Pain Behavior in a Comorbid Preclinical Model of Alcohol Use Disorder/Post-Traumatic Osteoarthritis Restricted; Files Only

Owusu, William (Spring 2026)

Permanent URL: https://etd.library.emory.edu/concern/etds/np193b769?locale=en
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Abstract

Osteoarthritis (OA) is a prevalent whole-joint disease that causes cartilage degeneration, inflammation, and chronic pain. Those with OA may turn to alcohol use to self-medicate pain, which increases their risk of alcohol use disorder (AUD) and potentially influences OA. The mechanisms linking these conditions remain unclear. Preclinical models combining OA with voluntary alcohol consumption are limited. To address this gap, we aim to develop a comorbid model in male Lewis rats by inducing post-traumatic OA through medial meniscal transection (MMT) and allowing continuous single-bottle access to ethanol or water. One MMT group received 10% ethanol, while another MMT group received water to examine OA alone. Sham-operated rats served as controls. Pain behaviors, joint structure, and synovial cytokines were assessed over a six-week period. Rats with OA that consumed alcohol exhibited increased hyperalgesia and potential allodynia compared with both the MMT + water and sham groups, while joint morphology remained unchanged. Synovial fluid from alcohol-consuming rats contained elevated IL-2 and IL-4, suggesting an inflammatory contribution to heightened pain. These findings indicate that alcohol use can exacerbate OA-related pain without causing additional structural damage. This model provides a platform to explore therapeutic strategies targeting the nervous system and related pathways in comorbid OA and AUD.

Table of Contents

Introduction ……………………………………………………………………………………..1 

Methods …………………………………………………………………………………………5 

Results …………………………………………………………………………………………..8 

Discussion ……………………………………………………………………………………..14   

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