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PubMed2005

Increased bone resorption in HD patients: is it caused by elevated RANKL synthesis?

BACKGROUND: The receptor activator of nuclear factor kappaB ligand (RANKL), produced by osteoblasts/stromal cells, is a member of the RANK/RANKL/OPG system, which regulates bone resorption by osteoclasts. Since RANKL and osteoprotegerin (OPG) production in bone is influenced by parathyroid hormone (PTH), we measured serum RANKL and OPG concentrations in haemodialysis (HD) patients, who commonly hypersecrete PTH. We aimed to determine if clinically demonstrated PTH-enhanced bone resorption is a consequence of increased RANKL synthesis. METHODS: RANKL, OPG, osteocalcin, intact PTH, bone-specific alkaline phosphatase, tartrate-resistant acid phosphatase 5b and beta-CrossLaps (CTx) were measured in blood samples from 80 HD patients and 50 age-matched controls. HD patients were stratified to tertiles according to their serum PTH levels: 29.3-103.0, 109.7-263.0 and 262.0-1700.0 pg/ml in the first, second and third tertiles, respectively. RESULTS: Mean serum RANKL levels were 1.6 times higher in HD patients than in age-matched controls (1.36+/-0.39 vs 0.83+/-0.70 pmol/l; P<0.001). All the measured bone markers significantly differed between patients and controls (P<0.001). Spearman's tests of correlation showed a statistically significant association of RANKL with PTH, osteocalcin and CTx (r=0.322, P=0.004; r=0.231, P=0.039; and r=0.230, P=0.040, respectively). Mean serum RANKL levels were significantly different between PTH tertiles (P = 0.003), but serum OPG levels were not (P=0.144). The highest RANKL levels were measured in the upper PTH tertile (1.54+/-0.39 pmol/l) and were significantly higher than in the middle or lower tertiles (1.27+/-0.42 and 1.23+/-0.26 pmol/l, respectively; P=0.003). Both of the measured bone-resorption markers, tartarate-resistant acid phosphatase 5b and CTx, as well as both bone formation markers, osteocalcin and bone-specific alkaline phosphatase were also significantly higher in the upper tertile, indicating that whole-bone remodelling is activated at high PTH and RANKL levels. CONCLUSIONS: Serum RANKL levels were significantly higher in HD patients than in healthy age-matched controls. Moreover, RANKL levels were significantly higher in the upper PTH tertile, indicating enhanced RANKL synthesis in a PTH-dependent fashion. Thus, our clinical findings clearly support published in vitro studies that demonstrated a stimulating effect of PTH on RANKL synthesis. Therefore, the hypothesis that PTH increases bone resorption in HD patients through RANKL appears valid.

Acid Phosphatase↗

PubMedDate not supplied

Bone resorption in chronic otitis media: the role of the osteoclast.

Most of the pathology associated with cholesteatoma is the result of osteoclast-mediated bone resorption in the middle ear. Cytokines, prostaglandins, nitric oxide, neurotransmitters and growth factors are associated with chronic inflammation and have been implicated in cholesteatoma-induced bone resorption. Although many different factors are known to regulate osteoclast activation, there is a final common pathway of osteoclast differentiation and resorption. Recent advances in molecular techniques and the increasing availability of genetically altered mice have provided valuable insight into the molecular mechanism of osteoclastic bone resorption. This review focuses on osteoclast biology, lessons from genetically altered mice, and their contribution to our understanding of cholesteatoma-induced bone resorption.

Animals↗

PubMed2006

MMP-9 antisense oligodeoxynucleotide exerts an inhibitory effect on osteoclastic bone resorption by suppressing cell migration.

