Effect of Parathyroid Hormone on Random Migration of Human Polymorphonuclear Leukocytes

Doherty, C C; LaBelle, Patrice; Collins, John; Brautbar, Nachman; Massry, Shaul G.

doi:10.1159/000167585

Cited by 43 publications

(13 citation statements)

References 22 publications

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“…Analysis of our data, while speculative at this point, suggests that PTH administration neutralizes LPS-mediated inflammation. In this regard, analysis of the data collected over the last decade indicates that PTH may act as an immunomodulating hormone (Doherty et al, 1988). For example, random migration of polymorphonuclear leukocytes (PMNLs) is impaired in chronic renal failure (CRF) patients, and an inverse relationship exists between random migration of PMNLs and blood levels of PTH in these patients (Doherty et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, analysis of the data collected over the last decade indicates that PTH may act as an immunomodulating hormone (Doherty et al, 1988). For example, random migration of polymorphonuclear leukocytes (PMNLs) is impaired in chronic renal failure (CRF) patients, and an inverse relationship exists between random migration of PMNLs and blood levels of PTH in these patients (Doherty et al, 1988). Moreover, it is possible that PTH affects leukocyte functions directly, since both B-and T-cells contain receptors for the hormone (McCauley et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

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Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

et al. 2003

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Parathyroid hormone (PTH) functions as a major mediator of bone remodeling and as an essential regulator of calcium homeostasis. In addition to the well-established catabolic effects (activation of bone resorption) of PTH, it is now recognized that intermittent PTH administration has anabolic effects (promotion of bone formation). The aim of this study was to investigate whether intermittent administration of PTH in rodents would block the alveolar bone loss observed in rats when a ligature model of periodontitis is used. Morphometric analysis showed that intermittent PTH administration (40 microg/kg) was able to protect the tooth site from periodontitis-induced bone resorption. In addition, there was a significant reduction in the number of inflammatory cells at the marginal gingival area in sections obtained from animals receiving PTH compared with control animals. These findings demonstrated that intermittent PTH administration was able to protect against periodontitis-associated bone loss in a rodent model.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

et al. 2003

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“…Some investigators reported impaired phagocytosis with the defect residing in the PMNL [1,2], while others found that the serum of uremic patients contains an inhibitor of phagocytosis [3][4][5], In contrast, several stud ies could not confirm defective phagocytosis in CRF [6, affects random migration of these cells [12] as well as their degranulation [13]. It is theoretically possible that the high blood levels of PTH in CRF patients affect the phagocytic function of their PMNL.…”

Section: Introductionmentioning

confidence: 99%

Impaired Phagocytosis in Dialysis Patients: Studies on Mechanisms

et al. 1991

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Dialysis patients have increased susceptibility to infection and this is, in part, due to impaired phagocytic and bactericidal activities of polymorphonuclear leukocytes (PMNL). The mechanisms responsible for the reduced phagocytosis are not known. Dialysis patients have elevated blood levels of parathyroid hormone (PTH), and available data indicate that PMNL is a target cell for PTH. Chronic exposure to excess PTH may cause accumulation of calcium in PMNL which in turn could adversely affect cellular events leading to their dysfunction. We studied phagocytosis, resting levels of cytosolic calcium ([Ca²⁺]_i), ATP content and the rise in [Ca²⁺]_i in response to ligation of Fcγ RIII receptors with 3G8 monoclonal antibody in PMNL from 37 dialysis patients and 48 normal subjects. The PMNL from the dialysis patients displayed impaired phagocytosis, elevated resting levels of [Ca²⁺]_i, decreased ATP content and a smaller rise in [Ca²⁺]_i in response to various doses of 3G8 monoclonal antibody as compared to values obtained in PMNL of normal subjects. Our results suggest that derangements in cellular metabolism and possibly an abnormality in Fcγ RIII interaction with antibody and/or the consequences of such interaction are responsible, at least in part, for the impaired phagocytosis of PMNL of dialysis patients. Our data are consistent with the notion that excess PTH may play an important role in the processes leading to impaired phagocytosis.

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“…A link between PTH and immune function has been suggested since immune cells such as T and B lymphocytes and leukocytes express PTH receptors (21, 22) . In fact, neutrophils from patients with hyperparathyroidism exhibit defects in chemotaxis, migration, and phagocytosis (23-25) and these defects are rescued when parathyroidectomy is performed (26). Thus, the concept that PTH is a negative modifier of the host immune system has been established (27, 28).…”

Section: Discussionmentioning

confidence: 99%

Intermittent Administration of Parathyroid Hormone Ameliorates Periapical Lesions in Mice

Otawa¹,

Tanoue²,

Kakemoto³

et al. 2015

Journal of Endodontics

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Introduction Intermittent administration of parathyroid hormone (PTH) promotes oral osseous wound healing and protects against ligature-induced alveolar bone loss. However, its therapeutic value on periapical periodontitis is unknown. The goal of this study was to determine the effect of intermittent PTH administration on the progression of periapical periodontitis. Methods Seven lymphotoxin alpha deficient mice received pulp exposures of mandibular first and second molars. Exposed pulp in the right mandible was covered with plaque-contaminated fibrin, while exposed pulp in the left mandible was left open. After four weeks, the periapical tissues were examined to determine the effect of plaque-contaminated fibrin to induce periapical lesions. Fourteen mice received pulp exposure covered with plaque-contaminated fibrin. PTH (40μg/kg/day) was administered intermittently to half of the mice for three weeks beginning one week after pulp exposure. The remaining half received saline injections as vehicle control. At sacrifice, mandibles and tibiae were harvested and processed for histological examination. Evaluation of neutrophils and blood vessels was performed after staining with immunofluorescence and periradicular bone was histomorphometrically analyzed. Results The exposed pulp covered with plaque-contaminated fibrin resulted in significantly larger periapical lesions compared to control. Intermittent PTH administration reduced the size of periapical lesions significantly. Significantly less neutrophil infiltration around the root apex was found in PTH-treated animals compared to control. Conclusions PTH treatment suppressed periapical inflammation by reducing neutrophil infiltration and protected against tissue destruction by periapical periodontitis.

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Effect of Parathyroid Hormone on Random Migration of Human Polymorphonuclear Leukocytes

Cited by 43 publications

References 22 publications

Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

Impaired Phagocytosis in Dialysis Patients: Studies on Mechanisms

Intermittent Administration of Parathyroid Hormone Ameliorates Periapical Lesions in Mice

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