title: Joint contact stress: a reasonable surrogate for biological processes?
abstract: A joint's normal mechanical history contributes to the maintenance of articular cartilage and underlying bone. Loading facilitates the flow of nutrients into cartilage and waste products away, and additionally provides the mechanical signals essential for normal cell and tissue maintenance. Deleteriously low or high contact stresses have been presumed to result in joint deterioration, and particular aspects of the mechanical environment may facilitate repair of damaged cartilage. For decades, investigators have explored static joint contact stresses (under some more or less arbitrary condition) as a surrogate of the relevant mechanical history. Contact stresses have been estimated in vitro in many joints and in a number of species, although only rarely in vivo. Despite a number of widely varying techniques (and spatial resolutions) to measure these contact stresses, reported ranges of static peak normal stresses are relatively similar from joint to joint across species, and in the range of 0.5 to 5.0 MPa. This suggests vertebrate diarthrodial joints have evolved to achieve similar mechanical design criteria. Available evidence also suggests some disorders of cartilage deterioration are associated with somewhat higher peak pressures ranging from 1-20 MPa, but overlapping the range of normal pressures. Some evidence and considerable logic suggests static contact stresses per se do not predict cartilage responses, but rather temporal aspects of the contact stress history. Static contact stresses may therefore not be a reasonable surrogate for biomechanical studies. Rather, temporal and spatial aspects of the loading history undoubtedly induce beneficial and deleterious biological responses. Finally, since all articular cartilage experiences similar stresses, the concept of a "weight-bearing" versus a "non-weight-bearing" joint seems flawed, and should be abandoned.
authors.affiliation: Clinical Orthopaedics & Related Research, 3550 Market St., Suite 220, Philadelphia, PA 19104, USA. dick.brand@clinorthop.org
authors.forename: Richard A
authors.initials: RA
authors.lastname: Brand
mesh_terms: D000818:Animals; D002358:Cartilage, Articular / Q000503:physiopathology*; D006801:Humans; D007596:Joints / Q000503:physiopathology*; D013314:Stress, Mechanical