Parathyroid Hormone Protects against Periodontitis-associated Bone Loss (original) (raw)

Effects of parathyroid hormone and cytokines on prostaglandin e synthesis and bone resorption by human periodontal ligament fibroblasts

Archives of Oral Biology, 1990

Cultured human periodontal ligament fibroblasts showed synergistic elevations in the synthesis of prostaglartdin E and production of CAMP by the administration of parathyroid hormone and cytokines (interleukin-la, -lb, or tumour necrosis factor-a). Unstimulated conditioned media derived from these fibroblasts contained bone-resorbing activity. In addition, conditioned media generated by cytokine-or parathyroid hormone-treated fibroblasts showed further increases in bone-resorbing activity. The effects were additive when the hormone was combined with either one of the cytokines in stimulating bone resorption. These findings suggest that the effect of parathyroid hormones and cytokines together on bone resorption can be mediated in part by human periodontal ligament fibroblasts via PGE production and subsequent PGE action on the osteoclasts.

Intermittent PTH administration improves alveolar bone formation in type 1 diabetic rats with periodontitis

Journal of Translational Medicine, 2018

Background: Periodontitis is an infectious disease that manifests as alveolar bone loss surrounding the roots of teeth. Diabetes aggravates periodontitis-induced alveolar bone loss via suppression of bone formation. Intermittent parathyroid hormone (PTH) administration displays an anabolic effect on bone. In this study, we investigated the effect of intermittent PTH administration on alveolar bone loss in type 1 diabetic rats with periodontitis. Methods: Rats were divided into control (C), periodontitis (P), periodontitis treated with PTH (P + PTH), diabetes with periodontitis (DP), and diabetes with periodontitis treated with PTH (DP + PTH) groups. To induce type 1 diabetes, rats were injected with streptozotocin and periodontitis was induced bilaterally by applying ligatures to the mandibular first molars for 30 days. During the experimental period, the P + PTH and DP + PTH groups were subcutaneously injected with PTH (40 μg/kg) three times per week, whereas the C, P, and DP groups were injected with citrate buffer. To observe the mineralization of the alveolar bone, the DP and DP + PTH groups were injected with calcein on days 10 and 27, and with alizarin red on day 20. Thirty days after ligation, histological findings and fluorescence labeling were analyzed in the furcations of the mandibular first molars. Sclerostin-positive osteocytes were assessed by immunohistochemical analyses. Results: The DP groups had smaller areas of alveolar bone than the other groups, and the DP + PTH group had a larger alveolar bone area than the DP group. The DP group had less osteoid formation than the C group, whereas the DP + PTH had greater osteoid formation than the DP group. Fluorescence labeling results revealed that the DP + PTH group had more mineral deposition on the alveolar bone than the DP group. The DP + PTH group exhibited lower percentage of sclerostin-positive osteocytes in alveolar bone than the DP group. Conclusions: Intermittent PTH administration diminishes alveolar bone loss and sclerostin expression in osteocytes, but increases osteoid formation and mineralization, suggesting that intermittent PTH administration attenuates diabetes-aggravated alveolar bone loss by the induction of bone formation. PTH-induced bone formation may be related to the regulation of osteocytic sclerostin expression in type 1 diabetic rats with periodontitis.

Effect of intermittent PTH administration in the periodontitis-associated bone loss in ovariectomized rats

Archives of Oral Biology, 2005

Objective: Parathyroid hormone intermittent administration has been considered to treat bone mass decrease in osteoporotic individuals. The present study evaluates whether PTH can affect alveolar bone loss in ovariectomized rats, since estrogen deficiency has been proposed as a risk factor for periodontal disease. Design and methods: Thirty female rats were set in groups: ovariectomized (Ovx) and Sham operated. Ovx were divided in two groups: Ovx-PTH (1-34) treated and Ovx, which received vehicle. After 1 week, cotton ligature was placed around one lower first molar of all animals to induce periodontal disease. Ovx treated received PTH doses of 40 mg/kg, three times a week for 30 days. After that, the animals were sacrificed, the mandibles extracted, X-rayed and samples prepared for histological evaluation. Histomorphometry was performed using image analyzer software. Scanning electron microscopy (SEM) of the tibias was also performed in all animals to evaluate possible changes in bone structure caused by the estrogen deficiency. Optical densities of the radiographs were measured by aluminum step-wedge equivalent thickness. Results: Histomorphomery indicated the anabolic PTH effect in ovariectomized rats with significant inhibition of periodontitis manifestation (p < 0.05) thus neutralizing the periodontitis inductor effects. The photo densitometry showed a lower mandibular optical density in the ovariectomized group that did not receive PTH (p < 0.05).

