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PubMed2000

Immobilization on the day 14th does not disrupts the basic diurnal rhythm of bone resorption.

Weight bearing and physical activity are important mechanical stimuli to bone growth and metabolism, and microgravity, such a space flight and/or bed rest, induces bone resorption and bone loss. An increased excretion of urinary Ca, an increased bone resorption and a decreased bone mineral density (BMD) have been observed in bed rest experiment of healthy subjects. Bone resorption markers show the specific circadian rhythms in human. Cross-linked carboxyl-terminal telopeptide of type I collagen (ICTP) and the urinary excretion of deoxypyridinoline (Dpy) are the highest in the early morning and the lowest late at night. Bed rest immobilization might influence these rhythms, due to no mechanical loading with loss of daily life activity. Bone resorption markers in healthy subjects had been compared between before and during bed rest to determine disruption of diurnal rhythms of bone resorption.

Acid Phosphatase↗

PubMed1989

Dichloromethylenebisphosphonate (Cl2MBP) inhibits bone resorption through injury to osteoclasts that resorb Cl2MBP-coated bone.

Dichloromethylenebisphosphonate (Cl2MBP, formerly Cl2MDP) inhibits bone resorption in vivo and in vitro. The mechanism by which it inhibits osteoclastic bone resorption has not been established. To investigate this, osteoclasts were isolated from rat long bone and incubated with Cl2MBP (10(-9)-10(-5) M) on bone slices. Bone resorption was assessed as plan area resorbed after 6 and 24 h by scanning electron microscopy. Although Cl2MBP inhibited bone resorption in the first 6 h of culture, inhibition was more marked in the incubation period between 6 and 24 h. This pattern of accelerating inhibition is unlike the pattern we have observed using other resorption-inhibitors, and suggested resorption-mediated osteoclast injury. In keeping with this, we found reduced numbers of osteoclasts, and morphological features of cell injury and degeneration of osteoclasts, after incubation with Cl2MBP on bone slices. Bone seemed to be an essential component in Cl2MBP-mediated injury, since osteoclast numbers and morphology on plastic coverslips were unaffected by the bisphosphonate. Moreover, bone slices preincubated with Cl2MBP showed similar effects on resorption and morphology to cultures in in which osteoclasts on bone were continuously immersed in Cl2MBP. Neither non-resorptive cells (macrophages, UMR 106 cells), nor osteoclasts prevented from resorption by calcitonin, showed evidence of cytotoxicity after incubation on bone slices with Cl2MBP. These results suggest that even relatively high concentrations of Cl2MBP in the fluid phase do not affect osteoclasts, nor does contact with Cl2MBP-coated bone surfaces, but that injury to osteoclasts, and a consequent reduction in bone resorption, occurs when osteoclasts excavate bone surfaces upon which Cl2MBP is adsorbed.

Animals↗

PubMed2005

TNF-alpha and pathologic bone resorption.

Chronic inflammatory bone diseases, such as rheumatoid arthritis, periodontal disease and aseptic periprosthetic osteolysis, are characterized by bone loss around affected joints and teeth caused by increased osteoclastic bone resorption. This resorption is mediated largely by the increased local production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFa). These cytokines may induce resorption indirectly by affecting the production of the essential osteoclast differentiation factor, receptor activator of NF-kB ligand, and/or its soluble decoy receptor, osteoprotegerin, by osteoblast/stromal cells or directly by enhancing proliferation and/or activity of cells in the osteoclast lineage. The importance of TNFa in the pathogenesis of various forms of bone loss is supported by both experimental and clinical evidence. However, TNFa is not absolutely required for osteoclastogenesis, erosive arthritis, or osteolysis, as all these events could occur in the absence of TNFa and whether TNFa promotes osteoclast formation independently of RANK signaling is still a topic of debate. Here we review our current understanding of the mechanisms whereby TNFa increases osteoclastogenesis in vitro and in vivo.

Animals↗

PubMed1993

Experimental model in vivo for quantitative assessment of bone resorption inhibition.

