Ringbone and Sidebone (High and Low Ringbone / Osteoarthritis of the Pastern and Coffin Joints)

Ringbone is a chronic, progressive, proliferative osteoarthritis (OA) affecting the synovial joints and/or periarticular structures of the distal interphalangeal (coffin) joint (low ringbone) or the proximal interphalangeal (pastern) joint (high ringbone). It is characterized by periarticular new bone formation, joint capsule thickening, synovitis, and cartilage degradation, leading to pain, lameness, and reduced athletic performance. Sidebone is a separate but often concurrent condition involving ossification of the collateral cartilages of the distal phalanx (cartilages of the foot), which can be associated with trauma or chronic inflammation. Both conditions are common in performance horses, particularly those involved in disciplines requiring high-impact foot placement, such as jumping, dressage, eventing, and Western performance events. The disease can be classified as articular (involving the joint) or periarticular (involving the joint capsule and ligaments), and as high (pastern joint) or low (coffin joint) based on anatomical location. Ringbone is a leading cause of chronic forelimb lameness, especially in middle-aged horses, and can significantly shorten an athletic career if not managed appropriately.

The etiology of ringbone is multifactorial, involving biomechanical stress, trauma, and conformational predispositions. Primary causes include: 1) Repetitive concussive forces and torsional stress on the pastern and coffin joints, particularly in horses performing rapid turns, jumping, or working on hard surfaces. 2) Acute trauma, such as kicks, falls, or overextension of the joint, leading to periarticular soft tissue injury and subsequent new bone formation. 3) Conformational abnormalities, including upright pasterns, toe-in or toe-out limb deviations, and unbalanced feet, which alter joint loading and predispose to OA. 4) Osteochondrosis or other developmental orthopedic diseases that may lead to joint incongruity and early cartilage damage. 5) Chronic low-grade infection or septic arthritis, though less common, can initiate degenerative changes. 6) In some cases, a genetic predisposition is suspected, particularly in certain breeds like Quarter Horses and Warmbloods. Sidebone specifically is often associated with trauma to the collateral cartilages, such as from stepping on uneven ground or direct blows, and may also be linked to chronic laminitis or poor foot conformation. The exact pathogenesis involves a cycle of cartilage damage, release of inflammatory mediators (e.g., cytokines, matrix metalloproteinases), synovitis, and subchondral bone remodeling, leading to periarticular osteophyte formation and progressive joint degeneration.

Ringbone is most commonly diagnosed in middle-aged horses (8-15 years old), though it can occur in younger horses, especially those with conformational predispositions. There is no strong sex predilection, but some studies suggest a higher incidence in geldings and stallions, possibly due to increased athletic use. Breeds commonly affected include Thoroughbreds, Warmbloods, Quarter Horses, and Arabians, reflecting their use in disciplines with high joint stress. The condition is more frequent in the forelimbs, particularly the front feet, due to the greater weight-bearing load (approximately 60% of body weight). High ringbone (pastern joint) is more common in horses used for jumping and dressage, while low ringbone (coffin joint) is often seen in Western performance horses and racehorses. Sidebone is more prevalent in heavy breeds and draft horses, but can occur in any breed. The overall prevalence in the general equine population is estimated at 5-10%, but it is significantly higher in performance horses, with some studies reporting up to 30% in jumping horses. Morbidity is high in affected populations, and the condition is a common cause of chronic lameness, leading to premature retirement from athletic activity. Mortality is negligible, but euthanasia may be considered in severe, unmanageable cases.

The pathophysiology of ringbone involves a complex interplay of mechanical, inflammatory, and degenerative processes. Initially, excessive or abnormal biomechanical stress on the articular cartilage leads to chondrocyte injury and release of pro-inflammatory cytokines (e.g., IL-1, TNF-α) and matrix metalloproteinases (MMPs). These mediators degrade the extracellular matrix, particularly proteoglycans and collagen, leading to cartilage fibrillation and erosion. Synovitis develops as the joint capsule becomes inflamed, producing increased synovial fluid volume and altered viscosity. The subchondral bone undergoes remodeling, with increased bone turnover and sclerosis, which can lead to subchondral bone cysts or microfractures. In response to chronic inflammation and instability, periarticular osteophytes form at the joint margins, which are the hallmark radiographic feature of ringbone. These osteophytes can restrict joint motion and cause mechanical pain. In sidebone, ossification of the collateral cartilages occurs, likely due to trauma or chronic inflammation, leading to calcification and eventual bone formation. The ossified cartilages can impinge on the hoof capsule or cause pressure on the digital nerves, contributing to lameness. Pain arises from synovitis, periostitis, and increased intra-articular pressure, as well as from mechanical impingement of osteophytes on surrounding soft tissues. The disease is progressive, with ongoing cartilage loss and bone remodeling leading to joint ankylosis in severe cases, which may paradoxically result in pain relief once complete fusion occurs.

