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PubMed2004

(23S)-25-Dehydro-1{alpha}-hydroxyvitamin D3-26,23-lactone, a vitamin D receptor antagonist that inhibits osteoclast formation and bone resorption in bone marrow cultures from patients with Paget's disease.

Osteoclast (OCL) precursors from patients with Paget's disease (PD) and normal OCL precursors transduced with the measles virus nucleocapsid protein gene (MVNP) are hyperresponsive to 1alpha,25-dihydroxyvitamin D(3) [1alpha,25-(OH)(2)D(3)] and can form OCLs at physiologic concentrations of 1alpha,25-(OH)(2)D(3). This hyperresponsivity to 1alpha,25-(OH)(2)D(3) is due to increased expression of TATA box-associated factor II-17, a potential coactivator of the vitamin D receptor. Hyperresponsivity to 1alpha,25-(OH)(2)D(3) may permit OCL formation in PD patients with low levels of 1alpha,25-(OH)(2)D(3) and play a role in the pathogenesis of PD. Therefore, we tested the effects of a vitamin D antagonist, (23S)-25-dehydro-1alpha-hydroxyvitamin D(3)-26,23-lactone (TEI-9647), to determine its potential to inhibit the enhanced OCL formation and bone resorption seen in patients with PD. TEI-9647, by itself, was not a vitamin D receptor agonist and did not induce OCL formation in vitro, even at 10(-6) m. However, it dose-dependently (10(-10) m to 10(-6) m) inhibited osteoclast formation induced by concentrations of 1alpha,25-(OH)(2)D(3) (41 pg/ml, 10(-10) m) detected in PD patients by bone marrow cells of patients with PD and MVNP-transduced colony-forming unit-granulocyte macrophage (CFU-GM) cells, which form pagetic-like OCL. Moreover, bone resorption by OCLs derived from MVNP-transduced CFU-GM treated with 10(-9) m 1alpha,25-(OH)(2)D(3) was dose-dependently inhibited by TEI-9647 (10(-9) m to 10(-6) m). Furthermore, 10(-7) m TEI-9647 by itself did not cause 1alpha,25-(OH)(2)D(3)-dependent gene expression but almost completely suppressed expression of the TATA box-associated factor II-17 and 25-hydroxyvitamin D(3)-24-hydroxylase genes induced by 1alpha,25-(OH)(2)D(3) treatment of MVNP-transduced CFU-GM cells. These results demonstrate that TEI-9647 can suppress the excessive bone resorption and OCL formation seen in marrow cultures from patients with PD.

Bone Marrow Cells↗
PubMed1992

Stimulative effects of cadmium on bone resorption in neonatal parietal bone resorption.

Effects of cadmium on bone resorption were investigated using neonatal mouse parietal bone culture system. Cadmium at 0.5 microM and above stimulated hydroxyproline release as well as 45Ca release. As cadmium-stimulated bone resorption was inhibited by calcitonin, bone resorption induced by cadmium is osteoclast-mediated bone resorption. CI-1, collagenase inhibitor, depressed cadmium-stimulated bone resorption in a dose-dependent manner. Osteoblasts are also involved in cadmium-induced bone resorption. Indomethacin-inhibited cadmium-stimulated bone resorption and cadmium-treated bones released prostaglandin E2 to a greater extent than untreated bones. Cadmium-stimulated bone resorption was shown to be dependent on the production of prostaglandin E2. 3-Isobutyl-1-methylxanthine potentiated cadmium-stimulated bone resorption and verapamil depressed it. It is possible that an increase in levels of cAMP and calcium ion in bone cells is involved in cadmium-induced bone resorption. From these results, cadmium was found to stimulate osteoclast-mediated bone resorption which is dependent on prostaglandin E2. Second messengers in cadmium-induced bone resorption may be cAMP and calcium ion.

Animals↗
PubMed2004

Soluble cathepsin-L: a marker of bone resorption and bone density?

We sought to evaluate cathepsin L serum levels in the peripheral blood of patients with low bone density. Blood samples from 60 patients (32 osteoporotic, 28 osteopenic) and 16 healthy controls were taken and quantitative measurements of cathepsin L were performed with the use of a commercially available enzyme-linked immunosorbent assay. Dual x-ray absorptionometry measurements and serum levels of alkaline phosphatase, bone-specific alkaline phosphatase, osteocalcin, parathyroid hormone, sexual hormones, and N -terminal crosslinks of type I collagen were examined. Group comparisons between patients with osteoporosis and controls showed significant differences with respect to cathepsin L ( t = -2.839; df = 29; P =.008). Osteoporosis treatment decreased the serum level of cathespsin L in a statistically significant fashion ( P =.002). These results suggest that the serum level of cathepsin L can serve as a marker of bone resorption and bone density.

