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Results for “Bone Resorption”

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PubMed1992

Suramin inhibits bone resorption and reduces osteoblast number in a neonatal mouse calvarial bone resorption assay.

The antineoplastic properties of suramin, a polyanionic agent with demonstrated antigrowth factor activity, are under evaluation in vitro, in vivo, and in clinical trials. Suramin has been shown to have antitumor activity in patients with advanced, hormone refractory prostate cancer. During these trials, significant resolution of osseous pain was observed in nearly three quarters of the patients treated with suramin. To evaluate the effect of suramin on bone cells, we studied the effect of suramin on bone resorption in a neonatal mouse calvarial assay. Suramin inhibited bone-resorbing activity in a dose-related fashion and had an additive effect with calcitonin. Calvaria pretreated with suramin had less bone-resorbing activity, fewer attached osteoblasts, and less medium alkaline phosphatase activity than control calvaria. Suramin also inhibited osteoclastic release of tritiated proline from labeled bone in a dose-dependent fashion. The effect of metastatic prostate carcinoma on bone is incompletely understood, but may be moderated by tumor-produced factors and/or cytokines. The effects of several such agents, therefore, were examined in combination with suramin. Bone resorption induced by PTH, epidermal growth factor, tumor necrosis factor, and a tumor-produced factor, PTH related-protein, was blocked by suramin. The ability of suramin to inhibit the bone-resorbing effects of several cytokines suggests that its mechanism may involve direct action on bone metabolism. Autoradiography performed on calvaria treated with labeled suramin demonstrated heavy deposition of suramin on the outer surface of the matrix, adjacent to osteoblasts and osteoclasts lining the outer table, suggesting that bone cells may be subject to high local concentrations of the drug, in keeping with this hypothesis.

Alkaline Phosphatase↗

PubMed1997

Advanced glycation end products enhance osteoclast-induced bone resorption in cultured mouse unfractionated bone cells and in rats implanted subcutaneously with devitalized bone particles.

Advanced glycation end products (AGE) are formed in long-lived matrix proteins by a nonenzymatic reaction with sugar. The presence of AGE in beta 2-microglobulin-amyloid fibrils of dialysis-related amyloidosis, one of the characteristic features of which is an accelerated bone resorption around amyloid deposits, was recently demonstrated. This suggested a potential link of AGE in bone resorption and initiated this investigation of whether AGE enhance bone resorption. When mouse unfractionated bone cells containing osteoclasts were cultured on dentin slices, both AGE-modified beta 2-microglobulin and BSA increased the number of resorption pits formed by osteoclasts, whereas their normal counterparts of those modified with the early glycation products did not. AGE proteins, however, did not increase the number of newly formed osteoclasts, even in the coculture of mouse bone marrow cells with osteoblastic cells isolated from mouse calvaria. Enhanced bone resorption was also observed when unfractionated bone cells were cultured on AGE-modified dentin slices. AGE-enhanced bone resorption was effectively inhibited by calcitonin and ipriflavone, both of which are inhibitors of bone resorption. AGE-enhanced bone resorption was further supported by in vivo evidence that rat bone particles-upon incubation with glucose for 60 days (AGE-bone particles)-when implanted subcutaneously in rats, were resorbed to a much greater extent than control bone particles upon parallel incubation without glucose. These findings suggest that AGE enhance osteoclast-induced bone resorption. Although the mechanism remains unknown, AGE are unlikely to promote differentiation of osteoclast progenitors into osteoclasts, suggesting that AGE activate osteoclasts or alter microenvironments favorable for bone resorption by osteoclasts. The modification of bone matrices with AGE might play a role in the remodeling of senescent bone matrix tissues, further implicating a pathological significance of AGE in dialysis-related amyloidosis or osteoporosis associated with diabetes and aging.

Amyloidosis↗

PubMed1989

Coordinated regulation of endothelial and fibroblast cell proliferation and matrix synthesis in periodontal ligament adjacent to appositional and resorptive bone surfaces.

