Short-term PTH administration increases dentine apposition and microhardness in mice

Guimarães, Gustavo Narvaes; Cardoso, Guinéa Brasil Camargo; Naves, Lucas Zago; Correr-Sobrinho, Lourenço; Line, Sérgio Roberto Peres; Marques, Marcelo Rocha

doi:10.1016/j.archoralbio.2012.03.007

Cited by 7 publications

(2 citation statements)

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“…Acetaminophen †† was used for pain control. After the surgery, every 2 days, 40 μg/kg hPTH (1‐34) ‡‡ 15 was subcutaneously administered in 16 rats (group 2: treated group) for 14 days (T14; n = 8) and 21 days (T21; n = 8), whereas another 16 (group 1: control group) rats received a PTH vehicle (0.01% acetic acid §§ ) for 14 days (C14, control; n = 8) and 21 days (C21; n = 8). The animals were sacrificed at days 14 or 21, and their right hemimandibles were retrieved for histologic evaluation.…”

Section: Methodsmentioning

confidence: 99%

Intermittent Parathyroid Hormone Administration Improves Periodontal Healing in Rats

Vasconcelos

Marques²,

Benatti

et al. 2014

Journal of Periodontology

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Section: Methodsmentioning

confidence: 99%

Intermittent Parathyroid Hormone Administration Improves Periodontal Healing in Rats

Vasconcelos

Marques²,

Benatti

et al. 2014

Journal of Periodontology

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“…24 Although dentin metabolism turnover is considerably slower than that of bone tissue, systemic changes that interfere with bone mineral density also interfere with dentin formation. 25 Since ZOL has a high affinity for calcium and phosphate and also interferes with bone metabolism, 26 it is likely that bisphosphonates directly interfere with odontoblasts, leading to this inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-17 plays a role in dental pulp inflammation mediated by zoledronic acid: a mechanism unrelated to the Th17 immune response?

CARLOS,

LEMOS,

BORGES

et al. 2023

J. Appl. Oral Sci.

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Objective To evaluate the influence of RORγT inhibition by digoxin on inflammatory changes related to interleukin-17 (IL-17) in the pulp of rats treated with zoledronate (ZOL). Methodology Forty male Wistar rats were divided into a negative control group (NCG) treated with saline solution, a positive control group (PCG) treated with ZOL (0.20 mg/kg), and three groups treated with ZOL and co-treated with digoxin 1, 2, or 4 mg/kg (DG1, 2, and 4). After four intravenous administrations of ZOL or saline solution in a 70-day protocol, the right molars were evaluated by histomorphometry (number of blood vessels, blood vessels/µm 2 , cells/µm 2 , total blood vessel area, and average blood vessel area) and immunohistochemistry (IL-17, TNF-α, IL-6, and TGF-β). The Kruskal-Wallis/Dunn test was used for statistical analysis. Results PCG showed an increase in total blood vessel area (p=0.008) and average blood vessel area (p=0.014), and digoxin treatment reversed these changes. DG4 showed a reduction in blood vessels/µm 2 (p<0.001). In PCG odontoblasts, there was an increase in IL-17 (p=0.002) and TNF-α (p=0.002) immunostaining, and in DG4, these changes were reversed. Odontoblasts in the digoxin-treated groups also showed an increase in IL-6 immunostaining (p<0.001) and a reduction in TGF-β immunostaining (p=0.002), and all ZOL-treated groups showed an increase in IL-17 (p=0.011) and TNF-α (p=0.017) in non-odontoblasts cells. Conclusion ZOL induces TNF-α- and IL-17-dependent vasodilation and ectasia, and the classical Th17 response activation pathway does not seem to participate in this process.

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Parathyroid Hormone (1-34) Modulates Odontoblast Proliferation and Apoptosis via PKA and PKC-Dependent Pathways

et al. 2014

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Parathyroid hormone (PTH) plays a key role in the development and homeostasis of mineralized tissues such as bone and dentine. We have reported that PTH (1-34) administration can increase dentine formation in mice and that this hormone modulates in vitro mineralization of odontoblast-like cells. The purpose of the present study was to investigate whether PTH (1-34) participates in the proliferative and apoptotic signaling of odontoblast-like cells (MDPC23). MDPC23 cells were exposed to 50 ng/ml hPTH (1-34) or vehicle for 1 (P1), 24 (P24), or 48 (P48) hours, and the cell proliferation, apoptosis, and cell number were evaluated. To examine whether changes in the proliferative and apoptotic signaling in response to PTH involve protein kinases A (PKA) and/or C (PKC), MDPC23 cells were exposed to PTH with or without PKC or PKA signaling pathway inhibitors. Overall, the results showed that the PKA pathway acts in response to PTH exposure maintaining levels of cell proliferation, while the PKC pathway is mainly involved for longer exposure to PTH (24 or 48 h), leading to the reduction of cell proliferation and increase of apoptosis. The exposure to PTH reduced the cell number in relation to the control group in a time-dependent manner. In conclusion, PTH modulates odontoblast-like cell proliferative and apoptotic response in a time-dependent manner. Both PKC and PKA pathways participate in PTH-induced modulation in an antagonist mode.

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Short-term PTH administration increases dentine apposition and microhardness in mice

Abstract: These findings indicate that intermittent administration of hPTH (1-34) increases apposition and mineralization of the dentine during young mice incisor formation.

Cited by 7 publications

References 35 publications

Intermittent Parathyroid Hormone Administration Improves Periodontal Healing in Rats

Intermittent Parathyroid Hormone Administration Improves Periodontal Healing in Rats

Interleukin-17 plays a role in dental pulp inflammation mediated by zoledronic acid: a mechanism unrelated to the Th17 immune response?

Parathyroid Hormone (1-34) Modulates Odontoblast Proliferation and Apoptosis via PKA and PKC-Dependent Pathways

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