Intrinsic predisposing factors include: 1) Conformation: upright pasterns, short, steep pasterns, and small, boxy feet increase concussive forces on the joints. Toe-in or toe-out deviations and base-narrow or base-wide limb conformations also alter joint loading. 2) Age: older horses have cumulative wear and tear, and cartilage becomes less resilient. 3) Breed: certain breeds, such as Quarter Horses and Warmbloods, may have a genetic predisposition. 4) Pre-existing joint disease: osteochondritis dissecans (OCD) or subchondral bone cysts can predispose to OA. 5) Foot balance: improper hoof trimming and shoeing, such as long toes and low heels, increase stress on the pastern and coffin joints. Extrinsic factors include: 1) Athletic discipline: high-impact activities like jumping, eventing, and barrel racing increase risk. 2) Training surfaces: hard or uneven footing increases concussive forces. 3) Trauma: direct injury to the pastern or foot. 4) Poor farriery: infrequent or incorrect trimming/shoeing. 5) Obesity: increased body weight exacerbates joint stress. 6) Inadequate warm-up or conditioning. 7) Previous lameness or injury to the same limb, leading to altered gait and overload of the affected joint.

Clinical signs of ringbone vary depending on the severity and location. Early signs may include subtle lameness that worsens with exercise or on hard surfaces, and improves with rest. Lameness is often graded on the AAEP scale (0-5): Grade 0 is sound, Grade 1 is mild lameness that is inconsistent, Grade 2 is consistent lameness under certain conditions, Grade 3 is consistent lameness at all times, Grade 4 is obvious lameness with marked head nod, and Grade 5 is severe lameness with minimal weight-bearing. Horses with high ringbone may show a shortened stride, reduced flexion of the pastern joint, and pain on flexion tests. Low ringbone often presents with a characteristic 'pointing' of the foot at rest, and pain may be elicited by hoof testers applied over the affected area. Digital pulse amplitude is often increased in the affected limb. Swelling and heat may be palpable around the pastern or coronary band. In advanced cases, visible bony enlargement (ring-like callus) may be present. Sidebone may cause lameness if the ossified cartilage impinges on the hoof or nerves, but many cases are asymptomatic. Horses may also exhibit reluctance to turn, stumble, or have a 'pottery' gait. In severe cases, joint effusion and crepitus may be detected. Chronic cases may show muscle atrophy in the shoulder or gluteal region due to disuse.

Differential diagnoses for ringbone include: 1) Pastern joint osteoarthritis (high ringbone) vs. other causes of pastern lameness such as fractures (e.g., proximal phalanx fractures), desmitis of the collateral ligaments of the pastern joint, or osteochondrosis. 2) Coffin joint osteoarthritis (low ringbone) vs. navicular disease, laminitis, pedal bone fractures, or septic arthritis. 3) Sidebone vs. hoof wall cracks, abscesses, or keratoma. 4) Other causes of lameness in the distal limb include: - Laminitis: acute or chronic, characterized by divergent sole growth, rotated distal phalanx on radiographs, and severe pain. - Navicular syndrome: lameness localized to the heel region, positive response to navicular bursa blocks, and radiographic changes such as cysts or erosions on the navicular bone. - Pedal osteitis: inflammation of the distal phalanx, often due to trauma or laminitis, with radiographic evidence of bone resorption. - Septic arthritis: acute severe lameness, joint effusion, fever, and positive synovial fluid culture. - Fractures: such as proximal phalangeal fractures or distal phalanx fractures, diagnosed by radiography or MRI. - Desmitis of the collateral ligaments of the distal interphalangeal joint: diagnosed by ultrasound or MRI. - Keratoma: a benign tumor of the hoof wall, causing lameness and characteristic radiographic lucency. - Hoof abscess: acute severe lameness, positive response to hoof testers, and drainage of purulent material. - Pastern dermatitis (scratches): skin infection causing lameness if severe. - Flexural deformities: such as club foot, which can cause abnormal joint loading. - Osteochondritis dissecans (OCD) of the pastern or coffin joints: usually in young horses, diagnosed by radiography. - Chronic progressive lymphedema: swelling of the distal limbs, but not typically causing lameness. - Tarsal osteoarthritis (bone spavin) can cause hindlimb lameness, but is less likely to be confused with ringbone. Each differential can be ruled out by specific diagnostic tests: nerve blocks (e.g., palmar digital block for navicular, abaxial sesamoid block for pastern), radiography (for fractures, OA, laminitis), ultrasound (for soft tissue injuries), MRI (for early cartilage or bone changes), and synovial fluid analysis (for sepsis).

