Bone cells predispose bone surfaces to resorption by exposure of mineral to osteoclastic contact.
نویسندگان
چکیده
The cell-free endocranial surface of young adult rat parietal bones was used as a substrate for osteoclastic bone resorption, either without prior treatment, or after incubation of the parietal bones with collagenase or neonatal rat calvarial cells. Untreated, the endocranial surface consisted of unmineralized organic fibres; incubation with calvarial cells or collagenase caused disruption and removal of these fibres, with extensive exposure of bone mineral on the endocranial surface, without morphologically detectable mineral dissolution. Neonatal rabbit osteoclasts resorbed bone to a greater extent from parietal bones pre-incubated with calvarial cells or collagenase than from untreated bones; mineral exposure and subsequent osteoclastic resorption were both increased if calvarial cells were incubated with parathyroid hormone; removal of bone mineral after incubation with calvarial cells removed the predisposition to osteoclastic resorption. These experiments demonstrate that calvarial cells are capable of osteoid destruction, and indicate that one mechanism by which osteoblasts induce osteoclastic bone resorption may be through digestion of the unmineralized organic material that covers bone surfaces, to expose the underlying resorption-stimulating bone mineral to osteoclastic contact.
منابع مشابه
Noninvasive optical detection of bone mineral.
UNLABELLED FRFP binds to mineral at osteoblastic, osteoclastic, and quiescent surfaces, with accumulation likely modulated by vascular delivery. In vivo visualization and quantification of binding can be accomplished noninvasively in animal models through optical tomographic imaging. INTRODUCTION The development of near-infrared optical markers as reporters of bone metabolism will be useful f...
متن کاملEffects of cyclic pressure on bone marrow cell cultures.
The present in-vitro study used bone marrow cell cultures and investigated the effects of cyclic pressure on osteoclastic bone resorption. Compared to control (cells maintained under static conditions), the number of tartrate resistant acid phosphatase (TRAP)-positive, osteoclastic cells was significantly (p<0.05) lower when, immediately upon harvesting, bone marrow cells were exposed to cyclic...
متن کامل1,25-Dihydroxyvitamin D3 stimulates rat osteoblastic cells to release a soluble factor that increases osteoclastic bone resorption.
Although 1,25-dihydroxyvitamin D3 stimulates osteoclastic bone resorption in vivo and in organ culture, the mechanism by which it effects this stimulation is unknown. We have recently found that the agent does not stimulate resorption by osteoclasts mechanically disaggregated from bone and incubated on slices of cortical bone. This suggests that the osteoclasts were removed by disaggregation fr...
متن کاملRoles of Renin-Angiotensin System in the Regulation of Prostate Cancer Bone Metastasis: A Critical Review
Mestastatic prostate cancer cells (MPCCs) frequently metastasize to bone, which is a “favorite soil” for colonization and proliferation of MPCCs. Prostate cancer bone mestastasis is tightly associated with tumor-induced bone lesions, most commonly caused from the etiological imbalance between osteoblastic bone formation and osteoclastic bone resorption, and from the anti-tumor immune response. ...
متن کاملBisphosphonates act on rat bone resorption through the mediation of osteoblasts.
Bisphosphonates are generally considered to act on bone resorption by binding to bone mineral and subsequently inhibiting the activity of the osteoclasts which ingest them. This has been supported by the fact that bisphosphonates adsorbed on mineralized tissue inhibit the resorbing activity of isolated osteoclasts in vitro. However, the effectiveness of different bisphosphonates determined in t...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Journal of cell science
دوره 76 شماره
صفحات -
تاریخ انتشار 1985