Objective: The menisci play an important role in the blomechanics of the kn
ee, and loss of meniscal function has been associated with progressive dege
nerative changes of the joint in rheumatoid arthritis as well as in osteoar
thritis. However, little is known about the underlying mechanisms that link
meniscal injury or degeneration to arthritis. Meniscal fibrochondrocytes r
espond to environmental mediators such as growth factors and cytokines, but
the influence of mechanical stress on their metabolic activity is not well
understood. Nitric oxide (NO) is believed to play a role in mechanical sig
nal transduction, and there is also significant evidence of its role in car
tilage and meniscus degeneration. The goal of this study was to determine i
f meniscal fibrochondrocytes respond to mechanical stress by increasing NO
production in vitro.
Design: Explants of lateral and medial porcine menisci were dynamically com
pressed in a precisely controlled manner, and NO production, nitric oxide s
ynthase antigen expression and cell viability were measured. The relative r
esponses of the meniscal surface and deep layers to dynamic compression wer
e also investigated separately.
Results: Meniscal NO production was significantly (P <0.01) increased by dy
namic compression in both the medial and lateral menisci. Dynamically compr
essed menisci contained inducible nitric oxide synthase antigen, while unco
mpressed menisci did not. Significant (P <0.05) zonal differences were obse
rved in basal and compression-induced NO production.
Discussion: Our findings provide direct evidence that dynamic mechanical st
ress influences the biological activity of meniscal cells. These results su
ggest that NO production in vivo may be in part regulated by mechanical str
ess acting upon the menisci. Since NO affects matrix metabolism in various
intraarticular tissues, alterations in the distribution and magnitude of st
ress in the menisci may have important metabolic as well as biomechanical c
onsequences on joint physiology and function. (C) 2001 OsteoArthritis Resea
rch Society International.