# PARATHYROID HORMONE-OSTEOBLAST MODULATED BONE RESORPTION

> **NIH NIH R01** · SAINT LOUIS UNIVERSITY · 1987 · $87,886

## Abstract

Osteopenia is a major cause of morbidity and mortality in an aging
population, yet its precise pathophysiology remains unclear.  Since bone
resorption increases as individuals age, the mechanism of control of the
osteoclast, the primary resorbing cell of the skeleton, is of tremendous
importance.  Despite these observations, the mechanisms by which bone
seeking agents, such as parathyroid hormone (PTH), activate osteoclasts are
unknown.  Such agents can theoretically stimulate resorption by 1) a direct
interaction with osteoclasts, 2) enhancement of differentiation of
osteoclast precursors or 3) interaction with an intermediary (modulator)
cell which can in turn stimulate osteoclastic activity and/or promote
osteoclast differentiation.  Available evidence suggests that parathyroid
hormone enhances resorption via modulator cells.  We propose that
osteoblasts have the capacity to modulate parathyroid hormone induced bone
absorption because 1) they produce agents which stimulate osteoclasts, 2)
osteoblasts bind parathyroid hormone and are responsive to the hormone and
3) bone resorption by isolated macrophages (surrogate osteoclasts) is not
stimulated by the PTH unless osteoblasts are also present.  This proposal
is directed toward examining the mechanisms by which parathyroid hormone
stimulates osteoblast modulated bone resorption.  The initial studies will
address the isolation of the factor produced by osteoblasts in response to
parthyroid hormone which is capable of increasing bone resorption.  Other
studies will address the mechanisms by which this effect takes place both
at a biochemical and cellular level.  The studies will also address the
modulation of this response in osteoblasts by other hormones as well as the
modulation of the response of the resorbing cell.  These experiments will
focus on the properties of the various cell types which are known to
enhance their capacity to degrade bone matrix.  These properties include a)
enhance differentiation of immature macrophages, b) enhancement of the
capacity of resorptive macrophages to bind the bone, c) enhanced
multinucleation of macrophages and d) increased macrophage number.

## Key facts

- **NIH application ID:** 3157140
- **Project number:** 5R01AR035287-03
- **Recipient organization:** SAINT LOUIS UNIVERSITY
- **SAM.gov UEI:** JNBLLTBTLLD8
- **Principal Investigator:** HORACE M PERRY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $87,886
- **Award type:** 5
- **Project period:** 1985-04-01 → 1988-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157140

## Citation

> US National Institutes of Health, RePORTER application 3157140, PARATHYROID HORMONE-OSTEOBLAST MODULATED BONE RESORPTION (5R01AR035287-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3157140. Licensed CC0.

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