement develops in 30-60% of cases over time, often emerging within 5 years of diagnosis and contributing to spinal fusion if unmanaged.^[103]^[104] Uveitis occurs in about 20-30% of HLA-B27-positive ERA patients, typically presenting as acute, unilateral anterior inflammation that can recur and impair vision if not screened regularly.^[16]^[65] Chronic inflammation also elevates cardiovascular disease risk, with psoriatic arthritis linked to higher rates of stroke and myocardial infarction due to accelerated atherosclerosis from persistent cytokine release.^[105] Iatrogenic complications stem from therapeutic interventions and disease-related immobility. Local infections, including bacterial abscesses, can occur post-injection at entheseal sites, with glucocorticoid administration carrying a noted risk of swelling, bleeding, and septic events.^[8] Prolonged immobility from pain and stiffness in chronic enthesitis contributes to secondary osteoporosis, particularly in axial forms like ankylosing spondylitis, where reduced weight-bearing exacerbates bone density loss.^[106] In pediatric patients with ERA, untreated hip enthesitis poses specific risks for growth disturbances, including leg length discrepancies and avascular necrosis due to chronic synovitis and vascular compromise in the proximal femur.^[107] These alterations can manifest as radiographic abnormalities, such as coxa magna or shortened femoral neck, impacting long-term gait and function if not addressed early.^[108] Early initiation of biologic therapies, such as TNF-alpha inhibitors, has been shown to mitigate these complication rates by suppressing inflammation promptly, with 2025 analyses indicating improved remission and reduced structural damage in ERA and psoriatic arthritis cohorts.^[103]^[109] This approach limits progression to axial disease and extra-articular involvement, enhancing overall prognosis when combined with routine monitoring.^[110]

Spondyloarthropathies

Enthesitis serves as a defining characteristic of spondyloarthropathies (SpA), a group of interrelated inflammatory disorders that primarily affect the axial skeleton, peripheral joints, and entheses, with enthesitis often manifesting as a key clinical feature alongside axial pain and peripheral arthritis.^[111] In this spectrum, enthesitis reflects the unique pathophysiology involving mechanical stress at tendon and ligament insertions, contributing to both diagnostic classification and disease progression across subtypes.^[2] In ankylosing spondylitis (AS), enthesitis is reported in approximately 25-40% of patients, frequently involving axial sites such as the spinal ligaments and iliac crests, where inflammation at the entheses of the annulus fibrosus and vertebral endplates can lead to erosions and subsequent reactive bone formation known as syndesmophytes.^[112]^[113] These syndesmophytes bridge vertebral bodies, promoting spinal fusion and ankylosis, which underscores enthesitis as a driver of structural damage in AS.^[114] Psoriatic arthritis (PsA), another core SpA subtype, exhibits enthesitis in up to 50% of cases, often at distal peripheral sites like the Achilles tendon, plantar fascia, and hand entheses, frequently coinciding with psoriatic skin lesions and nail dystrophy that exacerbate local inflammation.^[115] The Classification Criteria for Psoriatic Arthritis (CASPAR) explicitly incorporate enthesitis—either current or a history of it at a site distant from the affected joint—as a scoring element, aiding in distinguishing PsA from other arthritides when combined with psoriasis evidence and negative rheumatoid factor.^[115] Among other SpA forms, reactive arthritis, typically triggered by post-infectious mechanisms such as genitourinary or gastrointestinal pathogens, involves enthesitis in about 30% of cases, commonly at lower limb sites like the heels, reflecting an immune-mediated response to microbial antigens.^[116] Undifferentiated SpA, which encompasses early or atypical presentations not fitting specific subtypes, also features enthesitis prominently, often as an initial manifestation alongside peripheral arthritis or uveitis, with prevalence exceeding 70% in some cohorts.^[117] Diagnostic criteria for SpA highlight enthesitis as a pivotal element, particularly in the Assessment of SpondyloArthritis international Society (ASAS) framework, where it serves as an entry criterion for peripheral SpA (alongside arthritis or dactylitis) and as a supportive SpA feature in axial presentations when combined with imaging evidence of sacroiliitis or chronic back pain onset before age 45.^[118] This overlap facilitates early classification, enabling targeted interventions before radiographic progression. The 2022 ASAS-EULAR recommendations for the management of axial spondyloarthritis emphasize a treat-to-target approach using the Ankylosing Spondylitis Disease Activity Score (ASDAS) less than 2.1 for remission or low disease activity, with enthesitis managed as a peripheral manifestation through local glucocorticoid injections if appropriate.^[80] The 2025 British Society for Rheumatology guideline further updates treatment for axial SpA, emphasizing biologics for persistent enthesitis.^[83]

Other Inflammatory Disorders

Enthesitis is a recognized extraintestinal manifestation in inflammatory bowel disease (IBD), occurring in approximately 20-30% of patients with Crohn's disease or ulcerative colitis, predominantly affecting peripheral sites such as the Achilles tendon and plantar fascia without concomitant axial involvement.^[119] Clinical evidence of enthesitis, characterized by tenderness or swelling, has been reported in up to 33% of IBD cases, with ultrasound-detected abnormalities suggesting even higher subclinical prevalence, particularly in active disease states.^[18] This peripheral predominance distinguishes IBD-associated enthesitis from more axial-focused patterns in other conditions. In juvenile idiopathic arthritis (JIA), the enthesitis-related arthritis (ERA) subtype accounts for 10-15% of cases and frequently features enthesitis as a hallmark, often involving lower limb sites like the heels and knees.^[103] HLA-B27 positivity is observed in about 70% of ERA patients, correlating with increased risk of enthesitis at diagnosis and a more chronic course.^[14] Approximately 50% of children with ERA progress to adult-onset spondyloarthritis, with radiographic spinal involvement developing in around 43% over time.^[120] Metabolic disorders can also manifest with enthesitis-like changes. In gout, tophaceous deposits of monosodium urate crystals frequently accumulate at entheseal sites, such as the Achilles tendon and plantar aponeurosis, leading to erosive enthesopathy detectable by computed tomography.^[121] The SAPHO syndrome, encompassing synovitis, acne, pustulosis, hyperostosis, and osteitis, involves enthesopathy in a subset of cases, with ultrasound revealing inflammatory changes at tendon insertions, particularly in the lower extremities and sternoclavicular region.^[122] Infectious and post-infectious conditions occasionally present with enthesitis. Whipple's disease, caused by Tropheryma whipplei, may include enthesitis alongside migratory arthritis in up to 20% of cases, often as part of a multisystem involvement mimicking seronegative spondyloarthropathy.^[123] Sarcoidosis can feature entheseal granulomas, contributing to inflammatory enthesopathy, typically with underlying bone involvement and tenosynovitis in affected joints.^[124] Recent investigations highlight links between enthesitis and diffuse idiopathic skeletal hyperostosis (DISH), a metabolic disorder characterized by enthesophyte formation that can mimic inflammatory enthesitis on imaging, particularly at spinal and peripheral ligamentous attachments.^[125] In DISH, these non-erosive enthesophytes often lead to diagnostic confusion with inflammatory conditions, though the absence of HLA-B27 association and inflammatory markers helps differentiate it.^[126]

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