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Proliferative tenosynovitis (PT) is an inflammatory and proliferative disorder of the synovial membrane of the tendon sheath that is rare in animals. The histological alterations are characterized by multinodular neovascularization, with infiltration of histiocytic and multinucleated giant cells and haemosiderin deposition. We reviewed necropsy and biopsy records of horses submitted to the Setor de Anatomia Patológica of the Universidade Federal Rural do Rio de Janeiro from January 2017 to December 2020 to select cases of PT. We identified PT in three adult Brazilian Mangalarga Marchador horses with nodular lesions on the metacarpophalangeal, metatarsophalangeal or carpal joints. The three horses were under 6 years of age and presented with lameness and pain on palpation. There were recurrences in two horses after surgical removal. Radiographic and ultrasound examinations detected masses in the flexor or extensor tendons and subtendinous bursa. Histological study of synovial membrane and tendon sheath revealed an increased number of vessels, fibroplasia, osseous metaplasia and infiltration of lymphocytes, plasma cells and siderophages. This is the first description of PT in horses, which should be included as an orthopaedic differential diagnosis, especially in Mangalarga Marchador horses with lameness., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Reasons for Performing Study: To describe the clinical symptoms, treatment, and outcome of meniscal cysts in horses. These structures have not been previously described in the literature as a potential cause of lameness in the horse., Hypothesis: Meniscal cysts are an uncommon condition of the femorotibial joint but can be a significant cause of lameness. Symptoms can be resolved by arthroscopic excision., Methods: Records of horses diagnosed with meniscal cysts and treated by cyst excision and meniscal debridement at 2 surgical practices were reviewed. Clinical outcome was determined by repeat veterinary examination and contact with owner., Results: Seven cases of meniscal cyst were treated with arthroscopic cyst excision and meniscal debridement. Five of 7 horses had lameness attributable to femorotibial joint pathology, while the remaining 2 horses had meniscal cysts found incidentally during diagnostic arthroscopy for the treatment of osteochondritis dissecans of the lateral trochlear ridge of the femur. Five of 6 horses with long-term follow-up were sound and a 7th horse was improved 11 months after surgery., Conclusions and Potential Relevance: Meniscal cysts, while uncommon, can be associated with progressive lameness in the horse. Surgical excision of the cysts results in resolution or improvement of symptoms, without evidence of recurrence on follow-up examination., (© 2011 EVJ Ltd.)

Objective: To compare macrostructural and microstructural features of proximal sesamoid bones (PSBs) from horses with and without PSB midbody fracture to gain insight into the pathogenesis of PSB fracture., Sample Population: PSBs from 16 Thoroughbred racehorses (8 with and 8 without a PSB midbody fracture)., Procedures: Parasagittal sections of fractured and contralateral intact PSBs from horses with a PSB fracture and an intact PSB from age- and sex-matched control horses without a PSB fracture were evaluated for visual, radiographic, microradiographic, histologic, and his-tomorphometric differences in bone porosity, vascular channels, heme pigment, trabecular anisotropy, and pathological findings., Results: Fractured PSBs and their contralateral intact PSBs had more compacted trabecular bone than did control PSBs. Focal repair or remodeling was evident in the palmar aspect of many fractured and contralateral intact PSBs. Fracture coincided with microstructural features and propagated from the flexor to the articular surface., Conclusions and Clinical Relevance: Fractured PSBs had adapted to high loading but had focal evidence of excessive remodeling and porosity that likely predisposed the horses to complete fracture and catastrophic injury. Detection of focal injury before complete fracture provides an opportunity for prevention of catastrophic injury. Development of diagnostic imaging methods to assess porosity of PSBs may help to identify at-risk horses and allow for modifications of training and racing schedules to reduce the incidence of PSB fracture in Thoroughbred racehorses.

Objective: To determine the clinical, radiographic, ultrasonographic, and arthroscopic findings associated with tenosynovitis of the carpal synovial sheath induced by exostoses that originate from the caudal surface of the physeal scar of the distal radius and determine the results of surgical removal of those exostoses in horses., Design: Retrospective study., Animals: 10 horses., Procedure: Medical records of horses with effusion in the carpal synovial sheath and lameness evaluated from 1999 to 2003 were examined., Results: All horses had a history of intermittent mild to moderate effusion of the carpal synovial sheath and lameness of 1 forelimb. Results of regional perineural and intrathecal anesthesia of the carpal synovial sheath confirmed that the lameness originated in the carpal synovial sheath. Radiography revealed exostoses originating from the caudal cortex of the distal radius at the level of the closed physis. Arthroscopy was performed for confirmation and removal of exostoses that penetrated the carpal synovial sheath and impinged on the deep digital flexor tendon. All horses returned to previous athletic activity. One horse had a recurrence of clinical signs 12 months after surgery, which resolved with medical treatment., Conclusions and Clinical Relevance: Tenosynovitis of the carpal synovial sheath and lameness were caused by impingement of exostoses of the caudal radius on the lining and contents of the carpal synovial sheath. Although the clinical signs and surgical treatment were similar to that caused by osteochondromas, these exostoses developed at the level of the closed physis of the distal radius and were not radiographically or histologically similar to osteochondromas.

