Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

Barros, Silvana P.; Silva, M.A.D.; Somerman, Martha J.; Nociti, Francisco Humberto

doi:10.1177/154405910308201006

Cited by 89 publications

(88 citation statements)

References 32 publications

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“…Miller et al (1997) administered intermittent PTH to the mandibles of aged ovariectomized rats and found that PTH stimulated bone formation in the mandible [237]. Similarly, using a ligature-induced periodontitis model in rodents, another group found that PTH protects against periodontitis-associated bone loss [238]. At a clinical level, analysis of the data published thus far suggested that PTH, which is currently approved for use in the treatment of osteoporosis, might also prove useful for treating other bone-associated diseases such as periodontal disease [236].…”

Section: Parathyroid Hormonementioning

confidence: 95%

A review on endogenous regenerative technology in periodontal regenerative medicine

et al. 2010

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Section: Parathyroid Hormonementioning

confidence: 95%

A review on endogenous regenerative technology in periodontal regenerative medicine

et al. 2010

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“…The latter has been derived from studies demonstrating the ability of PDL cells to differentiate into a more mature osteoblastic phenotype after hormonal stimulation [33] and to mineralize the extracellular matrix emphasizing their pivotal role in periodontal regeneration [42,43]. Previously, a promising role for PTH in the attempt to prevent hard tissue loss in the course of inflammatory periodontal disease was suggested from experiments in rodents [44][45][46]. Thus, the intermittent PTH(1-34) effect on osteoprotegerin protein expression provides another piece in the mosaic to explain possible anabolic effects of the hormone on periodontal hard tissues aiming at tissue preservation or regeneration.…”

Section: Discussionmentioning

confidence: 96%

Intermittent PTH(1–34) signals through protein kinase A to regulate osteoprotegerin production in human periodontal ligament cells in vitro

et al. 2011

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Periodontal ligament (PDL) cells have been associated with the regulation of periodontal repair processes by the differential expression of osteoprotegerin and RANKL in response to intermittent parathyroid hormone (PTH) resulting in a modified activity of bone-resorbing osteoclasts. Here, we examined the intracellular signaling pathways that PDL cells use to mediate the PTH(1-34) effect on osteoprotegerin production and hypothesized that those would be dependent on the cellular maturation stage. Two stages of confluence served as a model for cellular maturation of 5th passage human PDL cells from six donors. Intermittent PTH(1-34) (10(-12) M) and PTH(1-31), the latter lacking the protein kinase C (PKC) activating domain, induced a significant decrease of osteoprotegerin production in confluent cultures, whereas the signal-specific fragments PTH(3-34) and PTH(7-34), which both are unable to activate protein kinase A (PKA), had no effect. The addition of the PKA inhibitor H8 antagonized the PTH(1-34) effect, whereas the PKC inhibitor RO-32-0432 did not. In pre-confluent, less mature cultures, intermittent PTH(1-34) resulted in a significant increase of osteoprotegerin. Similar results were obtained when PTH(1-31) substituted for PTH(1-34) as opposed to a lack of an effect of PTH(3-34) and PTH(7-34). Likewise, in confluent cultures, H8 inhibited the PTH(1-34) effect in pre-confluent cultures contrasted by RO-32-0432 which had no effect. These findings indicate that PTH(1-34) signaling targeting osteoprotegerin production in PDL cells involves a PKA-dependent pathway. The PTH(1-34) effect is dependent on cell status, whereas intracellular signal transduction is not. Clinical trials will have to prove whether those in vitro data are of physiological relevance for interference strategies.

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“…For instance, some studies have measured the destruction in the furcation area, others in proximal sites, some in buccal and lingual areas, others with only one measurement, or repeated measurements, etc. 14,[17][18][19][20][21][22][23][24] To the best of our knowledge, there are no studies evaluating ligatureinduced alveolar bone loss in proximal and buccal/ palatal surfaces in rats. Although ligature-induced alveolar bone loss measurement in proximal surfaces may be difficult to perform in morphometric analyses, the focus of the present study was to examine differences in the prevalence and extension of periodontal disease in proximal surfaces in humans, which could also occur in animals.…”

Section: Discussionmentioning

confidence: 99%

Correlation analysis of alveolar bone loss in buccal/palatal and proximal surfaces in rats

Azambuja¹,

Cavagni²,

Wagner³

et al. 2012

Braz. oral res.

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Abstract:The aim was to correlate alveolar bone loss in the buccal/palatal and the mesial/distal surfaces of upper molars in rats. Thirty-three, 60-day-old, male Wistar rats were divided in two groups, one treated with alcohol and the other not treated with alcohol. All rats received silk ligatures on the right upper second molars for 4 weeks. The rats were then euthanized and their maxillae were split and defleshed with sodium hypochlorite (9%). The cemento-enamel junction (CEJ) was stained with 1% methylene blue and the alveolar bone loss in the buccal/palatal surfaces was measured linearly in 5 points on standardized digital photographs. Measurement of the proximal sites was performed by sectioning the hemimaxillae, restaining the CEJ and measuring the alveolar bone loss linearly in 3 points. A calibrated and blinded examiner performed all the measurements. Intraclass Correlation Coefficient revealed values of 0.96 and 0.89 for buccal/lingual and proximal surfaces, respectively. The Pearson Correlation Coefficient (r) between measurements in buccal/ palatal and proximal surfaces was 0.35 and 0.05 for the group treated with alcohol, with and without ligatures, respectively. The best correlations between buccal/palatal and proximal surfaces were observed in animals not treated with alcohol, in sites both with and without ligatures (r = 0.59 and 0.65, respectively). A positive correlation was found between alveolar bone loss in buccal/palatal and proximal surfaces. The correlation is stronger in animals that were not treated with alcohol, in sites without ligatures. Areas with and without ligature-induced periodontal destruction allow detection of alveolar bone loss in buccal/palatal and proximal surfaces.

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Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

Cited by 89 publications

References 32 publications

A review on endogenous regenerative technology in periodontal regenerative medicine

A review on endogenous regenerative technology in periodontal regenerative medicine

Intermittent PTH(1–34) signals through protein kinase A to regulate osteoprotegerin production in human periodontal ligament cells in vitro

Correlation analysis of alveolar bone loss in buccal/palatal and proximal surfaces in rats

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