Dexamethasone enhances the effects of parathyroid hormone on human periodontal ligament cells in vitro

Calcified Tissue International, 1995

Periodontal ligament cells (PDL) are thought to play a major role in promoting periodontal regeneration. Recent studies, focused on characterizing PDL ceils, have been directed at establishing their osteoblast-like properties and determining biological mediators and/or factors that induce osteoblastic cell populations in the PDL. The glucocorticoid, dexamethasone (Dex), has been shown to selectively stimulate osteoprogenitor cell proliferation and to induce osteoblastic cell differentiation in many ceil systems. In the present study the ability of Dex to modulate parathyroid hormone (PTH)-stimulated cAMP synthesis in cultured human PDL cells was examined. PDL cells, obtained from premolar teeth extracted for orthodontic reasons, were cultured with Dex (0-1000 nM) for 7 days prior to PTH (1-34) stimulation. The exposure of PDL cells to Dex resulted in a dose-dependent increase in cAMP production in response to PTH stimulation. This response was seen in cells obtained from three different patients. The first significant Dex effect was seen on day 7 when compared to day 1 for 100 nM Dex. PTH 0-34) stimulation caused a dose-dependent increase in cAMP synthesis after Dex (1000 nM) treatment for 7 days. Conversely, stimulation of the cells with PTH (7-34) (0-1000 nM) did not increase cAMP production in PDL cells after Dex treatment. Forskolin-(1 ~LM) and isoproterenol-(1 ~LM) stimulated cAMP synthesis was not augmented by Dex treatment. Dex treatment did not alter calcitonin-(1 txM) stimulated cAMP production in PDL cells. Glucocorticoid enhancement of PTH-stimulated cAMP synthesis in these cells supports the presence of an osteoblast-like population in the PDL, in vitro.

Comparative effects of parathyroid hormone on osteoblasts and cementoblasts

Journal of Clinical Periodontology, 1987

Lindskog S, Blomlof L and Hamman^trom L: Comparative effects of parathyroid hormone on osteobiasts and cementoblasts. J Clin Periodontol 1987: 14: 386-389. Abstract. Although bone, dentin and dental cementum are mesenchymal mineralized tissues composed mainly of collagen and hydroxy apatite, they ditTer markedly in their suceptibility to resorption. Bone undergoes physiological resorption to which the dental tissues appear to be resistant. Recently, the cells covering bone surfaces have been attributed a regulatory role in osteoclastic bone resorption by exposing the bone surface following stimulation with hormones and inflammatory mediators, thereby allowing osteoclasts to colonize the bone surface. In the present study, it was shown that reparative cementum-forming cells covering an experimental cavity in the root surface of replanted monkey incisors were unaffected by parathyroid hormone, a potent mediator of bone resorption. In parallel experiments, endocranial osteobiasts exposed bone surface by widening their inercellular spaces. It was concluded that the layer of cells covering the root ^^ *°'. ^' surface forms a protective barrier against resorption which serves to preserve the integrity of the dental root.

Dose-dependent effect of parathyroid hormone on fracture healing and bone formation in mice

Journal of Surgical Research, 2017

Authors' contributions: A.M. and B.W. participated in study design, operation, data acquisition in vivo, data analysis in vivo, data analysis in vitro, data interpretation, and drafting and critical revision of manuscript. D.H. contributed for data acquisition in vivo, data analysis in vivo, data acquisition in vitro, data analysis in vitro, data analysis in vitro, and data interpretation. N.G. participated in operation, data acquisition in vivo, data analysis in vivo, drafting and critical revision of manuscript. R.S. contributed for data analysis in vivo, data interpretation, drafting and critical revision of manuscript. T.P. contributed for study design, data interpretation, and drafting and critical revision of manuscript. M.R. contributed for study design, data interpretation, drafting, and critical revision of manuscript. P.G. contributed for study design, operation, data analysis in vivo, data analysis in vitro, data interpretation, and drafting and critical revision of manuscript.

Serum parathyroid hormone and active vitamin D in chronic periodontitis

Journal of clinical periodontology, 2015

To study the association between periodontitis and serum parathyroid hormone (PTH) and the response of PTH to periodontal therapy in type 1 diabetic patients (T1DM). We also investigated the PTH-1,25(OH)2 D axis in the T1DM group. Periodontal health status was recorded in 54 periodontitis patients and 30 periodontally healthy controls (case-control data). Data were also collected from patients with type 1 diabetes mellitus at the baseline (n = 76) and after periodontal therapy (intervention data) (n = 53). Periodontitis was not associated with serum PTH in the case-control data or at the baseline of the intervention data. A post-therapy increase in serum PTH was found in 61% of the T1DM patients; in patients with moderate or severe periodontitis (n = 26) the average increase was 0.6 pmol/l (p = 0.016) and in patients with no or mild periodontitis (n = 27) 0.2 pmol/l (p = 0.250). In 47% of the T1DM patients, an increase in PTH was associated with an increase in serum 1,25(OH)2 D. An ...