We have previously shown that matrix metalloproteinases (MMPs) play a role in osteoclastic bone resorption by facilitating migration of osteoclastic cells toward bone surface through matrices. Of MMPs identified so far, MMP-9 is likely the most important proteinase for the action, since osteoclasts express this enzyme at a tremendously high level. However, no direct evidence has been provided to demonstrate its contribution to bone resorption. In this study, to address this point, we used an MMP-9 antisense phosphothiorate oligodeoxynucleotide (S-ODN), which was shown to inhibit the protein synthesis of MMP-9 efficiently. We demonstrated that the antisense S-ODN inhibited osteoclastic pit formation on matrigel-coated dentine slices in a concentration-dependent manner with a maximum reduction of total pit volume by 53% at 10 microM. These results, taken together, suggest that MMP-9 is involved in osteoclastic bone resorption process possibly by facilitating migration of osteoclasts through proteoglican-rich matrices.

Animals↗

PubMed1995

Possible involvement of focal adhesion kinase, p125FAK, in osteoclastic bone resorption.

Involvement of tyrosine phosphorylation in osteoclastic bone resorption was examined using osteoclast-like multinucleated cells prepared from co-cultures of mouse osteoblastic cells and bone marrow cells in the presence of 1 alpha,25-dihydroxyvitamin D3. When osteoclast-like cells were plated on culture dishes in the presence of 10% fetal bovine serum, they were sharply stained in their peripheral region by anti-phosphotyrosine antibody. Western blot analysis revealed that 115- to 130-kD proteins were tyrosine-phosphorylated in osteoclast-like cells. Using immunoprecipitation and immunoblotting, one of the proteins with 115-130 kD was identified as focal adhesion kinase (p125FAK), a tyrosine kinase, which is localized in focal adhesions. Immunostaining with anti-p125FAK antibody revealed that p125FAK was mainly localized at the periphery of osteoclast-like cells. Herbimycin A, a tyrosine kinase inhibitor, not only suppressed tyrosine phosphorylation of p125FAK but also changed the intracellular localization of p125FAK and disrupted a ringed structure of F-actin-containing podosomes in osteoclast-like cells. Antisense oligodeoxynucleotides to p125FAK inhibited dentine resorption by osteoclast-like cells, whereas sense oligodeoxynucleotides did not. These results suggest that p125FAK is involved in osteoclastic bone resorption and that tyrosine phosphorylation of p125FAK is critical for regulating osteoclast function.

Animals↗

PubMedDate not supplied

Crestal bone resorption 5 years after implant loading: clinical and radiologic results with a 2-stage implant system.

PURPOSE: The aim of the present study was to assess crestal bone resorption 5 years after loading by conducting a clinical and radiographic evaluation of 112 Frialit-2 implants consecutively placed in 51 patients from January 1994 through June 1994. MATERIALS AND METHODS: All implants were placed in the same private-practice clinic by the same surgeon. Clinical assessment included plaque score monitoring, bleeding on probing, probing depth, type of occlusion, and prosthetic adaptation. Intraoral radiographs were taken and compared using suitable software to accurately measure peri-implant bone resorption. RESULTS: The survival rate of the implants was 100%. Plaque was present on 47 (42%) implants. Bleeding on probing was detectable at 17 implants (15.5%). Probing depth was > 5 mm for 5 implants (4.5%). Crestal bone resorption was > 3 mm for 32 implants (28.6%); the average observed crestal bone resorption was 2.17+/-1.6 mm. DISCUSSION: The survival rate of the implants may be the result of the relatively short functional period as well as the strict and frequent clinical evaluations associated with oral hygiene procedures during the supportive periodontal therapy. CONCLUSION: The results suggest that with strict plaque control, and provided that the patient follows a regular program of supportive therapy, crestal bone resorption around a 2-stage implant system may be limited.

Adolescent↗

PubMed2006

In long-term bedridden elderly patients with dietary copper deficiency, biochemical markers of bone resorption are increased with copper supplementation during 12 weeks.

