Functionally adaptive control of bone architecture

Adaptation of bone architecture in relation to functional loading is a characteristic feature of bone physiology. In mammals and birds at least it is the mechanism on which the establishment and maintenance of load-bearing competence depends.

In connective tissues, unlike muscle, loads are sustained by an extracellular matrix. In tendon, ligament and cartilage resident cells throughout the structure may produce, remove and adapt matrix in their immediate vicinity, so regulating the amount of tissue present and altering its mechanical properties. In contrast, since bone matrix is rigid any change in bone architecture has to be accomplished by deposition of new tissue, and/or removal of old, either on existing surfaces or within voids excavated within the existing structure. The process of bone formation is performed by local mesenchymally derived osteoblasts whereas resorption requires haematogenously derived osteoclasts. Osteoclasts are, however, substantially influenced in their activity by osteoblasts (Chambers, 1985).

In bone, as in the other load-bearing connective tissues, one of the prime responsibilities of the resident cells is to maintain sufficient tissue present, with appropriate material properties, to sustain, without damage, the loads applied to it. Tissues subject to tension (such as tendon and ligament) self-align with load and so their shape is not critical. In contrast bones must withstand tension, compression, bending and torsion while providing the constant shape necessary for the close tolerances of joint surfaces and the consistent location of muscle attachments.