Aged↗
PubMed1997

[Interrelations of the calcium concentration in breast milk with maternal intake of cow's milk and milk products, bone resorption and bone mineral density during lactation].

The interrelations of the calcium (Ca) concentration in breast milk with maternal intake of cow's milk and milk products, 24-hour urinary hydroxyproline and Ca concentrations adjusted by creatinine (H.P/Cre, Ca/Cre) and bone mineral density measured by ultrasonic bone densitometry were examined to study the mechanism regulating the calcium concentration in breast milk. Subjects were 105 lactating women, aged 21 to 42 years, at 21.590 days postpartum. 1) The geometric means (logarithmically transformed calculated M +/- SD) of H.P/Cre were 40.7 (31-61) and 36.3 (28-47) mg/g in women lactating less than 150 days and 150 days or more, respectively. These values indicated increased bone resorption. 2) Intake of cow's milk and milk products significantly negatively correlated with urinary H.P/Cre. For women consuming less than 100ml per day of cow's milk, a significant positive correlation was found between the urinary H.P/Cre and Ca concentration in breast milk. These results suggest that the extent of bone resorption depends on maternal Ca intake and the Ca transfer from maternal bone to breast milk in women with a low Ca intake. 3) For women with a cow's milk intake of less than 100ml per day, a significant positive correlation was found between the Ca concentration in breast milk and bone mineral density, indicating that women with bone mineral loss are not able to compensate for the low Ca level in breast milk. 4) Urinary Ca/Cre significantly negatively affected the Ca concentration in breast milk. This result indicates that some amount of Ca in breast milk is due to renal conservation.

Adult↗
PubMed2006

A TNF receptor loop peptide mimic blocks RANK ligand-induced signaling, bone resorption, and bone loss.

Activating receptor activator of NF-kappaB (RANK) and TNF receptor (TNFR) promote osteoclast differentiation. A critical ligand contact site on the TNFR is partly conserved in RANK. Surface plasmon resonance studies showed that a peptide (WP9QY) that mimics this TNFR contact site and inhibits TNF-alpha-induced activity bound to RANK ligand (RANKL). Changing a single residue predicted to play an important role in the interaction reduced the binding significantly. WP9QY, but not the altered control peptide, inhibited the RANKL-induced activation of RANK-dependent signaling in RAW 264.7 cells but had no effect on M-CSF-induced activation of some of the same signaling events. WP9QY but not the control peptide also prevented RANKL-induced bone resorption and osteoclastogenesis, even when TNFRs were absent or blocked. In vivo, where both RANKL and TNF-alpha promote osteoclastogenesis, osteoclast activity, and bone loss, WP9QY prevented the increased osteoclastogenesis and bone loss induced in mice by ovariectomy or low dietary calcium, in the latter case in both wild-type and TNFR double-knockout mice. These results suggest that a peptide that mimics a TNFR ligand contact site blocks bone resorption by interfering with recruitment and activation of osteoclasts by both RANKL and TNF.

Amino Acid Sequence↗
PubMed1997

Frequency of food intake and natural dietary components are potent modulators of bone resorption and bone mass in rats.

Prevention of low bone mass is important to reduce the incidence of osteoporotic fractures. In this report evidence is provided that feeding habits per se, that is, increased frequency of food intake as well as a diet containing soy and other raw components, decrease bone resorption and increase bone mass in growing rats. Interim results after 6 weeks indicate that food fractionation and natural dietary components are both capable of inhibiting trabecular bone loss in aged rats. These interim results indicate that the effect of both dietary interventions are additive and together are capable of nearly completely blunting the age-dependent loss of trabecular bone mineral density. These dietary manipulations are, however, only partially effective in inhibiting the strongly increased loss of trabecular bone mineral density induced by estrogen deprivation. The fact that the natural dietary components are not more effective in ovariectomized rats as compared to intact females confirms our contention that these components may not operate by mimicking the effect of estradiol. Whether bone mass in humans is also under the control of dietary habits is not known. If so, an increased frequency of meals of appropriate composition may be used to prevent osteoporosis.

Animals↗
PubMed1978

A tetracycline-based histomorphometric evaluation of bone resorption and bone turnover in hyperthyroidism and hyperparathyroidism.