BACKGROUND: Although the effect of copper on bone has been tested in animals and healthy subjects, no studies concerning the effect of copper supplementation on bone metabolism in patients with copper deficiency have been reported because of the rarity of these patients. This study was conducted to investigate the effect of copper supplementation on bone metabolism in copper-deficient patients. METHOD: This study included 10 patients (83.7 +/- 8.3 years) with dietary copper deficiency under long-term bed rest for more than 12 months. They had their diets supplemented with copper sulfate (3 mg/day) over 12 weeks in addition to their diet of only one kind of enteral food with a low concentration of copper. Serum copper and ceruloplasmin, urinary deoxypyridinoline (DPD) and collagen-type 1 N-telopeptide (NTX) (biomarkers of bone resorption), serum osteocalcin (OC) and bone-specific alkaline phosphatase (Bone ALP) (biomarkers of bone formation) were analyzed at baseline, 4 and 12 weeks after copper supplementation. RESULTS: DPD and NTX excretion were significantly increased 4 weeks after copper supplementation (p = 0.009 and p = 0.013, respectively). Serum bone ALP and OC were not significantly changed 12 weeks after copper supplementation (p = 0.051 and p = 0.594). CONCLUSIONS: In patients with nutritional copper deficiency, bone resorption markers are increased with copper supplementation.

Aged↗

PubMed1998

Comparison of urinary bone resorption markers in women of 40-70 years; day-to-day and long-term variation in individual subjects.

OBJECTIVES: Bone resorption can be judged using biochemical markers in urine and blood. Our aim was to study the patterns of markers in the postmenopausal period. METHODS: The urinary excretion of bone resorption markers was tested using different assays. The study was undertaken to determine the day-to-day and the long-term variation, over 8 years, of these markers in individual women. RESULTS: Over a period of 2 weeks, the median of the day-to-day variation of the pyridinium crosslink markers varied between 12 and 23%, the median value of the long-term variation over 8 years between 10 and 21%, for the telopeptide markers median day-to-day variation was 18 and 20% and the long-term variation was 17 and 19%. The correlations between the different crosslink markers varied between 0.63 and 0.92, depending on the kind of the crosslink and on the method of determination. The two telopeptide markers showed an excellent correlation with r of 0.95. The excretion of all bone resorption markers varied with postmenopausal age, some differences were found between the crosslink and the telopeptide excretions with age, in women more than 20 years postmenopausal the telopeptides decrease whereas the crosslinks show an increase. CONCLUSIONS: This study shows that crosslinks and telopeptides give similar information on the rate of bone resorption: an increase during the first 5 years and a slight decrease in the next 5 years after menopause, discrepancies were found after 10 or more postmenopausal years.

Adult↗

PubMed2002

Soybean isoflavones reduce postmenopausal bone resorption in female Japanese immigrants in Brazil: a ten-week study.

OBJECTIVE: Some human studies and animal models of experimental osteoporosis have shown that soy isoflavones may be effective on bone health. In this study, we carried out an intervention study to explore the effects of dietary isoflavone on bone metabolism. METHODS: Forty healthy female postmenopausal Japanese immigrants living in Brazil were divided into two groups: isoflavone-administered (n = 20) or placebo (n = 20). Subjects in the isoflavone-administered group ingested 37.3 mg per day for 10 weeks. The collection of 24-hour urine and the measurement of bone stiffness were performed at 0 and 10 weeks. Urinary excretion of isoflavones and bone resorption markers were analyzed. RESULTS: Urinary isoflavone excretion in the isoflavone-administered group was significantly increased at weeks 3 and 10. Urinary excretion of bone resorption markers was reduced in the isoflavone-administered group, while the placebo group did not show any significant reduction. Differences in levels of urinary isoflavones and bone resorption markers between the two groups were significant. CONCLUSION: This study demonstrated that the bone resorption was associated with the intake of soy isoflavones in postmenopausal women, and continuous dietary intake of isoflavone may inhibit postmenopausal osteoporosis.

Biomarkers↗

PubMed2003

S 12911-2 inhibits osteoclastic bone resorption in vitro.

