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- Severe Joint Damage in Canine Haemophilia B Revealed by MRI and Histology
Severe Joint Damage in Canine Haemophilia B Revealed by MRI and Histology
Vet Comp Orthop Traumatol 2025
Obi Veterinary Education
August 20, 2025
Sarah L. Pownder, Brian G. Caserto, Marjory B. Brooks, Kei Hayashi
Background
Factor VII deficiency (F7d) and Factor IX deficiency (F9d) are inherited bleeding disorders in dogs and humans, with F9d (haemophilia B) often leading to more severe bleeding manifestations. Haemophilic arthropathy (HA), a chronic joint disease caused by recurrent haemarthrosis, is a major complication in human haemophilia, but little is documented in canine cases. This study aimed to describe post-mortem MRI and histologic joint findings in two Beagles with naturally occurring F7d and F9d.
Methods
Two adult female Beagles—one with homozygous F7d and one with severe F9d—were examined post-mortem. Limbs were scanned using 3-T MRI with proton density fast spin echo imaging, and joints were assessed for known HA features. Selected joints with MRI abnormalities were processed for histopathology. MRI was interpreted by a board-certified veterinary radiologist, and histology assessed cartilage, synovium, and subchondral bone changes.
Results
Eight of nine recognized HA imaging features were identified, including cartilage degeneration, subchondral cysts, marginal erosions, neovascularization, synovial inflammation and hyperplasia, hemosiderin deposition, haematoma, and osteopenia. Changes were most severe in the F9d dog, with severe joint pathology in shoulders, elbows, stifles, and metacarpophalangeal joints. The F7d dog showed only mild degenerative changes similar to an age-matched non-haemophiliac Beagle. Histology confirmed thickened, hypervascular synovium with villous projections, marginal osseous erosions, cartilage thinning, and hemosiderin-laden macrophages in the F9d dog. An additional finding was chondroid metaplasia in the triceps tendon of the F9d dog.
Limitations
The study involved only two cases, limiting generalizability. No breed/age/sex-matched control histology was available. Poor hemosiderin staining may have been due to decalcification methods, chronic iron deficiency, or rapid clearance of blood from canine joints. Not all joints were available for examination.
Conclusions
Severe HA in the F9d Beagle closely resembled human disease, supporting MRI as a valuable tool for detecting joint pathology after repeated haemarthrosis in dogs. F7d was associated with only mild joint changes, suggesting that HA severity correlates with bleeding phenotype. These findings may guide both veterinary diagnosis and comparative haemophilia research.
Photomicrograph (haematoxylin and eosin stain) of the shoulder (A, D, G), proton density fast spin echo magnetic resonance
images (B, E, H), and corresponding three-dimensional reconstructions of the shoulder (C, F, I) in the transverse (A–C), dorsal (E, F), and sagittal
(G–I) planes of the Factor IX-deficient dog. Deep to the supraspinatus attachment (A–C, F, H, I; oval-headed black arrows), a large osseous erosion
is seen consistent with a pseudocyst. The pseudocyst (G) shows oedematous, loosely arranged concentric collagen fibres bordered by a rim of
bone (lower portion of image). The shoulder demonstrates a thickened synovium (E, H, white arrowheads) and a regionally thickened
infraspinatus tendon (E, white star). Microscopically, at low magnification (A), the joint capsule is thick, and a large lytic lesion at the area
between the tubercle and articular surface is seen (pseudocyst). The synovium (D) has short villous projections with small numbers of
lymphocytes and plasma cells in the supporting layer and contains increased collagenous connective tissue and congested vasculature.
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