Joint anatomy, design, and arthroses: insights of the Utah paradigm.

This model of joint design argues 1) that excessive fatigue damage (MDx) in articular cartilage collagen can be the "final cause" of an arthrosis; 2) that known responses of a growing joint's anatomy and geometry, and modeling and maintenance activities, to mechanical loads minimize that cause and thus arthroses; 3) and many biomechanical, biochemical, cell-biologic, genetic and traumatic "first causes" of arthroses could lead to that final cause. The model depends partly on the following facts (marked by a single asterisk) and ideas (marked by a double asterisk). A) During growth a joint's total loads can increase over 20 times without causing an arthrosis, yet in adults an equal loading increase would cause one. B) Fatigue damage (MDx) occurs in joint tissues, larger strains increase it, and minimizing strains reduces it. C) Bone can repair amounts of MDx below an "MDx threshold," but larger amounts can escape repair and accumulate. The model assumes articular cartilage has similar features. D) Bone modeling makes bones strong enough to keep their strains below bone's MDx threshold and minimize MDx. Chondral modeling shapes and sizes joints during growth; that would keep articular cartilage strains below the chondral MDx threshold to minimize chondral MDx and arthroses. Normal chondral modeling nearly stops in adults, which might explain point A above. E) Throughout life maintenance activities preserve optimal physical, chemical and biologic properties of a joint's tissues. To past emphases on the biochemical, genetic, cellular and molecular biologic features of adult joint physiology, this model adds organ-level, tissue-level and vital-biomechanical features of growing joints that invite study and understanding at lower levels of biologic organization.