The potential anti-osteoporotic activity of the strontium compound, S12911, was tested on osteoclast-like cells and on cultured fetal mouse long bones. From 1 mM Sr2+, S12911 reduced both basal and stimulated bone resorption by decreasing osteoclast activity and ruffled border formation. The aim of this study was to evaluate the effects of S 12911-2 on osteoclastic bone resorption using in vitro systems. Osteoclast-like cells, produced in vitro by co-culture of mouse bone marrow cells with primary osteoblasts, were allowed to settle on dentine slices, and the area of resorption pits formed after 48 h was measured using an image analysis system. S 12911-2, at a minimal active concentration of 1 mM Sr2+, significantly reduced pit formation by these cells (p < 0.05). Pretreatment of slices for 48 h with S 12911-2 (5 mM Sr2+) did not produce appreciable inhibition of resorption. Bone resorption in cultured fetal mouse long bones was assessed by measuring the release of pre-incorporated 45calcium. S 12911-2 inhibited resorption in control cultures (18.9%, p < or = 0.05) and in bones cultured with the active form of vitamin D3 [1,25(OH)2D3] (44.5%, p < or = 0.05). S 12911-2 had no effect on the number of osteoclasts observed histochemically in longitudinal sections prepared from fetal mouse long bones. Electron microscopy of mouse long bones treated with S 12911-2 (3 mM Sr2+) showed osteoclasts with clear zones facing the bone surface, but without well-developed ruffled borders; untreated bones contained osteoclasts with normal ruffled borders. These results indicate that S 12911-2 inhibits osteoclast activity. This effect is directly linked to the presence of strontium, is effective on basal and stimulated resorption, and involves a decrease in ruffled border formation by osteoclasts.

Animals↗

PubMed1994

In vivo effect of beta 2-microglobulin on bone resorption.

beta 2-Microglobulin (beta 2-M) deposits have been found in the destructive bone lesions associated with dialysis-related amyloidosis. To examine whether beta 2-M can cause bone resorption in vivo, doses of beta 2-M alone were compared with parathyroid hormone (PTH), aluminum, and vehicle alone. Eleven injections of 10 micrograms each were made over a period of 56 hours into the subcutaneous tissue overlying the occipital region of mice. Using a computerized image analysis system we measured (1) periosteal and inner bone length, (2) bone marrow interface length, and (3) the extent of resorption along these surfaces expressed as percentage of total length. Injections of either beta 2-M or PTH were associated with 22% +/- 4% and 25% +/- 4% resorption of periosteal surface, respectively, and 15.9% +/- 2% and 19.9% +/- 5% resorption of marrow bone surfaces, respectively, compared with control. In contrast, aluminum did not increase bone resorption over controls. The simultaneous injection of calcitonin, an osteoclast inhibitor, with beta 2-M or PTH did not increase periosteal resorption over controls. The resorption of inner bone surface was similar in all groups. These studies show that beta 2-M and PTH cause bone resorption in the bone surfaces proximate to the site of injection. This suggests that beta 2-M may contribute to the development of the bone cysts in dialysis-related amyloidosis.

Aluminum↗

PubMed1980

Sulfonamide inhibition of bone resorption: lack of a hypophosphatemia.

Calcitonin and acetazolamide inhibit bone resorption in the ureter-ligated rat. Calcitonin treatment results in an ensuing hypocalcemia and hypophosphatemia. Although acetazolamide treatment results in a hypocalcemic response similar to that seen with calcitonin, plasma phosphate concentrations increase or remain unchanged after drug treatment. Data are presented indicating that acetazolamide exhibits two effects that influence blood phosphate. Drug treatment of ureter-ligated rats results in an inhibition of bone resorption which tends to lower blood phosphate concentrations. However, this effect is masked by a drug-induced hypercapnia which results in an increase in plasma phosphate concentrations. Elevation of blood pCO2 also attenuates the hypophosphatemic response to calcitonin.

Acetazolamide↗

PubMed2006

Effect of adoptive transfer of antigen-specific B cells on periodontal bone resorption.