Quantitative assessment of bone resorption inhibition in vivo is not easily accomplished; methods relying on a count of osteoclasts are questionable, and histomorphometric evaluation of the bone mass presents several technical problems as well. The authors developed a simple method to measure the inhibition of bone resorption by study of the proximal tibial metaphysis of growing rats: the height of the perichondrial bone ring was taken as an index of the balance between osteoblastic and osteoclastic activity because any agent that inhibits osteoclasts (without interference with osteoblasts) produces an increase in the height of this anatomical structure. Since the ring is well demarcated by surrounding tissues, its height can be measured with accuracy and used for quantitative assessment of bone resorption inhibition. This model was tested with salmon calcitonin, and it provides evidence in vivo that this hormone inhibits osteoclastic bone resorption.

Animals↗

PubMed1990

Bone resorption by isolated osteoclasts in living versus devitalized bone: differences in mode and extent and the effects of human recombinant tissue inhibitor of metalloproteinases.

The incubation of isolated osteoclasts with devitalized bone has become a widely used method for the recent study of bone resorption. Although the studies employing this method have definitively demonstrated that isolated osteoclasts have an avid capacity to resorb devitalized bone, the resorption in this model appears to be different from that of living bone as observed in vivo and in organ culture studies. To evaluate how the resorption of living bone is different from that of devitalized bone, we have extended this bone resorption model using isolated osteoclasts by including both devitalized and living bone substrates. Living bone substrates were freshly prepared from calvaria of 8- to 12-month-old mice. Periosteum, cellular components, and osteoid were completely scraped off to leave a rigid, smooth, mineral-exposed surface for the isolated osteoclasts to act upon. Some of the bone pieces were devitalized by repeated freezing and thawing. Living and devitalized bones were cultured with isolated rabbit osteoclasts for 60 h with or without recombinant human tissue inhibitor of metalloproteinases (100 micrograms/ml). The extent of bone resorption was assessed by measuring both the area and the depth of resorption pits. Comparing the areas of the resorption pits showed significantly more resorption in living bone than in devitalized bone (27% of that of living bone). Recombinant human TIMP reduced the resorption of living bone by 73% but did not, however, inhibit the resorption of devitalized bone. Similarly, resorption pits formed on the living bones were significantly deeper (on the average, 12.4 microns) than those formed on the devitalized bones (on the average, 4.3 microns). The average depth of the resorption pits on living bone was significantly reduced by the presence of the inhibitor, whereas there was no difference between the control and inhibitor-treated devitalized bones. These results suggest that the mechanisms underlying the resorption of living bone and that of devitalized bone are not the same and that the resorption of living bone is aided by osteocytes.

Animals↗

PubMed1991

Inhibiting and stimulating effects of TGF-beta 1 on osteoclastic bone resorption in fetal mouse bone organ cultures.

The effects of TGF-beta 1 on osteoclastic resorption of fetal mouse calvaria and long bones at various stages of development was studied in organ culture. In resorbing calvariae and long bones with an established marrow cavity TGF-beta 1 (4-10 ng/ml) had a stimulating effect on 45Ca release that was partially inhibited by indomethacin. In primitive long bones, however, which were explanted before osteoclast invasion and excavation of a marrow cavity had started, TGF-beta 1 (1-4 ng/ml) inhibited 45Ca release by an indomethacin-insensitive mechanism. Histomorphometry of long bones after staining for tartrate-resistant acid phosphatase (TRAP) revealed that TGF-beta 1 treatment inhibited the migration of TRAP-positive cells from periosteum to developing marrow cavity and inhibited cell fusion. However, the formation of (mononuclear) TRAP-positive cells in the periosteum-perichondrium was strongly enhanced. These data suggest that TGF-beta 1 modulates various steps in the cascade of osteoclast development, recruitment, and activation in different ways, involving both prostaglandin-mediated and prostaglandin-independent pathways. Therefore the net effect of exogenous TGF-beta 1 on osteoclastic resorption in bone organ cultures depends on the relative prevalence of osteoclast progenitors, precursors, and mature osteoclasts in the tissue under study.

