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PubMed1990

Inhibition of osteoclast proton transport by bafilomycin A1 abolishes bone resorption.

Osteoclasts are the main bone resorbing cells with capacity to acidify their intimate contact area with bone. Recent studies have suggested that osteoclast acid secretion is carried out by an H(+)-ATPase. We demonstrate here, that specific inhibitor of vacuolar type H(+)-ATPases, bafilomycin A1, inhibits bone resorption in osteoclast cultures as well as blocks proton transport in isolated medullary bone derived microsomes containing a vacuolar type H(+)-ATPase. These results demonstrate an important role of vacuolar H(+)-ATPase in bone resorption.

Animals↗

PubMedDate not supplied

[Biochemical bone resorption markers in children with osteosarcoma].

UNLABELLED: Biochemical markers of bone resorption such as the bane collagen breakdown products and specific factors associated with osteoclastogenesis are useful for monitoring the response of anticancer therapy and to assess disease progression in patients with metastatic bone disease. AIM: the aim of present study was to assess bone resorption process by collagen type I crosslinked C-telopeptide and osteoprotegerin levels in children with osteosarcoma. SUBJECTS AND METHODS: in serum of 20 patients (10-19 years) with osteosarcoma, bone resorption markers were determined: at diagnosis (before treatment), during preoperative and postoperative chemotherapy and after treatment. The control group consisted of 15 healthy age-matched children. Bone resorption markers were measured by immunoenzymatic ELISA assays. RESULTS: mean serum concentration of collagen type I crosslinked C-telopeptide in patients at the time of diagnosis was 15206 +/- 6808 pM/L. then it decreased by 15% during preoperative chemotherapy and it increased during the postoperative chemotherapy. In addition, the mean osteoprotegerin level was 3.73 +/- 0.78 pM/L at diagnosis, it increased by 12% during preoperative chemotherapy and then it decreased during the postoperative phase. Patients after therapy were divided into two subgroups: with favourable and unfavourable prognosis, In patients with favourable prognosis we observed lower serum concentrations of both resorption markers in comparison to patients with poor prognosis. CONCLUSIONS: bone resorption markers: may be useful for assessing bone resorption process and can be used in diagnosis and monitoring therapy of patients with osteosarcoma. Higher serum concentration bone resorption markers (especially osteoprotegerin) may be related to poor prognosis.

Adolescent↗

PubMed1981

Bacterial bone resorption in noma (gangrenous stomatitis).

Bone resorption (gangrenous stomatitis) was found to be associated with extensive bacterial colonization of mandibular bone in three separate cases of noma. Light and electron microscopy revealed a heterogeneous bacterial population with a long, filamentous, Gram-positive organism predominantly in direct contact with the resorbing bone front. The bone was completely denuded and no osteoclastic activity was observed. The highly regular arrangement of the filamentous organism along the resorbing bone and the absence of osteoclastic activity suggested that bone resorption in noma is mediated by bacterial action.

Bacteria↗

PubMed1976

Direct stimulation of bone resorption by thyroid hormones.

Although hypercalcemia, osteoporosis, and increased bone turnover are associated with thyrotoxicosis, no direct effects of thyroid hormones on bone metabolism have been reported previously in organ culture. We have now demonstrated that prolonged treatment with thyroxine (T4) or triiodothyronine (T3) can directly increase bone resorption in cultured fetal rat long bones as measured by the release of previously incorporated 45Ca. T4 and T3 at 1 muM to 10 nM increased 45Ca release by 10-60% of total bone 45Ca during 5 days of culture. The medium contained 4 mg/ml of bovine serum albumin to which 90% of T4 and T3 were bound, so that free concentrations were less than 0.1 muM. The response to T4 and T3 was inhibited by cortisol (1 muM) and calcitonin (100 mU/ml). Indomethacin did not inhibit T4 response suggesting that T4 stimulation of bone resorption was not mediated by increased prostaglandin synthesis by the cultured bone. Matrix resorption was demonstrated by a decrease in extracted dry weight and hydroxyproline concentration of treated bones and by histologic examination which also showed increased osteoclast activity. The effects of thyroid hormones were not only slower than those of other potent stimulators of osteoclastic bone resorption (parathyroid hormone, vitamin D metabolites, osteoclast activating factor, and prostaglandins), but the maximum response was not as great. We conclude that T4 and T3 can directly stimulate bone resorption in vitro at concentrations approaching those which occur in thyrotoxicosis. This effect may explain the disturbances of calcium metabolism seen in hyperthyroidism.

Animals↗

PubMed2005

[Molecules which are involved in osteoclastic bone resorption: from the aspect of targets of treatment for osteoporosis].