BACKGROUND AND OBJECTIVES: Host immune responses to periodontal pathogens have been considered to contribute to the alveolar bone destruction in periodontitis. However, the role of B lymphocytes in the pathogenesis of periodontal bone loss is not clear. METHODS: We examined the effect of adoptive transfer of antigen-specific B cells from rat spleens on experimental periodontal bone resorption. Donor rats were immunized intraperitoneally (i.p.) with formalin-killed Actinobacillus actinomycetemcomitans. Antigen-specific B cells were prepared from splenocytes by first binding CD43(+) cells to Petri dishes coated with anti-CD43 antibody to remove T cells, and non-binding cells were passed through a nylon wool column to deplete accessory cells. The retained cells were then collected and bound to A. actinomycetemcomitans-coated Petri dishes for enrichment of A. actinomycetemcomitans-binding B cells (AAB). A. actinomycetemcomitans non-binding B cells (ANB) and B cells from non-immunized donor rats (NIB) were also collected from these procedures. Each type of B cell was injected into a group of recipient rats that were then orally infected with live A. actinomycetemcomitans. RESULTS: At termination, the antibody levels to A. actinomycetemcomitans in serum and gingival wash fluids were significantly higher in the recipients transferred with AAB when compared to the recipients transferred with ANB or NIB. A markedly elevated number of antibody-forming cells were observed in the spleens of the recipients transferred with AAB, and these recipient rats also exhibited significantly increased bone resorption when compared to the other groups. CONCLUSIONS: It is suggested that B cells can contribute to periodontal bone resorption and that antigen-triggering of B cells is required for the bone resorption.

Actinobacillus Infections↗

PubMed1988

A link between calcitriol and bone resorption.

Calcitriol exposure stimulated a human osteosarcoma cell line, U2-OS, to produce a factor(s) which stimulated bone degradation in human monocyte cultures and osteoclastic bone resorption in fetal rat long bone cultures. The factor(s) was elicited by as little as 10(-10) M calcitriol. The factor is effective in stimulating peripheral blood monocytes to degrade bone, suggesting a direct effect on cellular bone breakdown. The fetal long bone assays suggest that the osteoblast-like cells produce a factor(s) which stimulates osteoclasts. This is confirmed by the fact that human calcitonin added to the long bone cultures blocks the stimulation. The effect of PTH appears to be through the production of factors which stimulate osteoblasts. The present study suggests that a similar factor(s) may be responsible for the effect of calcitriol on bone resorption.

Bone Resorption↗

PubMed2006

[Increased bone resorption by sympathetic nervous activity].

Recent experimental studies showed the dynamic neural regulation of local bone metabolism. Increased sympathetic nervous activity has been demonstrated to cause bone loss via an increase in bone resorption and a decrease in bone formation. This review summarized both in vivo and in vitro evidences implicating sympathetic neuron action in bone resorption.

Animals↗

PubMed1986

Effects of prostacyclin and prostaglandin E1 (PGE1) on bone resorption in the presence and absence of parathyroid hormone.

Prostaglandins have been shown to stimulate osteoclastic bone resorption in organ culture but morphologic studies of isolated osteoclasts have shown a transient calcitonin-like inhibiting effect of these agents. We looked for a dual effect on bone resorption by comparing the early and late effects of prostaglandin E1 (PGE1), prostacyclin (PGI2), 6 alpha-carbaprostaglandin I2 (C-PGI2), a carbon substituted analog of PGI2, and salmon calcitonin (CT) on the release of previously incorporated 45Ca from fetal rat long bones cultured in the presence of an inhibitor of cyclooxygenase, RO-20-5720. Experiments were performed in both the presence and absence of PTH (400 ng/ml), which was administered 24 hours before addition of prostaglandins or CT. In control cultures not stimulated by PTH, CT (100 mU/ml) produced significant decreases in 45Ca release at 48, 72, and 96 hours while PGE1 (10(-6) M), PGI2 (10(-5)), and C-PGI2 (10(-6) M) each produced significant increases in resorption at 24 through 96 hours. PGE1 at 10(-5) M, but not 10(-6) M, caused a significant decrease in medium 45Ca of 21% at 1 and 2 hours. Medium calcium measurements suggest that the change in 45Ca was due to inhibition of release and not to increased uptake. PGI2 (10(-5) M) and C-PGI2 (10(-6) M) caused no significant inhibitory effect. In cultures stimulated by PTH, CT produced significant inhibition of bone resorption of 6 through 96 hours, but no inhibition of bone resorption was noted at either early or late time points with PGE1, PGI2, or C-PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗

PubMed1994

Nonsteroidal antiinflammatory drug modulation of prosthesis pseudomembrane induced bone resorption.