Animals↗

PubMed1982

Possible link between changes in plasma 24,25-dihydroxyvitamin D and healing of bone resorption in dialysis osteodystrophy.

Histomorphometric studies of bone biopsies were performed on 12 hemodialyzed patients before and after six months of treatment with 25-(OH) and 1 alpha-(OH) vitamin D3. Patients could be classified into three groups according to bone resorption: Group I with normal bone resorption; Group II with elevated initial bone resorption unresponsive to vitamin D treatment; group III with elevated initial bone resorption sensitive to vitamin D treatment. None of the patients had histological signs of osteomalacia. In Group I, plasma concentrations of 24,25-(OH)2D and the ratio of 24,25-(OH)2D to 25-(OH) D remained in the normal range throughout the study; in Group II these parameters were subnormal initially and did not increase above normal except in one case; in Group III, plasma concentrations of 24,25-(OH)2D were high before or at the beginning of vitamin D administration and normal at the time of the second biopsy and wide variations were observed in the ratio of 24,25-(OH)2D to 25-(OH)D. No difference was found between these last two groups with regard to the cumulative dose of vitamin D derivatives administered or the changes in plasma PTH, CT, calcium and phosphate. These observations suggest a specific regulation of plasma 24,25-(OH)2D concentrations in hemodialyzed patients and a possible link (independent of circulating PTH, CT, or phosphate) between this regulation and healing of bone resorption. However, no correlation was found between plasma 24,25-(OH)2D and either one of the simultaneously measured biochemical or histological parameters.

24,25-Dihydroxyvitamin D 3↗

PubMed2004

Bone resorption activity of osteolytic metastatic lung and breast cancers.

Production of bone resorption mediators and bone resorption activity were compared among osteolytic metastatic cancers, normal bone tissues, and soft tissue metastatic cancers to search for the possible factors leading to cancer-induced bone resorption. Twenty-five patients with untreated osteolytic metastatic breast or non-small cell lung cancers consisted of the study group. Normal bone tissues obtained from the same patient were used as internal controls; and tumor tissues from patients with soft tissue metastasis were used as external controls. Serum and urinary bone turnover markers were measured. Tissues harvested during surgery were subjected to tissue culture. The levels of prostaglandin E2 (PGE2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) in the supernatant after 72 h of culture were measured. Bone resorption activity was measured by calcium release from cultured calvarias, and bone volume as well as osteoclast number in bone sections. Patients with osteolytic metastatic cancers showed significantly decreased serum osteocalcin, increased serum alkaline phosphatase, and urinary deoxypyridinoline levels. Osteolytic metastatic cancers produced significantly more PGE2 than both controls. Conditioned medium from osteolytic metastatic tumors showed significantly enhanced bone resorption activity, and indomethacin significantly reduced this activity. Levels of PGE2, and bone resorption activity increased in osteolytic tumor tissues than soft tissue metastatic tissues in the same patient indicated that the same tumor cells might respond differently to different microenvironments. Our observation showed that PGE2 was produced by osteolytic metastatic cancers and stimulated bone resorption in mice calvarias. PGE2 inhibitor may be applicable in reducing bone resorption by osteolytic metastatic cancers.

Biomarkers↗

PubMed2006

Matrix metalloproteinase-9 regulates graft bone resorption.

OBJECTIVE: To explore the relationship between bone resorption and matrix metalloproteinase-9 (MMP-9) expression in autogenous and allogenic bone grafts. MATERIALS AND METHODS: A total of 18 critical-size (10 x 15 mm) defects were created in rabbit mandibles bilaterally. Three groups of six defects each were grafted with autogenous endochondral (EC) bone, autogenous intramembranous (IM) bone, and allogenic IM bone. Three months later, the defects were retrieved for quantitative analysis on the basis of histology, immunohistochemistry, and in situ hybridization. RESULTS: A close relationship existed between MMP-9 expression and graft bone resorption. The parallel between MMP-9 expression and graft bone resorption suggested that bone resorption was accomplished in part by increased MMP-9 production evident in preosteoclasts and osteoclasts. CONCLUSIONS: MMP-9 plays an important role in graft bone resorption. Autogenous EC bone grafts express higher levels of MMP-9 leading to more resorption than autogenous or allogenic IM bone grafts.