Increased bone, resorption previously found in hyperthyroidism might be caused by a direct stimulating effect of thyroid hormone(s) on bone cells or by an increased sensitivity to circulating parathyroid hormone. In order to disclose qualitative differences in the response of bone resorbing cells to excess parathyroid hormone and excess thyroid hormone(s), histomorphometric analysis of iliac crest biopsies was performed in 25 hyperparathyroid and 40 hyperthyroid patients after tetracycline double-labelling. The main target cells for parathyroid and thyroid hormones were different. Parathyroid hormone stimulated osteocytic osteolysis and increased osteoclastic resorption surfaces equally in trabecular and cortical bone. The osteoclastic resorption was inactive. Thyroid hormone(s) had no effect on osteocytes but increased the osteoclastic resorption surfaces in trabecular and cortical bone, with a pronounced preponderance in cortical bone. The osteoclastic resorption was active and followed by a significant loss of both cortical and trabecular bone. The findings support the assumption that increased bone resorption in hyperthyroidism is caused by a direct stimulating effect of thyroid hormone(s).

Adult↗
PubMed1991

The effects of disorders of cartilage formation and bone resorption on bone shape: a study with chondrodystrophic and osteopetrotic mouse mutants.

The shapes of scapulae and basi-occipital bones from three genetically distinct achondroplastic mutants and one osteopetrotic mutant in the mouse (achondroplasia, brachymorphic, stumpy and grey lethal), and appropriate controls, have been compared using Fourier analysis and multivariate statistical techniques. Normal littermates were generally similar in shape, but mutants were significantly different from these controls and from each other. The pattern of morphological differences between the mutants and between the mutants and normal controls is examined. These differences are discussed in relation to the different effects of the four genes on bone morphogenesis, and the significance of these findings in relation to the contributions of cartilage formation and bone resorption to skeletal morphogenesis is considered.

Animals↗
PubMed1998

Prednisolone prevents decreases in trabecular bone mass and strength by reducing bone resorption and bone formation defect in adjuvant-induced arthritic rats.

We examined the effects of prednisolone (PSL) administration in normal female Sprague Dawley rats and adjuvant-induced arthritic rats at the age of 6 weeks. Rats were intramuscularly injected with PSL twice a week at doses of 0 (control), 10, 30, 90, or 270 mg/kg body weight (b.w.). In the normal rats, serum osteocalcin level at 14 days and serum carboxyterminal pyridinoline cross-linked telopeptide of type 1 collagen (1CTP) level at 28 days in the 270 mg/kg dose group was lower than the respective value in control animals. The BMC and the trabecular bone formation rate (BFR/BS) of the lumbar body (L-4) in the 270 mg/kg dose group at 14 and 28 days were significantly lower than the values in the control rats. In the arthritic rats, however, serum osteocalcin levels in the PSL-treated groups did not differ compared with arthritic controls. The serum 1CTP levels in all of the PSL-treated groups were significantly reduced at 28 days. The age-dependent increases in the L4 BMC, BMD, and L-3 ultimate compressive load values were maintained. The BFR/BS values in the 90 mg/kg and 270 mg/kg dose groups were significantly higher than those in the arthritic control rats. The trabecular osteoclast number and surface values in all of the PSL-treated groups were significantly lower than the values in arthritic controls. These data demonstrate that PSL administration prevented reduction in bone mass and strength of the lumbar trabecular bone in adjuvant-induced arthritic rats by reducing the increase in bone resorption and the decrease in bone formation at both the local and systemic levels.

Animals↗
PubMed2004

The effects of hyaluronan on bone resorption and bone mineral density in a rat model of estrogen deficiency-induced osteopenia.

