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The incidence and predictors of premature physeal closure (PPC) after pediatric distal tibial fractures were investigated. PPC was defined as evidence of growth plate disturbance on the injured side compared with the uninjured side. Ninety-two fractures were reviewed with at least 1 year of follow-up, or until physiologic closure of the growth plates. Twenty-five fractures (27.2%) were complicated by PPC, as confirmed by CT scan in most cases. Salter-Harris III and IV (medial malleolar type) fractures resulted in the highest percentage of PPC by fracture type (38%). Salter-Harris I and II fractures resulted in PPC in 36% of cases, followed by triplane fractures (21%) and Tillaux fractures (0%). Initial displacement, number of reduction attempts, or treatment method did not significantly affect the incidence of PPC. More anatomic reductions resulted in a statistically significant decrease in PPC rates. Residual physeal gap (>3 mm) following reduction was determined from radiographs in Salter-Harris I and II fractures. If a residual gap was seen on the radiograph, the incidence of PPC increased to 60%; if no gap was present, the incidence decreased to 17%. Open reduction was performed in five Salter-Harris II fractures that had a residual gap. Periosteum was entrapped in the physis in all of these cases. Residual gaps in the physis following closed reduction may represent entrapped periosteum in Salter-Harris I and II fractures. This can lead to a higher incidence of PPC, suggesting that open reduction and removal of the entrapped periosteum may be beneficial.

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Tumoral calcinosis occurs as a well-defined pathologic entity in 3 heterologous groups of diseases--hyperphosphatemic familial tumoral calcinosis, normophosphatemic tumoral calcinosis, and secondary tumoral calcinosis. The histological lesion is stereotypic developing from the concurrence of a juxta-articular injury with an elevated calcium-phosphorus product. The reparative response to injury is histiocytic featuring synovial metaplasia forming bursa-like structures that create the characteristic compartmentalization of the lesion. Histiocytic-derived osteoclastogenesis occurs as a response to the calcifying process initiated in the mitochondria of necrotic histiocytes forming the bursa-like structures. These calcifications, propelled by a gamut of conditions elevating serum phosphorus, facilitate the further nucleation of hydroxyapatite in mitochondria, matrical lipidic debris located in the cytoplasm and lysosomes of osteoclasts and in the locular contents, and on collagen and other extracellular matrix materials. The lesions enlarge because of new locule formation and failure to reduce the calcified burden by the compartment lining histiocytes and dysmorphic osteoclasts that are unable to solubilize the hydroxyapatite. The histological landmarks of tumoral calcinosis may be lost when its development becomes quiescent. The classic calcifying classifications are inadequate for tumoral calcinosis requiring creation of a new category for this entity.