OBJECTIVE: To study the in vitro effect of therapeutic levels of select nonsteroidal antiinflammatory drugs (NSAID) on prosthesis associated pseudomembrane induced bone resorption and cytokine and prostanoid synthesis using tissue obtained from osteoarthritic patients undergoing revision of cemented implants. METHODS: Pseudomembranes were cultured in the presence and absence of therapeutic levels of select NSAID: Processed conditioned media were evaluated for bone resorbing capacity by assessing murine neonatal limb rudiment release of 45Ca. Interleukin 1 (IL-1) and tumor necrosis factor (TNF) were analyzed by bioassay and prostaglandin E2 (PGE2) by radioimmunoassay. RESULTS: Piroxicam, in contrast to indomethacin and sodium salicylate, significantly decreased membrane associated bone resorption. The NSAID effect correlated more consistently with piroxicam downregulation of TNF synthesis than that of IL-1. Consistent drug associated suppression of PGE2 synthesis did not enable differentiation of NSAID effectiveness in suppressing pseudomembrane induced bone resorption. CONCLUSION: Results provide a rational basis for design of animal models and/or further human studies to test the hypothesis that the prophylactic administration of an NSAID can potentially retard the pseudomembrane effected bone resorptive process associated with aseptic cemented prosthesis failure.

Adult↗

PubMed1998

Cloning and identification of human Sca as a novel inhibitor of osteoclast formation and bone resorption.

Increased osteoclast activity is responsible for the enhanced bone destruction in postmenopausal osteoporosis, Paget's disease, bone metastasis, and hypercalcemia of malignancy. However, the number of known inhibitory factors that block osteoclast formation and bone resorption are limited. Therefore, we used an expression-cloning approach to identify novel factors produced by osteoclasts that inhibit osteoclast activity. A candidate clone was identified and isolated from a human osteoclast-like multinucleated cell (MNC) cDNA library, named osteoclast inhibitory peptide-1 (OIP-1), and the cDNA sequence was determined. This sequence matched that of the recently identified human stem cell antigen, was structurally similar to the mouse Ly-6 gene family, and the sequence predicted it was a glycosyl phosphatidyl inositol (GPI)-anchored protein that had a cleavable COOH-terminal peptide. Western blot analysis of conditioned media from 293 cells transfected with the OIP-1 cDNA clone confirmed that OIP-1 was released into the media as a membrane-bound GPI-linked protein. Interestingly, both recombinant OIP-1 expressed in Escherichia coli (which does not have GPI linker) and OIP-1 expressed by mammalian cells significantly reduced osteoclast-like MNC formation induced by 1,25-dihydroxyvitamin D3 or PTH-related protein in mouse and human bone marrow cultures, and inhibited 45Ca release from prelabeled bone in fetal rat organ cultures. In contrast, recombinant OIP-1 did not inhibit the growth of a variety of other cell types. These data indicate that OIP-1 is a novel, specific inhibitor of osteoclast formation and bone resorption.

ATPases Associated with Diverse Cellular Activitie↗

PubMed1988

Bone resorption induced by transplanted bladder tumor (MBT-2) in mice.

The high incidence of metastatic bone resorption in urological cancer makes it necessary for clinicians to look for a valid experimental model to investigate basic interaction between cancer cells and bone in order to improve the treatment. A new model of bone resorption has been defined, namely the subcutaneous injection of tumor cell suspensions of invasive transitional cell carcinoma of the bladder (MBT-2) into mice after the periosteum of the calvaria has been disrupted. The tumor induced osteolysis associated with osteoclast proliferation with reactive bone formation. Moreover, we were able to show hypercalcemia accompanied with local bone resorption in this model.

Animals↗