SAM-e has been shown to have anti-inflammatory and analgesic properties in animal models when given both orally and parenterally (Stramentinoli, 1987). The mechanism by which this effect is achieved is not clear, but it does not seem to be mediated via the prostaglandin system, as inferred from the finding that oral administration of a single dose or repeated doses of up to 1200 mg/kg for 30 days in rats did not affect the integrity of the gastric mucosa, which suggests that SAMe does not interfere with the cytoprotective function of prostaglandins in gastrointestinal tissues. Furthermore, SAM-e does not influence platelet aggregation (Stramentinoli, 1987) and has not been demonstrated to affect the eicosanoid system (Di Padova, 1987).

A stimulatory effect of SAMe on chondrocytes has been suggested from studies using human chondrocyte cultures (Harmand, Vilamitjana, Maloche, et al., 1987), and SAM-e has also been shown to increase the incorporation of sulfate into proteoglycans (Harnand, Vilamitjana, Maoche et al., 1987). In addition, SAM-e does enter the synovial fluid following oral doses of 400 mg (Giulidori, Cortellaro, Moreo et al., 1984), which suggests a reasonable mechanism of action by which SAM-e may affect osteoarthritis. .