Hyaluronan, or hyaluronic acid (HA), is an essential component of extracellular matrices. HA of appropriate molecular weight and concentration can induce osteoblast differentiation and bone formation in vitro. The aim of our study was to evaluate the effects of HA of different molecular weights on ovariectomy (OVX)-induced bone loss in rats. Adult female Sprague Dawley rats were subjected to bilateral OVX or sham surgical procedure (sham). OVX rats were treated with: HA of molecular weight of 0.75 MDa at a dose of 1 mg/kg/day and with HA of molecular weight of 1.62 MDa at a dose of both 0.5 mg/kg/day and 1 mg/kg/day. HA was applied orally once a day during the 8-week period after ovariectomy. Body weight, urinary pyridinoline (Pyr), deoxypyridinoline (DPyr) corrected for urinary creatinine, serum nitrite/nitrate concentrations and whole body and femoral bone mineral density (BMD) were measured. HA treatment had no effect on the body weight gain in OVX rats. Excretion of urinary Pyr and Dpyr significantly increased in OVX rats compared to sham controls. The higher molecular weight HA (1.62 MDa) significantly reduced urinary Pyr and DPyr concentrations measured on day 28 after ovariectomy (p < 0.001). Serum concentrations of nitric oxide metabolites, nitrite/nitrate significantly decreased in OVX rats in comparison with sham controls (p < 0.001). HA of both 0.75 MDa and 1.62 MDa molecular weights significantly enhanced serum nitrite/nitrate concentrations in OVX rats. There was a clear reduction of whole body and femoral BMD in untreated OVX rats. The higher molecular weight HA decreased both whole body and femoral BMD loss. Our results show that orally applied HA of high molecular weight (1.62 MDa) inhibits bone resorption and provides a protective effect on bone density in ovariectomized rats.

Amino Acids↗
PubMed2000

Peptidomimetic antagonists of alphavbeta3 inhibit bone resorption by inhibiting osteoclast bone resorptive activity, not osteoclast adhesion to bone.

Osteoclasts are actively motile on bone surfaces and undergo alternating cycles of migration and resorption. Osteoclast interaction with the extracellular matrix plays a key role in the osteoclast resorptive process and a substantial body of evidence suggests that integrin receptors are important in osteoclast function. These integrin receptors bind to the Arg-Gly-Asp (RGD) sequence found in a variety of extracellular matrix proteins and it is well established that the interaction of osteoclast alpha v beta 3 integrin with the RGD motif within bone matrix proteins is important in osteoclast-mediated bone resorption. In this study, we characterized the effects of two synthetic peptidomimetic antagonists of alpha v beta 3, SC-56631 and SC-65811, on rabbit osteoclast adhesion to purified matrix proteins and bone, and on bone resorption in vitro. SC-56631 and SC-65811 are potent inhibitors of vitronectin binding to purified alpha v beta 3. Both SC-56631 and SC-65811 inhibited osteoclast adhesion to osteopontin- and vitronectin-coated surfaces and time-lapse video microscopy showed that osteoclasts rapidly retract from osteopontin-coated surfaces when exposed to SC-56631 and SC-65811. SC-56631 and SC-65811 blocked osteoclast-mediated bone resorption in a dose-responsive manner. Further analysis showed that SC-65811 and SC-56631 reduced the number of resorption pits produced per osteoclast and the average pit size. SC-65811 was a more potent inhibitor of bone resorption and the combination of reduced pit number and size led to a 90% inhibition of bone resorption. Surprisingly, however, osteoclasts treated with SC-65811, SC-56631 or the disintegrin echistatin, at concentrations that inhibit bone resorption did not inhibit osteoclast adhesion to bone. These results suggest that alphavbeta3 antagonists inhibited bone resorption by decreasing osteoclast bone resorptive activity or efficiency but not by inhibiting osteoclast adhesion to bone per se.

Aniline Compounds↗
PubMed2004

Sequential analysis of biochemical markers of bone resorption and bone densitometry in multiple myeloma.

BACKGROUND AND OBJECTIVES: Bone lesions often occur in multiple myeloma (MM), but no tests have proven useful in identifying patients with increased risk. Bone marker assays and bone densitometry are non-invasive methods that can be used repeatedly at low cost. This study was performed to evaluate these methods in predicting bone events in MM patients. DESIGN AND METHODS: Thirty newly diagnosed MM patients were enrolled. Serum C-terminal telopeptide (ICTP) and urinary N-terminal telopeptide (NTx) of collagen I were measured for assessment of bone resorption, and serum C-terminal (PICP) and N-terminal (PINP) propeptides of procollagen I, bone-specific alkaline phosphatase, and osteocalcin were measured to estimate bone formation. Dual energy X-ray absorptiometry (DEXA) was used to assess bone mineral density (BMD) of the lumbar spine, hip, and whole body. Serum and urine samples were collected every 6 weeks, DEXA-scans performed every 3 months, and skeletal radiographs were done every 6 months as well as when indicated. RESULTS: Serum ICTP and urinary NTx were predictive of progressive bone events. Markers of bone formation, bone mineral density assessments, and M component measurements were less informative. In Cox analysis, ICTP showed the highest predictive value, but should be replaced with NTx in patients with nephropathy. Pretreatment low lumbar BMD was predictive of early vertebral fractures. INTERPRETATION AND CONCLUSIONS: Sequential DEXA-scans showed heterogeneous local BMD changes, and our data do not support routine use of sequential DEXA-scans. However, lumbar DEXA-scans at diagnosis can identify patients with increased risk of early vertebral collapses. Sequential analyses of serum ICTP and urinary NTx are useful for monitoring bone damage.