Bone in vertebrates is continuously destroyed and reformed to maintain bone volume throughout their life. In normal bone remodeling, osteoblastic bone formation follows osteoclastic bone resorption in a precise and quantitative manner. In osteoporosis, the bone resorption surpasses the bone formation. Recent studies have shown that osteoclastic bone resorption is tightly regulated by bone-forming osteoblasts. Osteoblasts express RANKL (receptor activator of nuclear factor-KappaB ligand), which plays central roles in osteoclast differentiation and function. In this review article, we explain molecules which are involved in the RANKL-RANK interaction in the regulation of osteoclastic bone resorption.

Bone Resorption↗

PubMed1995

Altering tooth eruption by blocking bone resorption--the local delivery of bafilomycin A1.

Tooth eruption is a complicated process requiring a coordination of bone resorption and bone formation by a variety of factors in and around the dental follicle proper and bone resorption is the rate-limiting step early in the process. We have recently described a method to deliver to the crypt of erupting dog premolars a reversible blocker of bone resorption, bafilomycin A1, and shown that its delivery for two week blocks bone resorption and eruption during this period without effect on adjacent teeth or on bone formation. In this study we show that delivery of 10(-6) M bafilomycin A1 via a cannulated osmotic minipump for two weeks early in the eruption of premolars delayed the eruption of these teeth for eight weeks. Similar delivery of the vehicle to the contralateral premolar had no effect on eruption. These data are the first clinical application of this potent drug and show that a short term local delivery is reversible and that blocking resorption for two weeks causes a fourfold delay in tooth eruption. Modifications of this approach may have clinical applications in dentistry.

Animals↗

PubMed1998

Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption.

Loss of sex steroids causes an increase in both the resorption and formation of bone, with the former exceeding the latter. Based on evidence that the increased bone resorption after estrogen loss is due to an increase in osteoclastogenesis, we hypothesized that estrogen loss also stimulates osteoblastogenesis. We report that the number of mesenchymal osteoblast progenitors in the murine bone marrow was increased two- to threefold between 2 and 8 wk after ovariectomy and returned to control levels by 16 wk. Circulating osteocalcin, as well as osteoclastogenesis and the rate of bone loss, followed a very similar temporal pattern. Inhibition of bone resorption by administration of the bisphosphonate alendronate led to a decrease of the absolute number of osteoblast progenitors; however, it did not influence the stimulating effect of ovariectomy on osteoblastogenesis or osteoclastogenesis. These observations indicate that the increased bone formation that follows loss of estrogen can be explained, at least in part, by an increase in osteoblastogenesis. Moreover, they strongly suggest that unlike normal bone remodeling, whereby osteoblast development is stimulated by factors released from the bone matrix during osteoclastic resorption, estrogen deficiency unleashes signals that can stimulate the differentiation of osteoblast progenitors in a fashion that is autonomous from the need created by bone resorption, and therefore, inappropriate.

Alendronate↗

PubMed1989

Effects of atrial natriuretic factor on cyclic nucleotides, bone resorption, collagen and deoxyribonucleic acid synthesis, and prostaglandin E2 production in fetal rat bone cultures.

We examined the effects of synthetic human atrial natriuretic factor (human ANF 99-126) on adenylate cyclase activity, cAMP and cyclic GMP (cGMP) levels, bone resorption, collagen and DNA synthesis, and prostaglandin E2 (PGE2) production in fetal rat bone organ cultures. ANF (100 nM) inhibited PTH- and PGE2-stimulated cAMP production but had no effect on basal cAMP production in 21-day fetal rat calvaria. ANF increased cGMP levels, and this was not affected by PTH. ANF (10 nM) partially inhibited bone resorption stimulated by PGE2 but had no effect on control or PTH-stimulated resorption in 19-day fetal rat long bones. ANF had no effect on collagen and DNA synthesis or PGE2 production and did not alter responses to PTH or PGE2 in the fetal rat calvaria. Thus, ANF has no major direct effect on bone resorption or formation, but it is possible that ANF modulates the local regulatory function of PGE2 in bone.

Adenylyl Cyclases↗

PubMed2004

Isosorbide mononitrate increases bone formation and decreases bone resorption in postmenopausal women: a randomized trial.

