Joints: Narrowed Joint Space and Ankylosis
Bone bridges prior to joint.
Ankylosis correlates with the locations of fusion; surgical defects and hardware may be present.
Sequelae of septic arthritis
Frank destruction of joint leads to eventual ankylosis.
Joint space narrowing from cartilage loss leads to ankylosis.
Locations correspond to sites of inflammation.
Infantile cortical hyperostosis (Caffey syndrome)
Smooth interosseous bridging and cortical thickening between long bones (e.g., radius and ulna). Involves diaphysis and spares epiphysis.
Synostosis may occur between two adjacent long bones after resolution of the acute phase.
Proximal radius and ulna are fused by a bone bridge.
The trabecular bone between the proximal radius and ulna is continuous.
Fibrodysplasia ossificans progressiva
Soft-tissue ossification bridging joints.
Intermittent progressive heterotopic bone replaces skeletal muscle and connective tissues.
Fig. 5.40, p. 522
Cartilage loss, marginal osteophytes, subchondral bone marrow edema, sclerosis, and cysts.
Although typically seen in adults, secondary OA may complicate JIA or the later stages of AVN. Any disorder that causes abnormal m echanics may lead to OA: posttraumatic, after repair of anterior cruciate ligament.
Sequela of septic arthritis
Fig. 5.22, p. 509
Presumably, pyarthrosis increases intracapsular pressure and compromises epiphyseal blood flow. Inflammation contributes to acute cartilage loss.
Fig. 5.41a, b, p. 522
Joint space narrowing at sites of inflammation. May have imaging findings of synovial thickening and hyperemia, bone marrow edema (MRI), and erosions.
Inflammation contributes to acute cartilage loss.
Resembles JIA. Epiphyses of affected joints are often enlarged.
Narrowing of the joint space usually results from diseases that cause cartilage loss. A narrowed joint space may be a precursor to ankylosis.
Autosomal dominant and sporadic forms.
Associated skeletal anomalies
Developmental dysplasia of the hip, club feet, missing or diminutive thumb, coalescence of carpal bones, symphalangism, and dislocation of radius.
Multiple exostoses, acrocephalopolysyndactyly, Holt-Oram, mandibulofacial dysostosis, Nievergelt dysplasia and Apert, Williams, Klinefelter (and other variants of Klinefelter syndrome with extra sex chromosomes), Nievergelt-Pearlman, and fetal alcohol syndromes.
Proximal radioulnar synostosis may arise from a defect in longitudinal segmentation at the seventh week of development and is bilateral in 60% of cases. Surgery is rarely indicated (because bridge regrows) except for severe pronation deformities.
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