Absorptiometry, Photon↗
PubMed1997

A population-based study of the relationship between salt intake, bone resorption and bone mass.

OBJECTIVE: To explore the relationship between urinary sodium (the best measure of salt intake), urinary calcium, urinary deoxypyridinoline (DPYR) and bone mass. DESIGN: Cross-sectional study. SETTING: Population based sample of healthy Hobart residents. SUBJECTS: One hundred and fifty-four (M = 34, F = 120) subjects invited to take part from a systematic sample of the electoral roll and a single newspaper advertisement. RESULTS: In both sexes, urinary sodium correlated moderately with urinary DPYR (r = 0.32, P < 0.0001) and urinary calcium (r = 0.37, P < 0.0001). In multivariate analysis, the combination of urinary sodium, total body bone area, age and sex explained 22% of the variation in log-transformed DPYR (P < 0.00001). In univariate analysis, both urinary sodium and urinary DPYR were strongly associated with bone mineral content and bone mineral density at all sites but this association disappeared after adjustment for confounders particularly body weight. CONCLUSIONS: This study has shown that salt intake is associated with markers of bone resorption in a population-based sample of males and females and appears likely to be a risk factor for osteoporosis despite the lack of a demonstrable association between bone mass and a single measure of urinary sodium excretion. Further studies are needed to define the effect of salt intake on bone mass and fractures more clearly. These studies will need to be either longitudinal or interventional in design with repeated measures of urinary sodium so that habitual sodium intake can be accurately assessed and regression dilution bias can be minimised.

Adult↗
PubMed2003

Osteopontin facilitates bone resorption, decreasing bone mineral crystallinity and content during calcium deficiency.

Osteopontin null-mice were previously shown to have bones containing more mineral and larger mineral crystals. These bones were independently seen to be resistant to ovariectomy-induced remodeling. To separate the physicochemical effects of osteopontin, which is an in vitro inhibitor of mineral crystal formation and growth, from effects of osteopontin on in vivo bone remodeling, this study examined mature (5-month-old) osteopontin-null (Opn-/-) and wildtype (WT) mice given a calcium-deficient diet. Biochemical parameters were measured during 4 weeks of Ca deficiency, followed by 1 week of refeeding adequate Ca. Ca deficiency caused a transiently greater rise in bone resorption in WT than Opn-/- mice (P = 0.01), whereas only the Opn-/- mice tended to increase Ca absorption (P = 0.08), yet both groups showed elevated levels of parathyroid hormone (PTH) (P < 0.001). The rise in markers of bone formation due to Ca deficiency was similar in both groups during Ca deficiency. Fourier transform infrared microspectroscopy assessed mineral properties at 20 microm spatial resolution in different anatomic regions of the bone. The Ca-deficient Opn-/- animals had slightly increased mineral content as compared to the WT, and there was a significant increase in the mineral content of older (endosteal) bone, implying that osteoclast recruitment was impaired. Crystallinity in the Ca-deficient Opn-/- bones was increased relative to the Ca-deficient WT at all sites except adjacent to the periosteum (younger mineral). These data suggest that osteopontin has both a physicochemical effect (inhibiting crystal growth and crystal proliferation) and a role in osteoclast recruitment, and in its absence, extraskeletal organs maintain calcium homeostasis.

Amino Acids↗
PubMed2003

Comparison of change in bone resorption and bone mineral density with once-weekly alendronate and daily risedronate: a randomised, placebo-controlled study.

