Literature DB >> 24733252

The apoptosis of osteoblasts and osteocytes in femoral head osteonecrosis: its specificity and its distribution.

Eugène Mutijima1, Viviane De Maertelaer, Manu Deprez, Michel Malaise, Jean-Philippe Hauzeur.   

Abstract

The pathogenesis of nontraumatic osteonecrosis (ON) remains unclear. Some studies have suggested that nontraumatic ON is attributed to increased osteocytic apoptosis. To test this hypothesis, a controlled study must compare the apoptosis of osteocytes and osteoblasts in cases of ON and osteoarthritis (OA). To assess either the localized or diffuse patterns of this increased osteocytic and osteoblastic apoptosis, we evaluated both the proximal and distal regions of necrotic areas. Femoral heads resected for total hip prosthesis were included for this study. Of these, 10 were ON cases-three were induced by corticosteroids, three by alcohol abuse, one resulted from trauma, one resulted from hyperlipemia, and two were idiopathic-10 were osteoarthritis cases, and 1 from a patient suffering from a subcapital fracture. The TUNEL reaction was used to detect the apoptosis in osteoblasts and osteocytes. A semi-quantitative evaluation was conducted, at both distal and proximal areas relative to the lesions, specifically in the area surrounding the necrotic region in the osteonecrosis cases, in the eburnated bone in the osteoarthritis cases, and in the subchondral bone fracture. The apoptosis of osteoblasts and osteocytes was statistically more frequent in the regions close to the necrotic areas in the ON group. No difference was found in the unpaired areas. In the ON group, no difference was found in terms of the etiological factors. During ON, the apoptosis of osteocytes and osteoblasts is increased proximally to the necrotic regions in the patients presenting with osteoarthritis and subcapital fractures. This increase was found not only in the corticosteroid-induced ON cases but also in the idiopathic and alcohol abuse- and trauma-induced ON cases.

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Year:  2014        PMID: 24733252     DOI: 10.1007/s10067-014-2607-1

Source DB:  PubMed          Journal:  Clin Rheumatol        ISSN: 0770-3198            Impact factor:   2.980


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