Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis.

Background: Tracheal replacement is a challenge for thoracic surgeons due to stenosis in the trachea-prosthesis anastomosis. We propose that stenosis occurs due to fibrosis as a result of an abnormal healing process, characterized by an increased expression of wound healing growth factors (vascular endothelial growth factor [VEGF], survivin, and CD31), which promote angiogenesis and decrease apoptosis. We analyzed the immunoreactivity of VEGF, survivin, CD31, and caspase-3 in the development of fibrotic stenosis in prosthetic tracheal replacement.

A novel rat osteoarthrosis model to assess apoptosis and matrix degradation.

Matrix degradation and apoptosis are two crucial features of osteoarthrosis (OA), but the relationship between them needs to be clarified. We developed a novel OA model in partial meniscectomisized rats for the assessment in situ of these processes. The surgical procedure used permitted us to identify and remove 30-50% of the meniscus.

Apoptotic chondrocytes from osteoarthrotic human articular cartilage and abnormal calcification of subchondral bone.

Objective: Osteoarthrosis (OA) is accompanied by altered subchondral bone remodeling. We investigated the role of chondrocytes in the mechanism of abnormal cartilage calcification.

Methods: Knee articular cartilage samples from OA and normal tissue were studied.