Little is known about the remodeling of blood vessels and soft connective tissue or the proliferation of endothelial cells in the periodontal ligament (PL) of teeth undergoing physiological drift. To determine whether there is evidence for coordinated regulation of endothelial cell and fibroblast proliferation and matrix synthesis in sites within the PL adjacent to bone-appositional (A) and bone-resorptive (R) surfaces, the PL in mouse mandibular molar was subdivided into A and R sectors on the basis of 3H-proline incorporation into alveolar bone. Computer-assisted morphometry of radioautographs showed that the number and area of blood vessels were similar in A and R sectors. Proliferation of endothelial cells and fibroblasts was assessed from radioautographs prepared from mice continuously labeled with 3H-thymidine at times between 2 and 60 days. Significantly more labeled endothelial cells (P less than .001) and fibroblasts (P less than .05) were seen in the A sector. The percent of labeled endothelial cells and the percent of labeled fibroblasts increased linearly to 25 days and then formed a plateau. The rate of increase of labeled fibroblasts was higher in the A sector than in the R sector (P less than .025). In addition, 3H-proline grain counts over extracellular matrix were significantly higher in the appositional sector than in the resorptive sector (P less than .025).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Inhibitory effect of okadaic acid on bone resorption in neonatal mouse calvaria in vitro. Protein dephosphorylation as an important regulatory mechanism in the bone resorption process.

Okadaic acid (OA), a potent inhibitor of protein phosphatase type 1 and protein phosphatase type 2A was studied for its effect on bone resorption in neonatal mouse calvaria. OA (0.01 to 1000 ng/ml) had no effect on the basal bone resorption rate, except at 1000 ng/ml, were a small inhibitory effect was observed. Resorption stimulated by parathyroid hormone (10(-8) M) was abolished in the presence of OA, half maximal inhibition being observed at 1 ng/ml. However, at 50 ng/ml or higher, OA significantly increased lactate dehydrogenase activity in the medium, indicating a cytotoxic effect at these concentrations. Similar inhibitory effects were observed when bone resorption was stimulated by 1,25-dihydroxycholecalciferol (10(-8) M) or prostaglandin E2 (10(-6) M). From this it is concluded that protein dephosphorylation may represent an important regulatory mechanism in the bone resorption process.

Animals↗

PubMed1994

The effect of sodium salicylate on the osteoclast-like cell formation and bone resorption in a mouse bone marrow culture.

Salicylates are reported to have an inhibitory effect on bone resorption in vivo and in vitro. The present study examined the effect of sodium salicylate on the formation of osteoclast-like cells in vitro. When mouse bone marrow cells were cultured for 8 days with 10(-8) M 1 alpha, 25-dihydroxyvitamin D3 (1 alpha, 25(OH)2D3), numerous clusters of mononuclear and multinucleated cells (MNCs) formed, which stained positive for tartrate-resistant acid phosphatase (TRAP-positive). In similar cultures using sodium salicylate, the number of both TRAP-positive mononuclear and TRAP-positive MNCs were found to diminish in proportion to the concentration of sodium salicylate. A time-course experimental model showed that the number of TRAP-positive MNCs decreased slightly when sodium salicylate was given early in the culture period, and decreased markedly when the drugs were given later in the culture period. Pit formation and bone-resorption area on the bone slices were also inhibited by adding sodium salicylate continuously with 1 alpha, 25(OH)2D3. The sodium salicylate showed no cytotoxic effect because the total number of adherent cells, including both TRAP-positive and TRAP-negative cells, was independent of the presence of sodium salicylate. These results suggest that sodium salicylate has an inhibitory effect on the recruitment of osteoclast-like MNCs and that this inhibition is greater during the later stage of mouse bone marrow culture.

Acid Phosphatase↗

PubMed1986

Stimulation of bone resorption in cultured mouse calvaria by Lys-bradykinin (kallidin), a potential mediator of bone resorption linking anaphylaxis processes to rarefying osteitis.

Lys-Bradykinin (kallidin) stimulated bone resorption in vitro as assessed by the release of 45Ca and 3H from mouse calvaria radiolabelled in vivo with [45Ca]CaCl2 and [3H]proline, respectively. The stimulatory effect of Lys-bradykinin was reduced by calcitonin, indicating that the bone resorptive effect of Lys-bradykinin was dependent on osteoclastic activity. Different inhibitors of arachidonic acid metabolism, including glucocorticoids, inhibited Lys-bradykinin stimulated mobilization of mineral, implicating the synthesis of prostaglandins as an intermediary step. Lys-Bradykinin enhanced the biosynthesis of PGE2 in osteoblast-like cells isolated from mouse calvaria. In view of these findings and the capacity of mast cells to generate kininogenase activity, resulting in formation of Lys-bradykinin and bradykinin, the role of these cells in the pathogenesis of bone loss in rheumatoid arthritis, mastocytosis and osteoporosis is discussed.