Acid Phosphatase↗

PubMed1999

Effects of barrier membranes on bone resorption and implant stability in onlay bone grafts. An experimental study.

The objective of the present report was to study the effects of barrier membranes on bone resorption and implant stability in a rabbit onlay bone graft model, using resonance frequency analysis, coordinate measurements on plaster models, removal torque measurements and histology. Disc-shaped bone grafts were harvested from the calvarium and placed with titanium implants in the proximal tibial metaphyses of 9 rabbits. On one side (test) the bone graft/implant was covered by an e-PTFE barrier, while the contralateral side was not covered by a membrane and served as control. Three animals were sacrificed after 8 weeks for histology. In 6 animals the membranes were removed after 8 weeks and the animals were followed for an additional period of 16 weeks. Implant stability and bone height around the implants was assessed for the test and control sides at Day 0 and 8, 16 and 24 weeks postoperatively. Removal torque tests were performed after 24 weeks. The results showed an increase in volume of the bone graft on the test side as long as the barrier membrane was in place. However, after removal of the membrane at 8 weeks the resorption rate was higher on the test side compared to the control side, resulting in a similar bone height after 24 weeks. There were no statistically significant differences in implant stability between the test and control sides at any time point, as measured with resonance frequency analysis. Additionally, no statistically significant differences were found between the test and control sides after 24 weeks, using removal torque measurements, coordinate measurements and histomorphometric evaluation. Thus, in this experimental model, the use of non-resorbable barrier membranes did not improve the stability of implants simultaneously placed with onlay bone grafts. Moreover, extensive resorption of the grafted bone was seen after barrier removal, which resulted in similar bone graft volume for the test and control sides at the end of the observation period.

Animals↗

PubMed1995

Nitric oxide: a cytokine-induced regulator of bone resorption.

Nitric oxide (NO) has been reported to inhibit osteoclastic bone resorption, yet potent stimulators of bone resorption, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), are known to stimulate NO production. This paradox prompted us to reinvestigate the relationship between NO production and bone resorption in mouse calvarial organ cultures. Control cultures and those stimulated with calciotropic hormones and individual cytokines produced little NO, and under these conditions the NO synthase inhibitor, L-NG-monomethyl arginine (LMMA), had no significant effect on bone resorption. Cytokine combinations were much more potent stimulators of NO production than individual cytokines. Dramatic stimulation of NO production and inhibition of bone resorption resulted when gamma-interferon (IFN) was combined with IL-1 or TNF and these effects were reversed by LMMA. IFN had no effect on bone resorption and little effect on NO production when used alone or in combination with calciotropic hormones, however, suggesting that IFN selectively inhibits cytokine-induced bone resorption by generating large amounts of NO. IL-1 and TNF acted together to stimulate NO production but to a lesser degree than when combined with IFN. LMMA inhibited bone resorption induced by IL-1 and TNF, suggesting that lower concentrations of NO stimulate bone resorption. Experiments with the pharmacological NO donor S-nitroso-acetyl-penicillamine (SNAP) supported this view in showing generalized suppression of bone resorption at high SNAP concentrations, but potentiation of IL-1 induced bone resorption at lower SNAP concentrations. We conclude that cytokines are potent inducers of NO in bone and that cytokine-induced NO production has biphasic effects on bone resorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Role of gastrointestinal hormones in postprandial reduction of bone resorption.