OBJECTIVE: To compare the effects of alendronate (ALN) 70 mg once weekly (OW) and risedronate (RIS) 5 mg daily between-meal dosing on biochemical markers of bone turnover and bone mineral density (BMD) in postmenopausal women with osteoporosis. RESEARCH DESIGN AND METHODS: This was a 3-month, randomised, double-blind, placebo-controlled study with a double-blind extension to 12 months. The study enrolled 549 postmenopausal women (ALN 219, RIS 222 and placebo (PBO) 108) who were > or =60 years of age at outpatient centres. MAIN OUTCOME MEASURES: The primary endpoint was reduction in urine N-telopeptides of type 1 collagen (NTx) corrected for creatinine level at 3 months. Secondary parameters included change in BMD at the spine and hip at 6 and 12 months, NTx at 1, 6 and 12 months, and serum bone-specific alkaline phosphatase (BSAP) at 1, 3, 6 and 12 months. Adverse experiences (AEs) were recorded throughout the study for an assessment of treatment safety profiles and tolerability. RESULTS: Over 3 months, ALN produced a significantly greater mean reduction in urine NTx than did RIS (-52% vs -32%, p < 0.001), which was maintained at 12 months. ALN produced a significantly greater mean BMD increase than did RIS at 6 months, and it was maintained at 12 months at the lumbar spine (4.8% vs 2.8%, p < 0.001) and total hip (2.7% vs 0.9%, p < 0.001), as well as at the trochanter and femoral neck. Significant reductions in BSAP with ALN compared to RIS were maintained over the 12 months of treatment. Study size did not allow for meaningful assessment of differences in fracture rates. Tolerability was generally similar between ALN, RIS and PBO, and the incidence of upper GI AEs causing discontinuation and oesophageal AEs was similar in the ALN and RIS groups. CONCLUSION: In this study, ALN 70 mg OW produced a 50% greater reduction in bone resorption as measured by urine NTx and significantly greater increases in lumbar spine and hip BMD than did RIS 5 mg daily. The treatments had similar safety profiles and were generally well-tolerated. Additional studies are needed comparing OW ALN with OW RIS, which became available after the commencement of the present study.

Aged↗
PubMedDate not supplied

Tartrate-resistant acid phosphatase 5B is a specific and sensitive marker of bone resorption.

Bone resorbing osteoclasts contain high amounts of tartrate-resistant acid phosphatase (TRACP) 5b and secrete it into the blood circulation. Circulating TRACP 5b activity is derived exclusively from osteoclasts. We have developed a TRACP 5b-specific-immunoassay using a monoclonal antibody O1A that was developed using TRACP 5b purified from human osteoclasts as antigen. Serum TRACP 5b activity has a low diurnal variability, and it does not accumulate in the circulation in renal or hepatic failure. It is elevated in 80% of patients with osteoporosis, while decreased 40-50% after antiresorptive therapy with estrogen and the bisphosphonate alendronate. Preliminary results show that serum TRACP 5b activity is normal in breast cancer patients without bone metastases, and elevated in approximately 80% of breast cancer patients with bone metastases. These results suggest that serum TRACP 5b activity may be a useful marker for the early detection of the spreading of breast cancer cells to bone.

Acid Phosphatase↗
PubMed1995

Mycoplasma-mediated bone resorption in bone organ cultures.

Mycoplasmas have been identified as one of many aetiological factors associated with experimental or human joint disease. Mycoplasma hyorhinis and M. arthritidis, but not M. pulmonis were found to cause significant release of calcium from murine long bone explants. The resorption process is inhibited by calcitonin, acetazolamide and by indomethacin. Mycoplasma-derived bone resorbing activity (M-BRA) is not an endotoxin as its effect is equally potent in cultures of bones obtained from endotoxin-responsive and -unresponsive mice. M-BRA is a high molecular weight compound resistant to proteases and heat but sensitive to hyaluronidase, lipase, detergents and in part to alkali and acid conditions. The active component is associated with the particulate fraction of the mycoplasma and its yield is enhanced by sonication. The damage to the subchondral bone in arthritis associated with a mycoplasma infection may be caused by a potent bone resorption inducing agent of mycoplasma origin.

Animals↗
PubMed1998

Dissociation between bone resorption and bone formation in osteopenic transgenic mice.

Bone mass is maintained constant in vertebrates through bone remodeling (BR). BR is characterized by osteoclastic resorption of preexisting bone followed by de novo bone formation by osteoblasts. This sequence of events and the fact that bone mass remains constant in physiological situation lead to the assumption that resorption and formation are regulated by each other during BR. Recent evidence shows that cells of the osteoblastic lineage are involved in osteoclast differentiation. However, the existence of a functional link between the two activities, formation and resorption, has never been shown in vivo. To define the role of bone formation in the control of bone resorption, we generated an inducible osteoblast ablation mouse model. These mice developed a reversible osteopenia. Functional analyses showed that in the absence of bone formation, bone resorption continued to occur normally, leading to an osteoporosis of controllable severity, whose appearance could be prevented by an antiresorptive agent. This study establishes that bone formation and/or bone mass do not control the extent of bone resorption in vivo.

Animals↗