Anaphylaxis↗

PubMed2005

Alendronate inhibits bone resorption at the bone-screw interface.

In the current study, we investigated whether the systemic administration of alendronate, a third-generation bisphosphonate, suppressed the loosening of screws at the bone-screw interface. We systemically administered alendronate to rats fitted with external fixators. External fixators with two half pins were applied to the right femurs of rats, and alendronate was administrated once a week during a 5-week postoperative period. Radiographic, histologic, and immunohistochemical findings subsequently were analyzed. Treatment with alendronate reduced the width of the fibrous loosening membrane and the number of osteoclasts at the bone-screw interface. These findings indicate that systemic treatment with alendronate exerts an inhibitory effect on local bone resorption at the bone-screw interface.

Acid Phosphatase↗

PubMed1989

A radiographic investigation into bone resorption of mandibular alveolar bone in elderly edentulous adults.

Clinical experience suggests that severe alveolar bone resorption can limit the success of complete denture wearing. The loss of bone mineral with age occurs throughout the skeleton, which contributes to the high incidence of bone fractures later in life. Women are more commonly affected by some of these fractures. The decline in serum oestrogen concentration following the menopause has been implicated in the aetiology of these fractures. We have found that age is important in determining the bone resorption observed in females but not in males.

Aged↗

PubMed1994

Cholera toxin-stimulated bone resorption in cultured mouse calvarial bones not inhibited by calcitonin: a possible interaction at the stimulatory G protein.

We examined the effect of calcitonin in cultured mouse calvarial bones after prestimulation with different activators of adenylyl cyclase. Calcitonin (100 ng/ml), added after 48 h of culture, inhibited bone resorption (assessed as release of 45Ca from prelabeled bones cultured for 96-144 h) stimulated with parathyroid hormone (PTH, 10 nM; 0-144 h) or the adenylyl cyclase stimulator forskolin (2 microM; 0-144 h). However, no effect of calcitonin was demonstrated when bone resorption was prestimulated with the adenylyl cyclase stimulator cholera toxin, at and above 1 ng/ml, at any time point studied. In contrast, two other types of inhibitors of bone resorption in vitro, the carbonic anhydrase inhibitor acetazolamide (10 microM) and the aminobisphosphonate AHPrBP (10 microM), significantly inhibited cholera toxin-stimulated bone resorption. No cyclic AMP response to calcitonin was seen after preculture for 48 h with cholera toxin (0.1-100 ng/ml), although bones precultured in basic medium, in the absence or presence of forskolin, were still able to respond to calcitonin with elevation of cyclic AMP. Binding studies with [125I]calcitonin demonstrated that the preculture with cholera toxin did not affect the binding of calcitonin to the receptor. In summary, our data show that cholera toxin pretreatment makes calvarial bones insensitive to calcitonin-induced inhibition of bone resorption as a result of an interaction with cholera toxin at the level of calcitonin receptor-linked signal transduction. We suggest that the interaction, distal to the calcitonin receptor, is caused by the irreversible activation of Gs produced by cholera toxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

[Effects of protease inhibitors and protein synthesis inhibitors on cartilage tissue-dependent bone resorption].