Osteochondral fragments from the axial proximoplantar/proximopalmar region of the proximal phalanx were removed from 38 joints in 30 horses. Ninety-three percent of the horses were Standardbreds, and 28 of the 30 had a low-grade lameness. All but 1 of the horses had hind limb involvement. A total of 43 fragments were removed. Most (71%) of the fragments involved the medial aspect of the joint and had to be dissected from a covering of synovial tissue. Histologically, the circumference of most fragments consisted of a transition zone at the attachment of the joint capsule, a region of nonarticular, non-weight-bearing cartilage, a region where organized, dense connective tissue, presumably remnants of the short sesamoidean ligament were attached, and a region consisting of irregular truncated bony surfaces covered by healing of chronic fracture. There were several areas of degenerate hyaline cartilage, but no areas of normal hyaline cartilage or areas containing related cartilage cores or other evidence of delayed endochondral ossification. Immunohistochemical staining of 4 segments from 1 horse revealed sensory substance P immunoreactive nerves in the fibrous tissue surrounding the bony fragments and within the central cancellous spaces. The histologic appearance suggests that these osteochondral fragments may be a result of fracture, rather than a manifestation of osteochondrosis.

Destructive lesions of the axial region of the proximal sesamoid bones were identified by radiography in eight fetlocks and seven lame adult horses. Lameness ranged from 2 to 5 (mean 4; scale 1 to 5) at the time of examination, with a duration of 10 days to two years (mean 5.6 months). Destructive lesions involved both proximal sesamoid bones when examined radiographically and were situated primarily at the level of the mid-body and apical region of the axial borders. Some lesions were cystic, whereas others eroded the axial border more diffusely. Scintigraphy revealed markedly increased activity within the proximal sesamoid bones of the clinically lame limb of four of the five horses examined. In four horses, post mortem computed tomography revealed axial border bone destruction and cavitary lesions within cancellous bone of affected proximal sesamoid bones. Lesions seen by computed tomography were larger than those identified on radiographic examination. Cavitary lesions not seen radiographically were identified in the proximal sesamoid bones of two clinically unaffected fetlocks examined for comparison in two of the seven horses. Evidence of acute, subacute or chronic/reparative osteomyelitis of the axial region of the proximal sesamoid bones was seen in the 10 fetlocks identified as abnormal from radiography or computed tomography. Also, three horses had septic synovitis of the flexor sheath of the clinically affected limb; of these, two had septic arthritis of the fetlock joint.

Squamous cell carcinoma of the hoof wall, with resultant invasion of the right hind distal phalanx, was identified in a 15-year-old Thoroughbred stallion. The clinical features included a chronic grade 2/5 right hind limb lameness and a sessile dorsal hoof wall mass that was not sensitive to palpation. Radiography revealed a well-circumscribed circular lucency within the distal phalanx, beneath the clinically noticed hoof wall mass. These features were considered to be characteristic of a hoof wall keratoma. Surgical intervention was done 10 months later. The histologic diagnosis at the time of surgery was squamous cell carcinoma. Eight months after surgery, progressive tumor invasion of the distal phalanx resulted in a pathologic articular fracture. This case highlights the need for accurate histologic diagnosis of equine hoof wall masses to differentiate between benign and malignant conditions.

Many lesions of the musculoskeletal system of racing horses are either acute traumatic lesions or are chronic biomechanically induced lesions that become suddenly unstable and provoke acute clinical signs. The latter lesions along with those of DJD are much more common and are of much greater overall economic importance to the racing industry than are the acute traumatic injuries. Chronic biomechanical lesions occur at predictable sites and are the result of an imbalance between repetitive microtrauma sustained in athletic performance and adaptive repair mechanisms of skeletal tissues. The distribution of these lesions in the limbs reflects the patterns of biomechanical forces placed on the skeleton during work at racing speeds and, therefore, reflects the type of racing activity for which the horse was bred. Lesions result when there is a failure of the stressed skeletal structures to adapt to the biomechanical forces placed upon them. Rest or a reduction in the level of training activity permit the healing of many asymptomatic and presumably some symptomatic lesions of the bony tissues. Articular cartilage, tendons, and ligaments have a lower capacity to resolve the damage and return to normal structure and function.

Fracture of the lateral wing of the third phalanx with secondary infection of the distal interphalangeal joint occurred in a neurectomized mare. Puncture of the sole may have been the inciting cause, emphasizing the need for careful daily foot care in neurectomized horses.

Navicular syndrome is a degenerative disorder of the distal half of the flexor surface of the proximal sesamoid bone that is predisposed by faulty foot conformation. In horses that become symptomatic, the faulty conformation results in sustained application of nonphysiologic pressure by the deep digital flexor tendon against the flexor cortex of the bone. This force stimulates an intense bone remodeling response in order to attenuate the pressure. An unfortunate sequela of this response is active hyperemia and edema formation in the medullary cavity of the bone. The edema is organized by fibrous tissue resulting in venous entrapment, venous hypertension, vascular bone pain, and the onset of clinical signs.

Braided carbon fiber sutures were used to repair surgically transected or lacerated digital flexor tendons of 20 mature horses (10 experimental and 10 clinical cases). In addition, 4 experimental horses had tenectomies that were not surgically repaired; these served as controls for the horses with carbon-implanted tendons. Six of the 10 clinically affected horses were returned to their intended use; 2 were euthanatized because of complications and 2 were still recuperating. The experimental horses were euthanatized at 12 days and 1, 2, 4, 8, and 12 months. Tendon scars were structurally and functionally similar in all of these horses. The main histologic difference between the controls and principals was the more extensive remodeling in the latter group at 8 months.