# FIBRONECTIN AND CARTILAGE DESTRUCTION IN OSTEOARTHRITIS

> **NIH NIH R01** · CORNELL UNIVERSITY · 1987 · $149,394

## Abstract

Our objective is to document changes associated with the early stage of
osteoarthritis in dogs and to identify factors which modify the disease.
Our aim is to examine the role of fibronectin in articular cartilage
destruction at an early stage of the osteoarthritic process, before changes
in joints can be detected by radiographic methods.  We can study this
aspect of the disease because of the advantages of the canine model,
particularly the spontaneity of the disease, its predictability and
expression in several joints of disease-prone dogs (hip, shoulder and knee
joints), its slow onset, and our capacity to sample cartilage within and
surrounding lesions as well as tissue from unaffected joints.

The proposed studies would examine the mechanism for the recently observed
increased content and synthesis of fibronectin in the abnormal cartilage of
osteoarthritic joints.  We want to localize the sites of accumulation of
fibronectin using immunohistochemical methods at the electronmicroscopic
level.  We want to substantiate that fibronectin production is a useful and
early marker of osteoarthritis and that its presence is consistent with the
idea that chondrocytes from osteoarthritic cartilage have a changed
phenotype.  We wish to isolate chondrocytes from normal and osteoarthritic
cartilage and determine in what ways they differ.  We would compare the
level of mRNA for fibronectin using available cDNA probes.  We would also
compare the cell size and shape, DNA content, position in the growth cycle,
and the presence of fibronectin or its receptors on the cell surface using
both established and novel methods of flow cytometry.  Another, but
related, aim is to ascertain how to manipulate the culture conditions of
explants of "normal" cartilage in vitro in order to induce increased rates
of fibronectin production.

These proposed experiments taken together are designed to test the
hypothesis that increased fibronectin production is a primary event in the
pathogenesis and that chondrocytes from osteoarthritic cartilage are
"dedifferentiated."

## Key facts

- **NIH application ID:** 3157330
- **Project number:** 5R01AR035664-02
- **Recipient organization:** CORNELL UNIVERSITY
- **SAM.gov UEI:** G56PUALJ3KT5
- **Principal Investigator:** GEORGE LUST
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $149,394
- **Award type:** 5
- **Project period:** 1986-09-01 → 1989-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157330

## Citation

> US National Institutes of Health, RePORTER application 3157330, FIBRONECTIN AND CARTILAGE DESTRUCTION IN OSTEOARTHRITIS (5R01AR035664-02). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3157330. Licensed CC0.

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