We studied bone resorption of fetal rat femora in association with cartilage tissue. Some protease inhibitors, e.g., E-64, pepstatin A, phosphoramidon, amastatin, bestatin, foroxymithine, did not influence the bone resorption, but some serine protease inhibitors such as PMSF, TLCK, TPCK and elastatinal inhibited the bone resorption at 10(-5) M, 10(-4) M, 10(-4) M, 10(-4) M, respectively. A conditioned medium, obtained from cartilage tissue-cultured medium in the presence of 10(-4) M TPCK, which was then excluded from the medium by dialysis after the culture, stimulated the bone resorption. Cycloheximide (0.1 to 10 micrograms/ml) and puromycin (0.3 to 30 micrograms/ml) inhibited the cartilage tissue-dependent bone resorption. A A transient treatment of the femora with cycloheximide (3 micrograms/ml) for a day inhibited the bone resorption, but after the treatment, in the absence of cycloheximide, the femora gradually recovered the bone-resorbing activity. The conditioned medium, obtained from cartilage tissue-cultured medium in the presence of cycloheximide (3 micrograms/ml), which was then excluded from the medium by dialysis after the culture, failed to influence the bone resorption. These findings collectively suggest that cartilage tissue produces a bone resorption-stimulating factor(s) which is a serine protease or contains the protein as an inactive, latent form and then a certain serine protease converts it to an active form.

Animals↗

PubMed1990

Urinary excretion of pyridinium crosslinks: a new marker of bone resorption in metabolic bone disease.

The pyridinium derivatives hydroxylysylpyridinoline (HP) and lysylpyridinoline (LP) are intermolecular crosslinking compounds of collagen which are only present in its mature form. Contrasting to the wide distribution of type I and II collagens, HP and LP are absent from skin, ligament and fascia, and their major sources are bone and cartilage. Using a specific HPLC assay, we have determined the 24-h excretion of HP and LP crosslinks in normal adults of both sexes, in patients with primary hyperparathyroidism and in patients with Paget's disease of bone before and after intravenous treatment with amino-propylidene bisphosphonate (APB). Mean adult normal values were 33 +/- 13 pmol/mumol creatinine for HP and 6.3 +/- 3.4 pmol/mumol creatinine for LP. In women, menopause induced a 2-3-fold increase of HP and LP reflecting the well documented postmenopausal increase of bone turnover. In the urine of patients with primary hyperparathyroidism and of patients with active Paget's disease of bone, urinary crosslinks were significantly higher than in age-matched controls, with a mean 3- and 12-fold increase, respectively. Urinary excretion of hydroxyproline is a well recognized but poorly sensitive marker of bone turnover, reflecting resorption. In the same patients, the effect of menopause and disease state on hydroxyproline excretion was much less dramatic than on HP and LP. During intravenous APB treatment of pagetic patients, there was an early decrease of HP and LP, which was significant after 24 h and reached 62% at 4 days, contrasting with a late and milder decrease of urinary hydroxyproline. Because APB is a potent inhibitor of resorption which does not have a direct short-term effect on bone formation, these data also indicate that urinary excretion of HP and LP reflect only collagen degradation occurring during osteoclastic resorption and not the degradation of newly synthesized collagen. We conclude that urinary HP and LP excretion represents the first sensitive and specific marker of bone resorption. Its use should be valuable in the clinical investigation of metabolic bone diseases, especially osteoporosis.

Adult↗

PubMed1999

Activation of NF-kappaB in human osteoblasts by stimulators of bone resorption.

Several bone resorptive stimuli affect osteoclasts indirectly by modulating the production and release of osteoblastic factors. Using electrophoretic mobility shift assays, we found that not only tumour necrosis factor-alpha (TNF-alpha) but also interleukin-1beta and parathyroid hormone (PTH) caused dose and time-related increases in nuclear factor kappaB (NF-kappaB)-DNA binding in Saos-2 human osteoblastic (hOB) cells. Activation of NF-kappaB by TNF-alpha was reproduced in primary hOBs. In contrast, consistent with their previously reported lack of response to steroid hormones, Saos-2 cells did not respond to 1,25-dihydroxyvitamin D(3). We suggest that NF-kappaB activation in osteoblastic cells constitutes an important pathway in osteoblast-mediated resorptive signalling.

Adult↗

PubMed1993

Role of cytokines in bone resorption.

Osteoclastic bone resorption is modulated in humans by powerful osteotropic factors which are generated in the immediate vicinity of bone resorbing surfaces. These factors are released from marrow mononuclear cells and from some bone cells, and some are actually incorporated into the noncollagenous bone matrix from where they are released when bone is resorbed. They are likely important not only in the control of normal bone remodeling, but also in a number of disease states associated with disordered remodeling. In this review, current concepts of the effects of these factors on cells in the osteoclast lineage will be discussed.