UNLABELLED: Collagen type I fragments, reflecting bone resorption, and release of gut hormones were investigated after a meal. Investigations led to a dose escalation study with glucagon like peptide-2 (GLP-2) in postmenopausal women. We found a dose-dependent effect of GLP-2 on the reduction of bone resorption. INTRODUCTION: The C-terminal telopeptide region of type I collagen as measured in serum (s-CTX) can be used to assess bone resorption. This marker of bone resorption has a significant circadian variation that is influenced by food intake. However, the mediator of this variation has not been identified. MATERIALS AND METHODS: We studied the release of the gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2; a representative of the intestinal proglucagon-derived peptides) after ingestion of glucose, fat, protein, and fructose, as well as their effects after parenteral administration in relation to bone turnover processes in healthy volunteers. Furthermore, we studied the effect on bone turnover of a single subcutaneous injection of GLP-2 in four different dosages (100, 200, 400, or 800 microg GLP-2) or placebo in 60 postmenopausal women (mean age, 61 +/- 5 years). RESULTS: All macronutrients significantly (p < 0.05) reduced bone resorption as assessed by s-CTX (39-52% from baseline), and only the glucagon-like peptides were secreted in parallel. Parenteral administration of GIP and GLP-1 did not result in a reduction of the s-CTX level, whereas GLP-2 caused a statistically significant and dose-dependent reduction in the s-CTX level from baseline compared with placebo (p < 0.05). Urine DPD/creatinine, a marker of bone resorption, was significantly reduced by 25% from baseline in the 800-microg GLP-2 group (p < 0.01). An area under the curve (AUC(0-8h)) analysis for s-CTX after GLP-2 injection confirmed the dose-dependent decrease (ANOVA, p = 0.05). The s-osteocalcin level was unaffected by the GLP-2 treatment. CONCLUSION: These studies exclude both GIP and GLP-1 as key mediators for the immediate reduction in bone resorption seen after a meal. The dose-dependent reduction of bone resorption markers found after subcutaneous injection of GLP-2 warrants further investigation into the mechanism and importance of GLP-2 for the bone turnover processes.

Adult↗

PubMed1990

A morphometric study of the effects of pressure on bone resorption in the middle ear of rats.

Bone destruction is one of the clinical features of chronic otitis media with cholesteatoma. Bone resorption may be due to the epithelial debris accumulated in the cholesteatoma epidermal sac that acts as foreign body material inducing a destructive granulation tissue and creates pressure on the bony middle ear. This compressive force then induces bone resorption. The present study was designed to replicate certain conditions similar to those in cholesteatoma leading to bone resorption. Four types of materials were implanted into the middle ear cavity of rats: (1) laminaria, an expandable seaweed material, (2) preswollen laminaria, (3) keratin powder suspension, and (4) surgical grade silicone, which when bent exerts pressure on the bulla wall. The placement of laminaria segments in the middle ear cavity of rats was followed by swelling of the implanted materials within 7 days. The bulla bone response was by neo-osteogenesis as well as active bone resorption. The new bone was observed on the external and/or internal surface of the tympanic bone. The cochlear bone also showed extensive bone resorption in the animals. Osteogenesis was rarely observed on the capsule of the cochlea. We also observed no bone resorption at sites without presence of inflammatory connective tissue between laminaria and bone. The typical multinucleated osteoclasts were often seen at the resorption area but the majority of bone resorption sites were characterized by the presence of mononuclear cells and other inflammatory cells. Preswollen laminaria, keratin powder, and silicone strips induced minimal bone resorption. No resorption was observed in the bony cochleas of these experimental groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

[Bone resorption markers].

For many years, only two bone resorption markers, urinary hydroxyproline and serum tartrate-resistant acid phosphatase, have been clinically employed. However, these two markers have lacked the sensitivity and specificity to bone resorption. In the late 1980s, pyridinoline (Pyr) and deoxypyridinoline (Dpyr) which are mature crosslinks inter-molecular of collagen, were proposed as bone resorption markers. After newly synthesized collagen is incorporated into bone matrix, Pyr, Dpyr are synthesized by the post-translational modification of collagen molecules. Pyridinoline crosslinks occur in type I collagen at two sites, the carboxy- and amino- terminal telopeptides to helix. At the time of bone resorption, Pyr, Dpyr and amino-, and carboxy- terminal crosslinked telopeptides of type I collagen are excreted into the circulation through collagen degradation. Because the crosslinks and crosslinked telopeptides do not exist at the time of synthesis of collagen, the assay for the crosslinks and telopeptides are specific to bone resorption. Recently, novel assays for measuring crosslinked telopeptides have been developed. Amino-terminal pyridinolines crosslinked telopeptides (NTx) and carboxy-terminal telopeptide of type I collagen (CrossLaps) is assayed in urine, and carboxy-terminal pyridinolines crosslinked telopeptides (ICTP) is assayed in serum. Because those markers are specific to bone resorption, they are expected to reflect the minimum amount of bone resorption in postmenopausal women and osteoporosis. We reviewed the background of Pyr and cross-linked telopeptides markers and compared the performance of these bone resorption markers in the bone turnover in postmenopause and established osteoporosis.

