Ischaemic chondronecrosis as a novel causative factor in the aetiopathogenesis of infantile Blount’s disease

Infantile Blount’s disease primarily affects toddlers, leading to tibia vara with or without growth arrest. While the disease’s association with abnormal compressive forces on the proximal tibial physis is widely accepted, its precise aetiopathology remains elusive. This hypothesis suggests that ischaemic chondronecrosis serves as a previously unaddressed cause of Blount’s disease. Notably, it is also the foremost theory to offer a comprehensive explanation for the specificity of involvement of the posteromedial tibial epiphysis, addressing a crucial aspect that was overlooked in prior research. The theory of pressure-induced ischaemic chondronecrosis is supported by a compelling body of radiological and histological evidence. Experimental studies on femoral heads in animals highlight the susceptibility to ischaemic injury in the absence of an ossific nucleus. The proposed mechanism could explain the delayed ossification observed in the proximal medial tibial epiphysis in Blount’s disease. Comparisons with Perthes’ disease reveal striking parallels in radiographic and histological features, pointing toward a shared aetiology of vascular insult. Despite both conditions progressing through similar stages, the distinction lies in Perthes’ being characterised by osteochondral necrosis, while Blount’s results from chondronecrosis. The potential applications of this hypothesis extend to early detection and prevention, emphasising the avoidance of compression on the medial tibial epiphysis. The study suggests a reevaluation of brace therapy and exploration of the role of serial valgus casting, especially in the early stages of insult and limited to walking time, as a preventive measure against ischaemic chondronecrosis and its complications.

In conclusion, this hypothesis sheds light on a novel mechanism of Blount’s disease. Further research is warranted to validate and refine this proposition, offering promising avenues for addressing a century-long enigma in its aetiology.