Bone Histomorphometry and Bone Quality in Primary Hyperparathyroidism

Dempster, David W.; Silverberg, Shonni J.; Shane, Elizabeth; Bilezikian, John P.

doi:10.1016/b978-0-12-397166-1.00029-1

Cited by 7 publications

(4 citation statements)

References 72 publications

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“…The increase in trabecular bone without change in cortical bone in the PTG‐RGS5 mice is noteworthy because this phenotype mirrors the bone changes often found in normocalcemic or mild PHPT in humans . The plasma level of PTH but not calcium correlated positively with trabecular bone changes, a finding consistent with effects of exogenous PTH administration on bone in other mouse models .…”

Section: Discussionsupporting

confidence: 75%

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Parathyroid-Targeted Overexpression of Regulator of G-Protein Signaling 5 (RGS5) Causes Hyperparathyroidism in Transgenic Mice

Balenga

Koh²,

Azimzadeh

et al. 2019

Journal of Bone and Mineral Research

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The relationship between impaired calcium sensing, dysregulated parathyroid hormone (PTH) secretion, and parathyroid cell proliferation in parathyroid neoplasia is not understood. We previously reported that a GTPase activating protein, regulator of G‐protein signaling 5 (RGS5) is overexpressed in a subset of parathyroid tumors associated with primary hyperparathyroidism (PHPT) and that RGS5 can inhibit signaling from the calcium‐sensing receptor (CASR). In vivo, we found that RGS5‐null mice have abnormally low PTH levels. To gain a better understanding of the potential role of RGS5 overexpression in parathyroid neoplasia and PHPT and to investigate whether inhibition of CASR signaling can lead to parathyroid neoplasia, we created and characterized a transgenic mouse strain overexpressing RGS5 specifically in the parathyroid gland. These mice develop hyperparathyroidism, bone changes reflective of elevated PTH, and parathyroid neoplasia. Further, expression of exogenous RGS5 in normal human parathyroid cells results in impaired signaling from CASR and negative feedback on PTH secretion. These results provide evidence that RGS5 can modulate signaling from CASR and support a role for RGS5 in the pathogenesis of PHPT through inhibition of CASR signaling. © 2019 American Society for Bone and Mineral Research.

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Section: Discussionsupporting

confidence: 75%

“…The bone in PHPT is characterized by high turnover, cortical bone loss, and preserved or increased trabecular bone . To investigate skeletal changes in PTG‐RGS5 mice with HPT, we assessed the microstructure of trabecular and cortical bone in femurs from 12‐month‐old transgenic and control mice using μCT (Fig.…”

Section: Resultsmentioning

confidence: 99%

Parathyroid-Targeted Overexpression of Regulator of G-Protein Signaling 5 (RGS5) Causes Hyperparathyroidism in Transgenic Mice

Balenga

Koh²,

Azimzadeh

et al. 2019

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

show abstract

“…2(b) and (c) are optical and histological images of the experimental region. It can be clearly seen the typical bone structure, with Haversian canals (the lowest concentration of Ca, P and Si, were the blood vessels run) and lamellar bone (Dempster, 2005). According to the normalized fluorescence maps, it can be noticed that Ca and P are uniformly distributed in the cortical bone.…”

Section: Resultsmentioning

confidence: 93%

“…The EXAFS spectrum contains information on the type and number of atoms in coordination with absorber atoms, their interatomic distances, and the degree of local molecular bonding disorder. As was widely described (Dempster, 2005), bone is a composite material with a mineral (some type of carbonate-HA nanocrystals) and an organic (collagen fibrils) part. Also bone is composed by a mixture of amorphous carbonate calcium phosphates with some ion substitution, which will growth with time and to be re-arranging as crystals.…”

Section: Resultsmentioning

confidence: 99%