Cellular response to ectopically implanted silk sutures and osteopetrotic bone.

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 and ia rats to determine if ia bone could induce functionally active and morphologically identifiable osteoclasts at the implant surface. Assays of 45Ca released from the preparations showed that normal and ia recipients were capable of equivalent cell-mediated release of Ca over a 2-week implant period, indicating that the ia resorptive defect was not reproduced at the subcutaneous site. Freeze-thawed osteopetrotic bone released twice as much 45Ca as normal bone. This difference was eliminated by collagenase treatment. Cellular profiles were similar in both normal and ia 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 of ia osteoclasts, but more closely resembled suture-induced macrophage-polykaryons. We conclude that ectopically implanted ia 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 of 45Ca. Release of labeled Ca was probably due to the action of mononuclear phagocytes and macrophage-polykaryons rather than to osteoclastic resorption.