UNLABELLED: NO regulates bone remodeling in cellular and animal models. We examined the effect of administering ISMO, a NO donor, on bone turnover in 144 postmenopausal women. After 3 months, women randomized to ISMO had a greater decrease in bone resorption and a greater increase in bone formation compared with placebo. NO donors may prevent postmenopausal bone loss. INTRODUCTION: NO both stimulates bone formation and inhibits bone resorption in vitro. NO donors (nitrates) are inexpensive and widely available, but their value for postmenopausal osteoporosis has never been evaluated in a randomized trial. MATERIALS AND METHODS: We randomly assigned 144 healthy postmenopausal women with a hip BMD T score between 0 and -2.5 to 5 or 20 mg/day of isosorbide mononitrate (ISMO) or placebo for 12 weeks. We measured urine N-telopeptide (NTx), a marker of bone resorption, and serum bone-specific alkaline phosphatase (BSALP), a marker of bone formation. Markers were measured immediately before randomization and after 12 weeks of treatment. We calculated the percent change in NTx and BSALP for each of the treatment groups (placebo, 5 mg ISMO, and 20 mg ISMO). Our primary outcome was the percent change in NTx and BSALP in the 5- and 20-mg ISMO groups compared with placebo. RESULTS AND CONCLUSIONS: Compared with women randomized to placebo, women randomized to 20 mg of ISMO had a 45.4% decrease in NTx (95% CI, 25.8-64.9) and a 23.3% increase (95% CI, 8.9-37.8) in BSALP. Women randomized to 5 mg of ISMO had a 36.3% decrease in NTx (95% CI, 14.8-57.8) and a 15.9% increase in BSALP (95% CI, 1.1-30.7). ISMO decreases bone resorption and increases bone formation. These findings suggest that nitrates may be useful for the prevention of postmenopausal osteoporosis.

Aged↗

PubMed1994

Structure-activity studies of the s-echistatin inhibition of bone resorption.

Synthetic Arg-Gly-Asp (RGD)-containing peptides were examined in bone resorption or attachment and detachment assays with isolated mammalian osteoclasts in an effort to elucidate the mechanistic and structural basis for the inhibition of bone resorption by s-echistatin. Bone resorption was the process most sensitive to inhibition by s-echistatin, with IC50 = 0.3 nM; inhibition of attachment to bone or detachment (lamellipodial retraction) was 30- to 70-fold less sensitive, with IC50 = 10 or 20 nM, respectively. Single amino acid substitutions within the 49-residue sequence of s-echistatin showed that although the efficacy of s-echistatin is dependent on the Arg24-Gly25-Asp26 sequence, additional residues, including Asp27, Met28, and Cys39, are also critical for potent inhibition of the resorbing activity of isolated rat osteoclasts. Because of the identification of the av beta 3 as the primary integrin on rat osteoclasts interacting the RGD peptides (Helfrich et al.), we examined the possibility of modeling bone resorption with other beta 3-mediated processes. Specifically, av beta 3 endothelial cell (human or rat) attachment to vitronectin and aIIb beta 3 platelet aggregation were compared with bone resorption for sensitivity to s-echistatin analogs, linear RGD peptides, and cyclic RGD peptides. Essentially no similarity in sensitivity to RGD peptides were observed between bone resorption, platelet aggregation, or endothelial cell attachment. Because rat osteoclasts and human giant cell tumors (osteoclastomas) shared similar sensitivity to s-echistatin and rat and human endothelial cells showed a similar sensitivity profile to RGD peptides, the dissimilarity of bone resorption to other beta 3-mediated processes cannot be explained in terms of species differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1989

Interaction of cyclosporine A and calcitonin on bone resorption in vitro.

Cyclosporine A (CsA), which is a potent immunosuppressive agent, inhibits bone resorption in vitro. The inhibition of bone resorption by CsA is sustained, unlike the transient inhibition of bone resorption produced by calcitonin (CT). These different patterns of inhibition were studied by examining the interaction between CsA and CT on stimulated bone resorption in the neonatal mouse calvarial resorptive system. "Escape" from the CT inhibition of PTH stimulated bone resorption occurred after 24 hr of organ culture. Coincubation with CsA (1 micrograms/ml) delayed the "escape" response of CT + PTH treated bones, so that the full "escape" response did not occur until after 48 hr of organ culture. Likewise, a pretreatment of 24 hr with CsA (1 micrograms/ml) was sufficient to delay "escape" from CT inhibition of PTH stimulated bone resorption until after 48 hr of organ culture. A higher concentration of CsA (10 micrograms/ml) completely prevented the "escape" response. Our data could indicate an interaction between the CsA and CT inhibitory effects on resorption.

Analysis of Variance↗

PubMed1989

Cadmium stimulates prostaglandin E2 production and bone resorption in cultured fetal mouse calvaria.