Animals↗

PubMed1996

Lower serum 25-hydroxyvitamin D is associated with increased bone resorption markers and lower bone density at the proximal femur in normal females: a population-based study.

Subclinical vitamin D deficiency is considered to be a risk factor for osteoporosis. Therefore, we studied vitamin D status and bone mineral density (BMD) in an age- and sex-stratified population based sample (209 males and 206 females aged between 50 and 80 years). In addition, urinary excretion of pyridinium crosslinks of collagen was determined in order to monitor bone resorption. We found a seasonal variation of serum 25-hydroxyvitamin D (25(OH)D) levels with higher values detected in the summer (27 +/ - 10 ng/ml) and lower values measured in the winter (17 +/- 9 ng/ml). Further analyses were performed separately for winter and summer, respectively. We also excluded subjects taking osteotropic medication. In men, we found no significant relationship between vitamin D status and bone density or pyridinium crosslinks. In women, we found significant positive correlations between 25(OH)D and proximal femur BMD in winter (r = 0.21, p < 0.05) and in summer (r = 0.36, p < 0.01). The association between 25(OH)D and proximal femur BMD persisted after correction for age and body mass index. Serum 25(OH)D and urinary pyridinium crosslinks were inversely correlated in females in winter (r = -0.24, p < 0.02) and in summer (r = -0.32, p < 0.02). Our data support the hypothesis that already moderately low serum levels of 25(OH)D within the "normal" range lead to osteopenia via increased bone resorption.

Age Factors↗

PubMed1994

The purification and partial characterization of bone resorptive polypeptides from bovine bone matrix.

Matrix proteins were extracted from bovine cortical bone with EDTA/Tris-HCl under non-dissociative conditions at neutral pH. Four distinct bone resorptive proteins with molecular masses of 14, 25, 29 and 40 kDa were purified and partially characterized using an in vitro neonatal mouse calvarial assay and a growth factor assay using BALB/c/3T3 cells. The 14 kDa protein was purified by anion exchange chromatography (Mono Q) and gel filtration (Superdex 75HR) using FPLC (fast protein liquid chromatography); this factor stimulated the proliferation of MCF-7 human breast cancer cells, a bioassay which is specific for the insulin-like growth factors (IGFs). The 25, 29 and 40 kDa proteins were purified by sequential chromatography as follows: anion-exchange (Mono Q), heparin-Sepharose, hydroxyapatite, concanavalin A-Sepharose, phenyl-Superose, reversed phase high performance liquid chromatography (HPLC) and sodium dodecylsulfate polyacrylamide gelelectrophoresis (SDS-PAGE). The 25 kDa protein was identified as TGF-beta by its inhibitory effect on the proliferation of mink lung cells. The 40 kDa protein enhanced the formation of multinucleate tartrate-resistant acid phosphatase positive cells in a murine bone marrow differentiation assay, but was without effect in an isolated osteoclast assay and had no growth factor activity; this protein is likely to be a colony stimulating factor. The 29 kDa protein was also without growth factor activity; it was, however, able to stimulate bone resorption in the isolated osteoclast assay, suggesting a direct action in osteoclast function. The 29 and 40 kDa proteins may be osteoblast gene products that have been sequestrated by the bone matrix in a similar fashion to TGF-beta and the IGFs. This is the first report of proteins isolated from bone matrix which directly stimulate osteoclast differentiation and activity.

Animals↗

PubMed2004

Effects of TGF-beta, TNF-alpha, IL-beta and IL-6 alone or in combination, and tyrosine kinase inhibitor on cyclooxygenase expression, prostaglandin E2 production and bone resorption in mouse calvarial bone cells.

