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Bone formation and bone resorption in failed total joint arthroplasties: Histomorphometric analysis with histochemical and immunohistochemical technique
Author(s) -
Kadoya Y.,
Revell P. A.,
AlSaffar N.,
Kobayashi A.,
Scott G.,
Freeman M. A. R.
Publication year - 1996
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.1100140318
Subject(s) - osteolysis , bone resorption , osteoclast , vitronectin , immunohistochemistry , resorption , chemistry , pathology , alkaline phosphatase , acid phosphatase , medicine , dentistry , integrin , receptor , biochemistry , enzyme
To elucidate the reactions of bone around aseptically loosened total joint arthroplasties, 24 interface tissues with adjacent bone were obtained in 17 revision operations (11 hips and six knees). The morphology of the bone surface next to the interface membrane was investigated with histochemical and immunohistochemical techniques and then histomorphometrically analysed. One‐third of the total bone surface, 32.69 ± 5.16% (mean ± SE) (n = 24), showed positive alkaline phosphatase activity. The bone surface in contact with the cells positive for CD11b (a macrophage marker) amounted to 19.33 ± 5.16% (n = 24). The proportion of the osteoclastic bone resorption estimated by vitronectin receptor expression was 7.67 ± 1.82% (n = 21). Tissues retrieved from the sites where radiographic evidence of osteolysis was present (n = 12) had a significantly larger extent of the bone surface in contact with CD11b‐positive cells than did the tissues from areas without osteolysis (n = 12, p = 0.0067, Mann‐Whitney U test), whereas no significant difference was observed in the extent of osteoclastic bone resorption. These data demonstrate that active bone formation, regarded as a repair process, is the most common feature even in revised cases. They also highlight the role played by macrophages, not as cells producing inflammatory mediators that could activate osteoclasts, but as cells primarily responsible for the bone loss in osteolytic lesions.