Cyclic tensile strain suppresses catabolic effects of interleukin-1beta in fibrochondrocytes from the temporomandibular joint.
OBJECTIVE
To discern the effects of continuous passive motion on inflamed temporomandibular joints (TMJ).


METHODS
The effects of continuous passive motion on TMJ were simulated by exposing primary cultures of rabbit TMJ fibrochondrocyte monolayers to cyclic tensile strain (CTS) in the presence of recombinant human interleukin-1beta (rHuIL-1beta) in vitro. The messenger RNA (mRNA) induction of rHuIL-1beta response elements was examined by semiquantitative reverse transcriptase-polymerase chain reaction. The synthesis of nitric oxide was examined by Griess reaction, and the synthesis of prostaglandin E2 (PGE2) was examined by radioimmunoassay. The synthesis of proteins was examined by Western blot analysis of the cell extracts, and synthesis of proteoglycans via incorporation of 35S-sodium sulfate in the culture medium.


RESULTS
Exposure of TMJ fibrochondrocytes to rHuIL-1beta resulted in the induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), which were paralleled by NO and PGE2 production. Additionally, IL-1beta induced significant levels of collagenase (matrix metalloproteinase 1 [MMP-1]) within 4 hours, and this was sustained over a period of 48 hours. Concomitant application of CTS abrogated the catabolic effects of IL-1beta on TMJ chondrocytes by inhibiting iNOS, COX-2, and MMP-1 mRNA production and NO, PGE2, and MMP-1 synthesis. CTS also counteracted cartilage degradation by augmenting expression of mRNA for tissue inhibitor of metalloproteinases 2 that is inhibited by rHuIL-1beta. In parallel, CTS also counteracted rHuIL-1beta-induced suppression of proteoglycan synthesis. Nevertheless, the presence of an inflammatory signal was a prerequisite for the observed CTS actions, because fibrochondrocytes, when exposed to CTS alone, did not exhibit any of the effects described above.


CONCLUSIONS
CTS acts as an effective antagonist of rHuIL-1beta by potentially diminishing its catabolic actions on TMJ fibrochondrocytes. Furthermore, CTS actions appear to involve disruption/regulation of signal transduction cascade of rHuIL-1beta upstream of mRNA transcription.
Agarwal
S
S
University of Pittsburgh, Pennsylvania, USA.
Long
P
P
Gassner
R
R
Piesco
N P
NP
Buckley
M J
MJ
D000818:Animals; D019902:Chondrocytes / Q000378:metabolism; D051546:Cyclooxygenase 2; D015232:Dinoprostone / Q000096:biosynthesis; D007375:Interleukin-1 / Q000037:antagonists & inhibitors / Q000494:pharmacology; D007527:Isoenzymes / Q000235:genetics; D008349:Manipulation, Orthopedic; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000096:biosynthesis / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D010641:Phenotype; D026741:Physical Therapy Modalities; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics; D011509:Proteoglycans / Q000096:biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D013704:Temporomandibular Joint / Q000166:cytology*; D013705:Temporomandibular Joint Disorders / Q000534:rehabilitation; D013718:Tensile Strength / Q000502:physiology*; D019714:Tissue Inhibitor of Metalloproteinases / Q000235:genetics
D007375:Interleukin-1; D007527:Isoenzymes; D011509:Proteoglycans; D012333:RNA, Messenger; D019714:Tissue Inhibitor of Metalloproteinases; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D020781:Matrix Metalloproteinase 1; D015232:Dinoprostone