The effect of cadmium on bone resorption was studied using isolated fetal mouse calvaria. Cadmium stimulated bone resorption and PGE2 production in a dose-dependent manner. The minimal concentration of cadmium which stimulated bone resorption was the same as that stimulated prostaglandin E2 production. The stimulatory effects of cadmium (0.5 microM) on bone resorption and prostaglandin E2 production were completely inhibited by indomethacin. Exogenously added PGE2 (100ng/ml) abolished the inhibitory effect of indomethacin on bone resorption stimulated by cadmium. These results strongly indicate that cadmium stimulates bone resorption via prostaglandin E2 mediated mechanism.

Animals↗

PubMed1987

Effects of calcium and magnesium intakes and feeding level during the dry period on bone resorption in dairy cows at parturition.

A study was made of the influence of low and high calcium intakes at two feeding levels (experiments 1 and 2), and of different magnesium intakes (experiment 3) during the dry period, on the cellular resorptive activity in bone of dairy cows at parturition. In experiment 1 (26 cows) the feed intake was 1.12 times maintenance and the calcium intake was either 13.0 g d-1 or 83.5 g d-1. In experiment 2 (33 cows) the feed intake was 1.9 times maintenance and the calcium intake was either 26.4 g d-1 or 87.2 g d-1. In experiment 3 the cows feed intake was 1.4 times maintenance, the calcium intake was 71 to 72 g d-1 and the magnesium intake was either 16.6 g d-1 or 71.0 g d-1. Bone biopsies were taken from the tuber coxae between three and eight hours after parturition. In experiment 1 the cellular resorptive activity in bone from older cows was higher in the cows receiving the low calcium diet. In experiment 2 the differences between the bone resorptive activities of the two groups were small. In experiment 3 the bone resorptive activity was lower in the cows with a deficient supply of magnesium. There were significant relationships in young cows, but not in older cows, between the cellular resorptive activity in bone and the rate of calcium mobilisation measured biochemically. These results suggest that in older dairy cows bone resorption makes only a minor contribution to the total rate of calcium mobilisation at parturition and is therefore of minor importance for the prevention of periparturient hypocalcaemia.

Animals↗

PubMed2002

In vitro study of the effects of Epimedium on osteoclastic bone resorption in various oral mineralized tissues.

OBJECTIVE: To investigated the bone resorption caused by osteoclasts and modulating functions of a Chinese herb, Epimedium on bone resorption. METHODS: Osteoclasts were separated from long-limb bones of new born rabbits, cultured with de-activated human tooth slices and glass slices, and treated with different concentrations of Epimedium. Osteoclasts on glass slices were stained by HE staining, TUNEL staining and absorption pits on tooth slices were observed by light microscope. RESULTS: HE staining shows that the Epimedium treated cells showed shrinkage of cytosol and condensation of nuclei. Some treated cells showed breakage of nuclei. TUNEL staining shows that treated cells showed shrinkage of cytosol, dark stained nuclei and light stained cytosol. These results indicate that Epimedium can induce osteoclast to commit apoptosis. Further study shows that the number and area of absorption pits formed on treated tissues are significantly different from those on control tissues. So the effect of Epimedium on bone resorption is dose-dependent. CONCLUSIONS: Epimedium can induce osteoclast apoptosis and inhibit bone resorption. The effect of Epimedium on bone resorption is dose-dependent.

Animals↗

PubMed2006

Cytokine-induced osteoclastic bone resorption in charcot arthropathy: an immunohistochemical study.

BACKGROUND: Charcot arthropathy is a chronic, progressive destructive process affecting bone architecture and joint alignment in people lacking protective sensation. The etiologic factors leading to progressive bone resorption have not been elucidated. The purpose of this study was to histologically examine surgical specimens with Charcot arthropathy for cell type and immunoreactivity of known cytokine mediators of bone resorption. METHODS: Tissue samples of 20 specimens with known Charcot arthropathy were stained for Hematoxylin and Eosin (H&E) to quantify cell type. Nine of the specimens were stained with interleukin-1 (IL-1) antibody, nine with tumor necrosis factor (TNF) alpha antibody, and nine with interleukin-6 (IL-6) antibody. Distribution of staining was graded as focal (less than 10% of cells), moderate (10% to 50% of cells), and diffuse (more than 50% of cells) by two independent investigators. Inflammatory cells in tissue sections of rheumatoid synovium served as a positive control. RESULTS: Osteoclasts were seen in excessive numbers lining the resorptive bone lacunae. There was a disproportionate increase in osteoclasts to osteoblasts in the Charcot-reactive bone. In each case, osteoclasts demonstrated immunoreactivity for IL-1, IL-6 and TNF-alpha with a grade of moderate or diffuse reactivity. CONCLUSION: The findings of excessive osteoclastic activity in the environment of cytokine mediators of bone resorption (IL-1, IL-6, and TNF-alpha) suggest enhanced bone resorption through the stimulation of osteoclastic progenitor cells as well as mature osteoclasts. Alteration in the synthesis, secretion, or activity of these important regulatory molecules through the use of pharmacologic agents may, in turn, alter bone remodeling and loss and lead to accelerated healing without collapse or malalignment.

