ISSN:
1432-0878
Schlagwort(e):
Bone resorption
;
Implantation
;
Osteoclasts
;
Osteopetrosis
;
Mononuclear phagocytes
;
Rat
Quelle:
Springer Online Journal Archives 1860-2000
Thema:
Biologie
,
Medizin
Notizen:
Summary Faulty osteoclasts, characteristic of the incisors-absent (ia) rat mutation of osteopetrosis, cause a resorptive defect which results in the persistence of immature, highly mineralized bone matrix. We implanted osteopetrotic bone subcutaneously into normal andia rats to determine ifia bone could induce functionally active and morphologically identifiable osteoclasts at the implant surface. Assays of45Ca released from the preparations showed that normal andia recipients were capable of equivalent cell-mediated release of Ca over a 2-week implant period, indicating that theia resorptive defect was not reproduced at the subcutaneous site. Freeze-thawed osteopetrotic bone released twice as much45Ca as normal bone. This difference was eliminated by collagenase treatment. Cellular profiles were similar in both normal andia animals regardless of the implant preparation. At 3 days after implantation, both bone and suture were surrounded by mononuclear cells. By 14 days, multinucleated cells appeared at the implant surfaces. Morphological comparison of implant-induced multinucleated cells and tibial osteoclasts indicated that bone-elicited multinucleated cells lacked the ruffled borders characteristic of normal osteoclasts or the extensive clear zones typical ofia osteoclasts, but more closely resembled suture-induced macrophage-polykaryons. We conclude that ectopically implantedia bone as compared to normal bone elicits a different functional response from structurally similar cell populations. Bone-elicited multinucleated cells could not be classified as active osteoclasts despite evidence of release of45Ca. Release of labeled Ca was probably due to the action of mononuclear phagocytes and macrophage-polykaryons rather than to osteoclastic resorption.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1007/BF01239966
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