Vitamin D, Calcium, Alkaline Phosphatase, and Parathyroid Hormone in Patients with and without Chronic Periodontitis

Journal of Nepalese Society of Periodontology and Oral Implantology

Introduction: Periodontal diseases comprise a group of inflammatory diseases caused by bacteria that colonise the tooth surface and infect surrounding soft tissues, ultimately leading to tooth loss. Vitamin D, calcium, alkaline phosphatase, and parathyroid hormone have role in bone metabolism both in health or in disease. Objective: To compare serum Vitamin D, calcium, alkaline phosphatase, and parathyroid hormone levels in patients with generalised chronic periodontitis and healthy periodontium. Methods: A cross-sectional analytical study was done in 80 patients visiting Department of Dental Surgery from July to December 2019. Clinical parameters measured were plaque index, gingival index, clinical attachment level, and pocket depth in the healthy periodontium and generalised chronic periodontitis. Blood investigation for serum Vitamin D, calcium, alkaline phosphatase (ALP), and parathyroid hormone (PTH) level were done. Data was analysed in SPSS v.16. Results: Out of total 80 pat...

Effects of cyclic vs. daily treatment with human parathyroid hormone (1–34) on murine bone structure and cellular activity

Bone, 2007

Previously, we demonstrated that the human parathyroid hormone (1-34) fragment (hPTH(1-34)) increased bone strength in proportion to its effects on BMD and cortical bone structure in the murine femur by comparing cyclic vs. daily administration of hPTH(1-34). Both cyclic and daily regimens increased vertebral BMD similarly at 7 weeks. Here, we have examined the effects of daily and cyclic PTH regimens on bone structure and cellular activity by static and dynamic histomorphometry. Twenty-week-old, intact female C57BL/J6 mice were treated with the following regimens (n = 7 for each group): daily injection with vehicle for 7 weeks [control]; daily injection with hPTH(1-34) (40 μg/kg/day) for 7 weeks [daily PTH]; and daily injection with hPTH(1-34) (40 μg/kg/ day) and vehicle alternating weekly for 7 weeks [cyclic PTH]. At days 9 and 10, and 2 and 3 prior to euthanasia, calcein (10 mg/kg) was injected subcutaneously. At the end of study, the lumbar vertebrae 1-3 and the left femora were excised, cleaned, and processed for histomorphometry. In the lumbar vertebrae, daily and cyclic PTH regimens significantly increased cancellous bone volume (BV/TV), trabecular number, trabecular osteoclast and osteoblast perimeters, trabecular mineral apposition rate (MAR) and bone formation rate (BFR), and periosteal MAR and BFR compared to control, with no significant difference between the two PTH-treated groups. Increased trabecular tunneling was observed in both PTHtreated groups. Both regimens tended to increase vertebral cortical bone formation parameters with the effects at the periosteum site being more marked than those at the endosteum site, resulting in a significant increase in cortical width. In the femur, the effects of cyclic PTH on BV/TV, trabecular width and number, trabecular and endocortical osteoblast and osteoclast perimeters, cortical width, and trabecular and periosteal BFR were less marked than those of daily PTH. A cyclic PTH regimen was as effective as a daily regimen in improving cancellous and cortical bone microarchitecture and cellular activity in the murine vertebra.

The influence of parathyroid hormone-related protein (PTHrP) on tooth-germ development and osteoclastogenesis in alveolar bone of PTHrP-knock out and wild-type mice in vitro

Archives of Oral Biology, 2002

In a previous study, it was shown that tooth germs of neonatal homozygous parathyroid hormone-related protein (PTHrP)knockout mice are penetrated or compressed by the surrounding alveolar bone, suggesting an important role for PTHrP in the formation and activation of osteoclasts around growing tooth germs. In order to elucidate the role of PTHrP during the development of the tooth germ and related structures, mandibular explants containing cap stage tooth germs of embryonic day 14, homozygous mice were here cultured with or without surrounding alveolar bone. There was no difference in the number of tartrate-resistant acid phosphatase-positive multinucleated osteoclastic cells around the first molars of homozygous and wild-type mice. After 10 days of culture, osteoclastic cells were rarely present in explants from homozygous mice and penetration of alveolar bone into the dental papilla was observed. The decline in osteoclast number was partly restored by the addition of PTHrP to the culture. Tooth germs of both wild-type and homozygous mice cultured without alveolar bone developed well, with no apparent structural abnormality; dentine formation was evident after 10 days. These data suggest that PTHrP is not required for the development of the tooth germ proper but is indispensable in promoting the osteoclast formation required to accommodate that development.