Effects of Estrogen Deficiency and/or Caffeine Intake on Alveolar Bone Loss, Density and Healing: A Study in Rats.
ABSTRACT Background: To evaluate the effects of caffeine and/or estrogen deficiency on ligature-induced bone loss (BL), trabecular bone area (TBA) and post-extraction bone healing (BH). Methods: Rats were assigned into one of the groups: Control: non-ingestion of caffeine/sham-surgery (n=15); Caffeine: ingestion of caffeine/sham-surgery (n=15); Ovariectomized (OVX): non-ingestion of caffeine/ovariectomy (n=15); Caffeine/OVX: ingestion of caffeine/ovariectomy. The rats were under caffeine administration during 65 days and/or estrogen deficiency for 51 days. On the 21(st) day after ovariectomy, one first mandibular molar received a ligature while the contralateral tooth was left unligated. The first maxillary molars were extracted at 8 days before sacrifice. BL, TBA, the positive cells for tartrate-resistant acid phosphatase (TRAP), receptor activator of NF-(К)B ligand (RANKL) and osteoprotegerin (OPG) were analyzed in the furcation area of mandibular molars. Histometric BH and gene expression of bone morphogenetic protein (BMP)-2, BMP-7, osteopontin and bone sialoprotein were evaluated in alveolar sockets. Results: The caffeine group presented the greatest BL and the OVX group the highest number of TRAP+ cells around ligated teeth (p<0.05). The control group presented higher TBA and BH than the other groups (p<0.05). All test groups presented higher RANKL/OPG+ cells than the control group around ligated/unligated teeth. The OVX and caffeine/OVX groups presented greater number of TRAP+ cells around unligated teeth than the control group (p<0.05). There were no differences among groups for gene expression (p>0.05). Conclusions: Caffeine increased BL in the presence of ligature. Caffeine and/or estrogen deficiency decreased TBA in absence of ligature and reduced BH after tooth extraction.
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ABSTRACT: The purpose of this 2-year longitudinal clinical study was to investigate alveolar (oral) bone height and density changes in osteoporotic/osteopenic women compared with women with normal lumbar spine bone mineral density (BMD). Thirty-eight postmenopausal women completed this study; 21 women had normal BMD of the lumbar spine, while 17 women had osteoporosis or osteopenia of the lumbar spine at baseline. All subjects had a history of periodontitis and participated in 3- to 4-month periodontal maintenance programs. No subjects were current smokers. All patients were within 5 years of menopause at the start of the study. Four vertical bitewing radiographs of posterior sextants were taken at baseline and 2-year visits. Radiographs were examined using computer-assisted densitometric image analysis (CADIA) for changes in bone density at the crestal and subcrestal regions of interproximal bone. Changes in alveolar bone height were also measured. Radiographic data were analyzed by the t-test for two independent samples. Osteoporotic/osteopenic women exhibited a higher frequency of alveolar bone height loss (p<0.05) and crestal (p<0.025) and subcrestal (p<0.03) density loss relative to women with normal BMD. Estrogen deficiency was associated with increased frequency of alveolar bone crestal density loss in the osteoporotic/osteopenic women and in the overall study population (p<0.05). These data suggest that osteoporosis/osteopenia and estrogen deficiency are risk factors for alveolar bone density loss in postmenopausal women with a history of periodontitis.Osteoporosis International 02/1999; 10(1):34-40. · 4.04 Impact Factor
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ABSTRACT: The identity of the paracrine mediator(s) of the antiresorptive action of estrogen on bone cells is controversial. Osteoprotegerin (OPG) was recently identified as a soluble member of the tumor necrosis factor (TNF) receptor (TNF-R) superfamily that is secreted by osteoblast lineage cells and acts by binding to and neutralizing its cognate ligand, OPG-L, a required factor for osteoclastogenesis. OPG prevents bone loss when administered to ovariectomized rats, induces osteoporosis when ablated in knock-out mice, and induces osteopetrosis when overexpressed in transgenic mice. In conditionally immortalized, human osteoblastic hFOB/ER-3 and hFOB/ER-9 cell lines containing physiological concentrations of approximately 800 and approximately 8,000 functional estrogen receptors (ER)/nucleus, respectively, we found that 17beta-estradiol dose- and time-dependently increased OPG mRNA and protein levels to maximal levels of 370% and 320%, respectively (P < 0.001); co-treatment with the "pure" antiestrogen ICI 182,780 abrogated these effects completely. 17beta-Estradiol also dose-dependently increased OPG mRNA and protein levels in normal human osteoblasts with approximately 400 ER/nucleus by 60% and 73%, respectively. Thus, estrogen enhancement of OPG secretion by osteoblastic cells may play a major role in the antiresorptive action of estrogen on bone.Endocrinology 09/1999; 140(9):4367-70. · 4.72 Impact Factor
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ABSTRACT: The general public widely consumes caffeine (1,3,7-trimethylxanthine), which is contained in various foods, beverages and over-the-counter medications. We have shown previously that caffeine intake could affect bone metabolism in vivo. Because prostaglandin E2 (PGE2) is shown to be elevated in the periodontally diseased site, the possible interaction between caffeine and PGE2 was investigated in the present study using UMR106-01 rat osteoblast-like cells in vitro. Although neither 0.1 mM caffeine nor 0.1 microg/ml of PGE2 alone showed any inhibitory effects on cell proliferation, the combination of caffeine and PGE2 showed significant inhibition. However, in order to have inhibitory effects, both caffeine and PGE2 had to be present at least 72 or 96 hours in the medium. Addition of the endogenous PGE2 synthesis inhibitor, indomethacin, showed no effects on cell proliferation. Neither cAMP-inducing agent IBMX (0.01 mM and 0.1 mM) nor forskolin (0.001 mM) inhibited cell proliferation, but combined with PGE2 these agents strongly inhibited proliferation as was observed with the combination of caffeine and PGE2, suggesting possibly that the increase of intracellular cAMP concentration plays an important role in the inhibitory effects of cell proliferation. The present data for the first time demonstrate the possible implication of routine caffeine intake in the acceleration of pathological conditions of periodontitis. Thus, we propose that chronic caffeine intake is one of the possible risk factors in the advancement of pathology in the periodontitis patient. Further research in this area is warranted.Journal of Periodontology 04/1999; 70(3):283-8. · 2.40 Impact Factor