The diagnostic algorithm for ringbone follows a systematic approach: 1) History and physical examination: Obtain a detailed history including signalment, use, onset, and progression of lameness. Perform a thorough lameness examination at the walk and trot on a hard surface, noting the grade and response to flexion tests. Palpate the distal limbs for heat, swelling, and pain. Assess digital pulses. 2) Diagnostic anesthesia: Perform perineural nerve blocks to localize the source of lameness. For low ringbone, a palmar digital nerve block (at the level of the proximal sesamoids) may improve lameness. For high ringbone, an abaxial sesamoid nerve block (blocking the palmar nerves at the base of the proximal sesamoids) is often used. Intra-articular anesthesia of the coffin or pastern joint can confirm joint involvement. 3) Radiography: Obtain standard radiographic views of the foot and pastern, including lateromedial, dorsopalmar (or dorsoplantar), and oblique views. Look for periarticular osteophytes, joint space narrowing, subchondral bone sclerosis, and in advanced cases, ankylosis. For sidebone, radiographs may show ossification of the collateral cartilages. 4) Ultrasonography: Useful for evaluating periarticular soft tissue structures, such as the collateral ligaments and joint capsule, and for detecting early periarticular new bone formation. 5) Advanced imaging: MRI or CT may be indicated if radiographs are inconclusive or to assess early cartilage damage, subchondral bone changes, or soft tissue involvement. 6) Synovial fluid analysis: If septic arthritis is suspected, perform arthrocentesis and analyze synovial fluid for white blood cell count, total protein, and culture. 7) Scintigraphy (bone scan) can identify areas of increased bone turnover, but is less specific. 8) Response to treatment: A positive response to intra-articular corticosteroids or hyaluronan can confirm the diagnosis. The algorithm should be tailored to the individual case, but always begins with a thorough lameness exam and nerve blocks.

Laboratory findings in ringbone are generally non-specific, but may be helpful in ruling out other conditions. Complete blood count (CBC) is usually within normal limits, unless there is concurrent infection or inflammation. Serum biochemistry may show mild elevations in muscle enzymes (CK, AST) if there is muscle atrophy or exertional myopathy, but these are not specific. Synovial fluid analysis is more useful: in osteoarthritis, the fluid is typically clear to slightly yellow, with a normal to mildly elevated white blood cell count (<1,000 cells/µL) and total protein (<2.5 g/dL). In septic arthritis, the WBC count is >30,000 cells/µL, total protein >4 g/dL, and culture may be positive. Inflammatory markers such as serum amyloid A (SAA) may be elevated in acute inflammation or infection, but are not specific for ringbone. If laminitis is a differential, insulin and glucose levels may be measured to assess for insulin dysregulation. ACTH levels may be checked if PPID is suspected as a contributing factor. However, in typical cases of ringbone, laboratory findings are unremarkable, and the diagnosis is based on imaging and clinical signs.

