Authors:

Sophia Foerster

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under Inflammation Osteoarthritis (OA) is a degenerative joint disease driven by chronic inflammation that causes cartilage degeneration. The postmenopausal female population experiences primary OA at a 1. 3 higher incidence rate 158 UNIVERSITY OF OREGON • 2026 UNDERGRADUATE RESEARCH SYMPOSIUM TABLE OF CONTENTS than age-matched males, implicating sex as a risk factor for OA. The objective of this project is to understand the role of sex-specific hormones such as estrogen in cartilage matrix susceptibility to inflammation-driven degeneration. We hypothesize that estrogen will attenuate glycosaminoglycan (GAG) loss under inflammatory conditions, while leaving the ratio of collagen type II to type I in the matrix unchanged. Human chondrocytes were harvested from an osteochondral allograft and expanded to passage 3 before use. To engineer healthy cartilage spheroids, 250,000 cells were centrifuged and cultured in hormone- free chondrogenic media under physoxic conditions for 14 days. To study the chondroprotective effects of estrogen, cartilage spheroids underwent a 24hr incubation period with IL-1β and TNFα (1ng/mL each), with or without supplementation of estrogen (272 pg/mL E2). Brightfield imaging, biochemical assays and histological analysis were used to assess cartilage matrix composition. To evaluate matrix degradation, we collected media following inflammatory exposure. There was significantly less GAG loss in E2-supplemented inflammatory conditions compared to normal inflammatory conditions, indicating E2 had chondroprotective effects in an acute inflammatory environment.

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University of Oregon / 2026

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Co-authors:

Sophia Foerster