[Pathomorphological aspects and repair mechanisms of femur head necrosis]

Abstract

The pathomorphologies of non-traumatic femoral head osteonecroses (ON) are usually similar, despite various known pathogenetic factors. The size and position of the subchondral bone and marrow segment, becoming necrotic after the ischemic event(s), and the kind of repair processes determine the time course and thus the fate of this hip joint disease. Four cases of conservatively or core decompression-treated femoral head ON were selected to demonstrate differently effective repair mechanisms which are discussed in respect to existing therapeutic concepts. Diagnostic criteria from magnetic resonance imaging follow-ups were correlated with light microscopy findings on undecalcified ground and microtome sections from femoral heads retrieved at total joint replacement. Initial stage (ARCO 0) and reversible early stage ON (ARCO 1) after incomplete ischemias can apparently show spontaneous sufficient repair. After extensive and complete ischemia, however, ON progresses without detectable changes on plain radiographs into irreversible early stage ON (ARCO stage 2). Only in exceptional cases (with small, medially located necroses), a spontaneous sufficient repair seems possible. Usually, early ARCO stage 2 ON with intact articular surface shows no remodeling of the subchondral necrotic bone and fatty marrow, but only ineffective repair with fibrovascular tissue invasion and bone resorption at the vital bone border. Repeated bone appositions on partly resorbed necrotic trabeculae form the sclerotic rim in this pathognomonic reactive interface. New bone formation can also be increased underneath the necrotic area and reactive interface when surrounded by accompanying bone marrow edema. Core decompression in ARCO stage 2 ON, even if it reaches the necrotic lesion, can at best delay progression of the disease, but never leads to complete reconstruction of the necrotic area. More likely, after both conservative and operative treatment, destructive resorption without effective consecutive bone formation will lead sooner or later to collapse of the articular surface and thus to mechanical instability of transition stage ON (ARCO stage 3). On the other hand, this subchondral fracture can apparently also cause reconstructive repair which, by involving chondral and membranous ossification in this "creeping substitution", can reduce the necrotic area. However, it cannot prevent progression into late stage ON (ARCO stage 4) with secondary joint destructions. Principally, besides the rare sufficient repair in initial and certain early ON, three forms of insufficient repair in the necrotic area can be distinguished: lack of remodeling, destructive remodeling, and reconstructive remodeling. To date, no therapeutical intervention exists which leads to complete healing of irreversible ON stages by reconstructive repair. Improved understanding of pathomorphology and repair mechanisms, however, could be the basis for future therapeutical concepts which should aim at the complete regeneration of the osteonecrotic area.