Adult↗

PubMed1993

Peripheral monocyte culture supernatants of menopausal women can induce bone resorption: involvement of cytokines.

Increased bone resorption is a mechanism contributing to bone loss in the postmenopausal period. Cytokines are involved in osteoclastic differentiation and, therefore, may play a role in the regulation of bone resorption. Several previous works showed the implication of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF alpha) in the modulation of bone remodeling. This study determines the concomitant production of the three cytokines and tests the bone-resorbing activity of peripheral monocyte supernatants. Four groups of women were studied: premenopausal women (n = 13; mean age, 47 +/- 0.9 yr), untreated postmenopausal women (n = 21; mean age, 52 +/- 0.6 yr), postmenopausal women treated with estrogens (n = 14; mean age, 54.2 +/- 1.1 yr), or postmenopausal women treated with ethanehydroxydiphosphonate (n = 12; mean age, 53.2 +/- 2 yr). Assignment to clinical groups was verified by plasma FSH and estradiol determinations. Lumbar spine bone mineral density was significantly higher in the premenopausal women group than in the three postmenopausal groups. Peripheral blood monocytes were cultured for 48 h with 20% autologous plasma, and after stimulation with lipopolysaccharides. IL-1, IL-6, and TNF alpha levels were measured by RIA in the monocyte surpernatants. The three cytokines were highly correlated to each other, IL-1 with IL-6 (r = 0.76; P < 0.001), IL-1 with TNF alpha (r = 0.89; P < 0.001), and IL-6 with TNF alpha (r = 0.89; P < 0.001). The mean levels of the three cytokines could not be compared because of the variations in the values. However, a trend toward lower levels in the three cytokines was noted in estrogen-treated women compared to the untreated postmenopausals. The bone-resorbing activity of monocyte supernatants, assessed by fetal long bone-resorbing assay, increased in untreated postmenopausal compared to that in premenopausal women (1.22 +/- 0.08 vs. 0.87 +/- 0.11; P < 0.05). In estrogen-treated patients, this activity decreased to premenopausal levels (0.89 +/- 0.04 vs. 0.87 +/- 0.11; P = NS). The resorbing activity was correlated to IL-1 (r = 0.28; P = 0.03), IL-6 (r = 0.52; P < 0.01), and TNF alpha (r = 0.48; P < 0.01). The addition of cytokine inhibitors and IL-1 receptor antagonist and TNF alpha antibodies to the supernatant bone culture medium induced a significant decrease in the calcium release. Those data show the involvement of several cytokines in the bone resorption process after estrogen deficiency.

Bone Resorption↗

PubMed2004

Decreased bone resorption with soy isoflavone supplementation in postmenopausal women.