Cyclooxygenase-2 (COX-2) and tyrosine kinase, which are involved in the biosynthesis of prostaglandin E(2) (PGE(2)) in mouse calvarial osteoblasts, are stimulated by cytokine interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and/or interleukin-6 (IL-6). IL-1beta and IL-6 and, to a lesser extent, TNF-alpha, enhances COX-2 mRNA levels in calvarial osteoblasts. Simultaneous treatment with IL-6 and IL-1beta and TNF-alpha resulted in enhanced COX-2 mRNA levels accompanied by the cooperative stimulation of PGE(2) biosynthesis compared to cells treated with IL-1beta or TNF-alpha or IL-6 alone. In contrast, the presence of TGF-beta reduced COX-2 mRNA level, PGE(2) biosynthesis and bone resorption induced by IL-1beta, TNF-alpha, IL-6 or a combination thereof. However, neither IL-1beta, TNF-alpha, IL-6 nor a combination of IL-1beta, TNF-alpha, IL-6 enhanced COX-1 mRNA levels in calvarial osteoblasts. A novel Src tyrosine kinase inhibitor, Herbimycin A (HERB), reduced COX-2 mRNA levels as well as PGE(2) production induced by IL-1beta, TNF-alpha and IL-6 or a combination of IL-1beta, TNF-alpha, IL-6, whereas COX-1 mRNA levels remained unaffected. Finally, HERB was found to inhibit in vitro bone resorption. These results indicate that the cooperative effects of IL-beta, TNF-alpha, IL-6 on PGE(2) production are due to the enhanced expression of the COX-2 gene and that tyrosine kinase(s) are involved in COX-2 signal transduction in mouse calvarial osteoblasts. Thus, the Src family of kinase inhibitors may be useful in treating diseases associated with elevated bone loss.

Animals↗

PubMed1990

Bone resorption in orthotopic and heterotopic bone of dichloromethylene bisphosphonate-treated rats.

The effect of the bisphosphonate dichloromethylene bisphosphonate (Cl2MBP) on orthotopic and heterotopic bone, induced by implants of demineralized bone matrix (DBM) in rats, was analyzed, with special reference to bone resorption. The heterotopic bone was formed by induction for 3 weeks; at this time, the rats were given daily subcutaneous injections of 3 mg/kg of body weight of Cl2MBP or saline, until sacrifice. Prior to the start of treatment, the animals were given 45Ca and [3H]proline to label the inorganic and organic components of bone, respectively. Groups of rats were sacrificed at intervals from 1 to 31 days after isotope injection, and the net formation of bone and the elimination rates of the two isotopes were studied in the heterotopic bone, in diaphyseal and metaphyseal bone, and in teeth. The treatment with Cl2MBP caused a doubling of the daily net increase in mineral of the induced heterotopic bone, and a less pronounced increase in the ash content of tibiae. The treatment decreased the elimination rates of both isotopes in the orthotopic and heterotopic bone, showing that decreased bone resorption is the cause of the increased net bone formation.

Animals↗

PubMed2005

Two types of bone resorption lacunae in the mouse parietal bones as revealed by scanning electron microscopy and histochemistry.

To understand the bone resorption process on the basis of the morphology of bone resorption lacunae, the inner surface of parietal bones in juvenile mice was exposed with a treatment of ultrasonic waves or NaOCl treatment and examined by scanning electron microscopy (SEM). The bone resorption lacunae were divided into two types (I and II) according to differences in morphological features of their walls; the wall of type I lacunae was covered with loose collagen fibrils, while that of type II lacunae was smooth with almost no fibrillar structures. Collagen fibrils in type I lacunae treated with ultrasonic waves differed in appearance from those treated with NaOCl; the collagen fibrils were thin and displayed a smooth surface in type I lacunae treated with ultrasonic waves, while they were thick and showed a rough surface in those treated with NaOCl-probably because superficial uncalcified collagen fibrils were digested with the chemical. The results indicated that type I lacunae occupied 77% of all of the bone resorption lacunae treated with ultrasonic waves, but 51% of those treated with NaOCl. This finding led to the idea that type I lacunae can be subdivided into two: lacunae (Ia), covered with partially calcified fibrils as well as superficial uncalcified fibrils; and lacunae (Ib), covered only with uncalcified fibrils. The presence of uncalcified fibrils in the bone resorption lacunae was further confirmed by backscattered electron (BSE) imaging of SEM. Histochemistry for acid phosphatase or immuno-histochemistry for cathepsin B or carbonic anhydrase in combination with SEM revealed that type I lacunae were located under osteoclasts but type II lacunae were not. These findings indicate that type I lacunae are in the process of bone resorption by osteoclasts, while type II lacunae are in the final stage of bone resorption and free from osteoclasts. Bone resorption may thus proceed in the order of Ia, Ib, and II.

Animals↗