Biochemical and Cellular Assessment of Acetabular Chondral Flaps Identified During Hip Arthroscopy.

Purpose: To analyze chondral flaps debrided during hip arthroscopy to determine their biochemical and cellular composition.

Methods: Thirty-one full-thickness acetabular chondral flaps were collected during hip arthroscopy. Biochemical analysis was undertaken in 21 flaps from 20 patients, and cellular viability was determined in 10 flaps from 10 patients.

Stem cells catalyze cartilage formation by neonatal articular chondrocytes in 3D biomimetic hydrogels.

Cartilage loss is a leading cause of disability among adults and effective therapy remains elusive. Neonatal chondrocytes (NChons) are an attractive allogeneic cell source for cartilage repair, but their clinical translation has been hindered by scarce donor availability. Here we examine the potential for catalyzing cartilage tissue formation using a minimal number of NChons by co-culturing them with adipose-derived stem cells (ADSCs) in 3D hydrogels.

Direct subcutaneous injection of polyethylene particles over the murine calvaria results in dramatic osteolysis.

Purpose: The murine calvarial model has been widely employed for the in vivo study of particle-induced osteolysis, the most frequent cause of aseptic loosening of total joint replacements. Classically, this model uses an open surgical technique in which polyethylene (PE) particles are directly spread over the calvarium for the induction of osteolysis. We evaluated a minimally invasive modification of the calvarial model by using a direct subcutaneous injection of PE particles.

Flexor tendon tissue engineering: bioreactor cyclic strain increases construct strength.

Mutilating injuries of the hand and upper extremity result in tendon losses too great to be replaced by autologous grafts. The goal of this study was to use tissue engineering techniques to produce additional tendon material. We used a custom bioreactor to apply cyclic mechanical loading onto tissue-engineered tendon constructs to study ultimate tensile stress (UTS) and elastic modulus (E).

What are the local and systemic biologic reactions and mediators to wear debris, and what host factors determine or modulate the biologic response to wear particles?

New clinical and basic science data on the cellular and molecular mechanisms by which wear particles stimulate the host inflammatory response have provided deeper insight into the pathophysiology of periprosthetic bone loss. Interactions among wear particles, macrophages, osteoblasts, bone marrow-derived mesenchymal stem cells, fibroblasts, endothelial cells, and T cells contribute to the production of pro-inflammatory and pro-osteoclastogenic cytokines such as TNF-alpha, RANKL, M-SCF, PGE2, IL-1, IL-6, and IL-8. These cytokines not only promote osteoclastogenesis but interfere with osteogenesis led by osteoprogenitor cells.

Regulation of nitric oxide and bcl-2 expression by shear stress in human osteoarthritic chondrocytes in vitro.

Onset and progression of cartilage degeneration is associated with shear stress occurring in diarthrodial joints subjected to inappropriate loading. This study tested the hypothesis that shear stress induced nitric oxide is associated with altered expression of regulatory onco-proteins, bcl-2, and Fas (APO-1/CD95) and apoptosis in primary human osteoarthritic chondrocyte cultures. Shear stress induced membrane phosphatidylserine and nucleosomal degradation were taken as evidence of chondrocyte apoptosis.