Radiography is the primary imaging modality for ringbone. For high ringbone, lateromedial and dorsopalmar (or dorsoplantar) views of the pastern joint will show periarticular osteophytes on the dorsal and palmar/plantar aspects of the proximal and middle phalanges, joint space narrowing, and subchondral bone sclerosis. In advanced cases, there may be bony bridging across the joint (ankylosis). For low ringbone, lateromedial and dorsopalmar views of the foot will show osteophytes on the extensor process of the distal phalanx and on the distal aspect of the middle phalanx, as well as joint space narrowing. Sidebone is visible on dorsopalmar or oblique views as ossification of the collateral cartilages, which appear as radiopaque structures adjacent to the distal phalanx. Ultrasonography can be used to evaluate the joint capsule, collateral ligaments, and periarticular soft tissues, and may detect early periarticular new bone formation before it is radiographically visible. MRI is highly sensitive for detecting early cartilage damage, subchondral bone edema, and soft tissue injuries, and is particularly useful when radiographs are normal but lameness is localized to the pastern or coffin joint. CT provides excellent bone detail and is useful for surgical planning. Scintigraphy (bone scan) can identify areas of increased bone turnover, but is less specific. In all cases, imaging should be interpreted in conjunction with clinical findings and nerve blocks.

Cytology of synovial fluid from affected joints typically shows a mild increase in nucleated cell count (predominantly mononuclear cells) and total protein, consistent with non-septic inflammation. Histopathology of the joint capsule and periarticular tissues reveals synovial hyperplasia, fibrosis, and infiltration of inflammatory cells. Cartilage shows fibrillation, erosion, and loss of proteoglycans. Subchondral bone shows sclerosis, microfractures, and new bone formation. In sidebone, histopathology of the collateral cartilages shows endochondral ossification, with islands of cartilage within the bone. These findings are characteristic but not pathognomonic, and are rarely needed for diagnosis.

Treatment of ringbone aims to reduce pain, slow disease progression, and maintain athletic function. Conservative management includes: 1) Rest and controlled exercise: Initial rest (4-8 weeks) followed by a gradual return to work on soft footing. 2) Non-steroidal anti-inflammatory drugs (NSAIDs): Phenylbutazone (2.2-4.4 mg/kg PO q12h) or flunixin meglumine (1.1 mg/kg IV or PO q12h) for acute flare-ups, but long-term use is discouraged due to GI and renal side effects. 3) Intra-articular therapy: Corticosteroids such as triamcinolone acetonide (6-12 mg per joint) or methylprednisolone acetate (40-80 mg per joint) combined with hyaluronan (20-40 mg per joint) can provide significant pain relief. These are often used in conjunction with systemic hyaluronan (e.g., 40 mg IV q7d for 3 weeks). 4) Disease-modifying osteoarthritis drugs (DMOADs): Polysulfated glycosaminoglycan (Adequan) 500 mg IM q4d for 7 treatments, or oral glucosamine/chondroitin supplements. 5) Extracorporeal shockwave therapy (ESWT) may be beneficial in some cases. 6) Farriery: Corrective shoeing is crucial. For low ringbone, a shoe with a rolled toe and wide web, or a bar shoe with heel support, can reduce joint stress. For high ringbone, a shoe with a raised heel may help. 7) Surgical options: Arthrodesis of the pastern joint (for high ringbone) is a salvage procedure that can provide long-term pain relief, but is reserved for severe cases. Arthrodesis of the coffin joint is rarely performed. Palmar digital neurectomy may be considered for low ringbone, but carries risks of neuroma and recurrence. 8) Alternative therapies: Acupuncture, chiropractic, and regenerative medicine (e.g., stem cell therapy, platelet-rich plasma) are being explored, but evidence is limited. In all cases, a multimodal approach is recommended, with regular monitoring and adjustment of therapy based on response.

The prognosis for ringbone depends on the severity, location, and response to treatment. For low ringbone, the prognosis is generally guarded to fair, with many horses returning to light work, but some may require retirement. For high ringbone, the prognosis is more guarded, especially if there is significant periarticular new bone formation. Arthrodesis of the pastern joint has a good prognosis for pasture soundness, but not for high-level athletic performance. Sidebone is often an incidental finding and may not cause lameness; if it does, the prognosis is good with conservative management. Negative prognostic indicators include: advanced age, severe radiographic changes (e.g., joint space obliteration, large osteophytes), lack of response to intra-articular therapy, and involvement of multiple joints. Positive prognostic indicators include: early diagnosis, minimal radiographic changes, and good response to treatment. Overall, with appropriate management, many horses can continue in some capacity, but the athletic career may be shortened.