OBJECTIVE: To investigate the effect of soy isoflavone supplementation on bone mineral density (BMD) and markers of bone turnover in postmenopausal women. METHODS: In this randomized, placebo-controlled clinical trial, we used a crossover design to test the effect of soy isoflavone (110 mg/day) (1.3:1.0:0.22 ratio of genistein/daidzein/ glycitein) on bone formation, bone resorption, bone mineral content (BMC), and BMD for 6 months. RESULTS: Postmenopausal women (n = 19), mean age 70.6 +/- 6.3 years and mean time since menopause 19.1 +/- 5.5 years, were given isoflavone supplements for 6 months. There was a 37% decrease in urinary concentrations of type 1 collagen alpha1-chain helical peptide (HP), a marker of bone resorption, during the isoflavone supplementation compared with baseline (p < 0.05) and a significant difference in mean (SE) HP excretion levels when isoflavone was compared with placebo (43.4 +/- 5.2 vs. 56.3 +/- 7.2 microg/mmol creatinine [cr], p < 0.05). With isoflavone supplementation, mean spine BMD at L2 and L3 was significantly greater when treatment was compared with control, with a difference between means of 0.03 +/- 0.04 g and 0.03 +/- 0.04 g (p < 0.05), respectively. There were nonsignificant increases from baseline for total spine BMC (3.5%), total spine BMD (1%), total hip BMC (3.6%), and total hip BMD (1.3%) with the isoflavone treatment. CONCLUSIONS: Soy isoflavone, in isolated form, was effective in this study to significantly decrease bone resorption in postmenopausal women. Further investigation needs to be done to evaluate the long-term effects of soy isoflavone on bone mass and fracture risk.

Aged↗

PubMed1986

Histologic study of the inhibition of bone resorption in organ cultures by myo-inositol-2-monophosphate.

This study examines chemically and histologically the relative abilities of inositol monophosphate (IP1), inorganic phosphate (Pi), ethane-1-hydroxy-1, 1-diphosphonate (EHDP) and dichloromethylene disphosphonate (Cl2MDP) to inhibit parathyroid hormone (PTH)--induced resorption of fetal rat long bones in organ culture. Pregnant rats injected with 45Ca on the 18th day of gestation were killed the next day and their fetuses removed. Half of each pair of dissected long bones was incubated in a chemically defined control medium while the contralateral half was incubated in medium containing PTH or PTH plus the compound to be tested. 45Ca released into the medium was indicative of the amount of bone resorption. Bones were then processed histologically and examined microscopically. All compounds inhibited resorption to some extent with IP1 and Pi being less effective than EHDP or C12MDP at comparable phosphate concentrations. However, the disphosphonates damaged osteoclasts whereas IP1 and Pi did not. This suggests that IP1 may inhibit resorption by a different mechanism perhaps related only to prevention of crystal dissolution.

Animals↗

PubMed1992

Kinetics of immune cell and bone resorptive responses to endodontic infections.

Infection of the dental pulp stimulates a host immune response in the periapical region (the periapical "lesion") with the concomitant resorption of bone. The cell composition of human or rat periapical lesions is mixed, consisting of T, B, and "null" lymphocytes, plasma cells, macrophages, polymorphonuclear leukocytes, and mast cells. Cells are thus present which mediate a broad spectrum of immunological phenomena. In order to determine which of these mechanisms contribute to periapical bone resorption, a rat model system has been used in which periapical lesions are induced by pulp exposure and infection from the oral environment. In this model, a rapid period of lesion expansion and bone destruction occurs between days 1 and 15 after exposure (active phase), with a chronic phase characterized by lesion stabilization commencing thereafter. Phenotypic analysis of the cellular infiltrate has shown that T helper cells predominate during the active phase, whereas increased numbers of T suppressor cells are associated with chronicity. Extracts of periapical lesions contain bone-resorbing activity, as determined by the release of 45Ca from prelabeled a rat long bones in organ culture. Higher levels of bone-resorbing activity are present during the active than in the chronic phase. Characterization of bone-resorbing activity indicates the presence of resorptive mediators which are heat labile and protease sensitive and which are distinct from lipopolysaccharide. Preliminary biochemical fractionation indicates that resorptive mediators fractionate in the 15,000- to 60,000-dalton molecular mass range, presumably cytokines such as interleukin 1 and tumor necrosis factor. These studies demonstrate the utility of the rat model for studying mechanisms of periapical lesion pathogenesis and implicate T helper cell-mediated activities, in particular those leading to macrophage activation and cytokine production, in periapical lesion expansion.

Alveolar Bone Loss↗