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Abstract
Genetic predisposition, traumatic events, or excessive mechanical exposure provoke arthritic changes in the temporomandibular joint (TMJ). We analysed the impact of mechanical stress that might be involved in the development and progression of TMJ osteoarthritis (OA) on murine synovial fibroblasts (SFs) of temporomandibular origin. SFs were subjected to different protocols of mechanical stress, either to a high-frequency tensile strain for 4 h or to a tensile strain of varying magnitude for 48 h. The TMJ OA induction was evaluated based on the gene and protein secretion of inflammatory factors (Icam-1, Cxcl-1, Cxcl-2, Il-1ß, Il-1ra, Il-6, Ptgs-2, PG-E2), subchondral bone remodelling (Rankl, Opg), and extracellular matrix components (Col1a2, Has-1, collagen and hyaluronic acid deposition) using RT-qPCR, ELISA, and HPLC. A short high-frequency tensile strain had only minor effects on inflammatory factors and no effects on the subchondral bone remodelling induction or matrix constituent production. A prolonged tensile strain of moderate and advanced magnitude increased the expression of inflammatory factors. An advanced tensile strain enhanced the Ptgs-2 and PG-E2 expression, while the expression of further inflammatory factors were decreased. The tensile strain protocols had no effects on the RANKL/OPG expression, while the advanced tensile strain significantly reduced the deposition of matrix constituent contents of collagen and hyaluronic acid. The data indicates that the application of prolonged advanced mechanical stress on SFs promote PG-E2 protein secretion, while the deposition of extracellular matrix components is decreased.
Highlights
The temporomandibular joint (TMJ) is the connection point of cranium and mandible and presents a unique articulated joint
Synovial fibroblasts of the temporomandibular joint are expected to be exposed to a frequent tensile strain on a daily basis
Progressing arthritic changes are indicated by increased levels of local and systemic inflammation
Summary
The temporomandibular joint (TMJ) is the connection point of cranium and mandible and presents a unique articulated joint. A characteristic feature of inflammatory active synovial fibroblasts is the expression of proinflammatory cytokines such as IL-1β, IL-6, IL-8, and of enzymes with a matrix-degrading activity, the matrix metalloproteinases (MMPs) Elevated levels of these cytokines and MMPs promote further inflammatory and cartilage-degrading processes, as well as tissue vascularization [21,22,23,24]. Apart from cartilage degeneration, subchondral bone remodelling and increased bone metabolism takes place in orthodontically induced TMJ OA rat models [25], while a genetic model of TMJ OA showed increased levels of the receptor activator of nuclear factor kappa β ligand (RANKL) and osteoprotegerin (OPG) who are key players in osteoclast-activity regulating-processes [26]. The synthesis of collagen and hyaluronic acid is altered [32] and changes in the enzymatic activity of hyaluronic acid synthases, as well as a shift of type II to type I collagen can be observed [33,34,35]
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