Adult↗

PubMed1984

Sex differences in bone resorption: a scanning electron microscopic study of mouse parietal bones.

Bone resorption surfaces formed by osteoclasts can be identified as rough areas by scanning electron microscopy (SEM). In this study, the endocranial surfaces of mouse parietal bones were examined by SEM at 1, 4, 6, 8, 14 and 20 weeks of age in an attempt to understand the bone resorbing activity after the cessation of bone growth. On the inner surface of the parietal bones, the rough areas, composed of a group of 8 to 30 microns wide concavities, can be divided into two distinct groups (type I and type II). The surface of type I areas appeared irregularly rough and those of type II revealed feather, fire-flame, or wave-like patterns due to characteristic arrangements of the concavities. The rough areas occupying the inner surface of the parietal bones made up about 60% of the surface area at 1 week and about 5% at 4 weeks in both sexes. The rough areas were all type I at this age. After puberty, the rough areas in males occupied about 10% of the inner surface until 20 weeks and consisted of large type I and small type II areas. In females, the proportion of the rough areas increased after puberty and occupied about 40% of the endocranial surface at 14 and 20 weeks. The type I areas were much larger, increasing in size with age and eventually occupying a large proportion of the rough areas. The sex differences in the rough areas were reversed by gonadectomy. The results suggest that male and female gonadal products, possibly sex hormones, have respective inhibitory and stimulatory effects on the formation of bone resorptive surfaces, and may be responsible for the sex differences in the size and morphological features of the areas on the bone surfaces.

Age Factors↗

PubMed1997

Role of estrogen deficiency in pathogenesis of secondary hyperparathyroidism and increased bone resorption in elderly women.

Whether the increased bone resorption and secondary hyperparathyroidism in elderly women is due to aging or to estrogen deficiency is unclear. To address this issue, we measured serum intact parathyroid hormone (PTH) and biochemical markers in serum and urine samples from 30 premenopausal women (32 +/- 0.5 years, mean age +/- SE), 30 estrogen-deficient postmenopausal women (74.2 +/- 0.6 years), and 30 elderly women (73.8 +/- 0.6 years) receiving long-term estrogen treatment. Because of the first and third groups were comparable in estrogen status but not in age, whereas the second and third groups were comparable in age but not in estrogen status, the independent effects of age and estrogen deficiency could be assessed quantitatively. Mean values were higher in the estrogen-deficient postmenopausal women than in the premenopausal women for serum PTH (by 33%, p < .01) and for bone resorption markers [by 50% p < .001) for urine cross-linked N-teleopeptide of type I collagen (NTx); 34% (p < .001) for urine pyridinoline (Pyd); and 36% (p < .001) for urine deoxypyridinoline (Dpd)]. However, mean values for serum PTH in the postmenopausal women receiving estrogen treatment did not differ from those in the premenopausal women, and mean values for bone resorption markers were not different (urine NTx and Pyd) or were lower [urine Dpd, by -12%, (p < .005)]. These findings suggest that late consequences of estrogen deficiency rather than age-related processes per se are the principal causes of the secondary hyperparathyroidism and increased bone resorption in elderly women.

Adult↗

PubMed1992

Mediators of bone resorption around implants.

An important cause of prosthetic loosening is bone resorption that results from the interaction of macrophages with implant surfaces and particulate debris. The mediators involved in this bone resorption were investigated in vitro. Medium conditioned by macrophages interacting with foreign materials was assayed for bone resorption stimulation and inhibition, and for prostaglandin E2 (PGE2). In some experiments, the medium was dialyzed, and in others indomethacin was added. Macrophages were found to release stimulators and inhibitors of bone resorption. The relative amount of these was variable. When macrophages interacted with foreign surfaces, their stimulatory effect was ten times their inhibitory effect. Further activation by phagocytosis caused a further 15-fold increase in stimulation, with no change in inhibition. It is probable that before macrophages encounter foreign materials their stimulatory and inhibitory effects are the same so that they do not cause net bone resorption. Important stimulatory and inhibitory mediators were not dialyzable and so were probably cytokines or possibly collagenase. Prostaglandins were neither important stimulators nor inhibitors. There was only enough PGE2 released to account for 2% of the bone resorption that was stimulated.

Animals↗