Follow-up for ringbone should include regular re-evaluation every 4-8 weeks initially, then every 3-6 months. Serial lameness examinations and radiographs are recommended to monitor disease progression. Farriery should be checked every 4-6 weeks to maintain proper foot balance. A controlled exercise program should be implemented, with gradual increases in duration and intensity. Owners should be educated on signs of pain and lameness, and advised to adjust work accordingly. In cases of intra-articular therapy, repeat injections may be needed every 6-12 months. If surgery is performed, post-operative care includes stall rest for 4-8 weeks, followed by a gradual return to exercise. Long-term follow-up is essential to manage the disease and maintain quality of life.

Pearls: 1) Always perform a thorough lameness exam with nerve blocks before imaging, as ringbone can be masked by other conditions. 2) Use intra-articular anesthesia to confirm joint involvement. 3) Radiographs should include multiple views to detect subtle osteophytes. 4) Early aggressive treatment with intra-articular therapy and corrective shoeing can slow progression. 5) Consider MRI if radiographs are normal but lameness persists. 6) In sidebone, many cases are asymptomatic; do not attribute lameness to sidebone unless other causes are ruled out. Pitfalls: 1) Failing to rule out navicular disease or laminitis, which can coexist. 2) Over-reliance on radiographs, which may not show early changes. 3) Using NSAIDs long-term without addressing the underlying joint disease. 4) Neglecting farriery, which is critical for management. 5) Performing neurectomy without considering the risk of neuroma and recurrence. 6) Assuming that ankylosis will always resolve pain; it may not. 7) Not considering the horse's intended use when recommending treatment.

Current drug protocols for ringbone include: 1) NSAIDs: Phenylbutazone (2.2-4.4 mg/kg PO q12h for 3-5 days, then as needed), Flunixin meglumine (1.1 mg/kg IV or PO q12h for 2-3 days), Firocoxib (0.1 mg/kg PO q24h for 14 days, then 0.1 mg/kg q48h). 2) Intra-articular corticosteroids: Triamcinolone acetonide (6-12 mg per joint for coffin joint, 10-20 mg for pastern joint) combined with hyaluronan (20-40 mg per joint). Methylprednisolone acetate (40-80 mg per joint) is an alternative. 3) Systemic hyaluronan: 40 mg IV q7d for 3 weeks, then as needed. 4) Polysulfated glycosaminoglycan (Adequan): 500 mg IM q4d for 7 treatments, then monthly. 5) Pentosan polysulfate: 3 mg/kg IM q7d for 4 weeks, then monthly. 6) Oral supplements: Glucosamine (10 g/day) and chondroitin sulfate (5 g/day) are commonly used, though evidence is limited. 7) For acute flare-ups, a short course of dexamethasone (0.04-0.1 mg/kg IV) may be used. 8) In cases of septic arthritis, antibiotics such as penicillin G (22,000 IU/kg IV q6h) and gentamicin (6.6 mg/kg IV q24h) are indicated. 9) For pain management, opioids such as morphine (0.1-0.2 mg/kg IM or IV q4-6h) or butorphanol (0.01-0.02 mg/kg IV) may be used in severe cases. 10) Adjunct therapies: ESWT (2000-3000 shocks at 0.15-0.25 mJ/mm²) may be applied to the affected joint. All protocols should be tailored to the individual horse, with monitoring for adverse effects.

Evidence-based literature on ringbone is limited but growing. A landmark study by Dyson et al. (2003) evaluated the clinical features and response to treatment in horses with pastern joint OA, finding that intra-articular corticosteroids and corrective shoeing improved lameness in 60% of cases. A study by Sherlock et al. (2016) compared arthrodesis vs. medical management for high ringbone, showing that arthrodesis provided better long-term soundness but had a higher complication rate. A systematic review by Van Weeren and de Grauw (2017) on DMOADs concluded that there is moderate evidence for the use of polysulfated glycosaminoglycan and hyaluronan in equine OA. A consensus statement from the American College of Veterinary Surgeons (ACVS) on management of osteoarthritis recommends a multimodal approach including weight management, exercise modification, and intra-articular therapy. A study by Ribera et al. (2011) on the use of triamcinolone in the coffin joint showed significant improvement in lameness for up to 6 months. Regarding sidebone, a study by Ruohoniemi et al. (1997) found that ossification of the collateral cartilages is common in Finnhorses and is often incidental. Overall, the evidence supports the use of intra-articular corticosteroids and hyaluronan, as well as corrective farriery, but more research is needed on long-term outcomes and regenerative therapies.