Effects of aging on articular cartilage homeostasis

Abstract

This review is focused on aging-related changes in cells and extracellular matrix of the articular cartilage. Major extracellular matrix changes are a reduced thickness of cartilage, proteolysis, advanced glycation and calcification. The cellular changes include reduced cell density, cellular senescence with abnormal secretory profiles, and impaired cellular defense mechanisms and anabolic responses. The extracellular and cellular changes compound each other, leading to biomechanical dysfunction and tissue destruction. The consequences of aging-related changes for joint homeostasis and risk for osteoarthritis are discussed. This article is part of a Special Issue entitled "Osteoarthritis".

Fig. 1. Macroscopic images of human femoral condyles

Images represent normal young (left, age 40), normal aging (center, age 76) OA (right, age 88) tissue. The old normal condyle shows intact cartilage with yellow discoloration, which is in part due to the formation of advanced glycation end products. The OA sample features large areas with complete loss of articular cartilage (dashed line on the left femoral condyle), osteophytes at the joint margins (red arrowheads) and the intercondylar notch (blue arrowheads). M=medial; L=lateral

Fig. 2. Safranin O stained sections of human femoral condyles

Images show young normal (left, age 40), old normal (center, age 76) and OA donors (right, age 88). The old normal sample has reduced tissue height, reduced safranin O staining in the superficial zone but no structural defects at the surface. The OA sample shows loss the superficial and part of the mid zone, fibrillations extending into the deep zone, areas with low cell density and cell clusters and duplication of the tidemark. All images are shown at 2.5x magnification.