Transient-steady state phenomena in microdamage physiology: A proposed algorithm for lamellar bone

Abstract

This algorithm suggests that in steady states the momentary burden of unrepaired microdamage (MDx) in lamellar bone equals the rate of creation of new MDx multiplied by the time taken to repair a locus of MDx completely in the biomechanical sense. That "repair period" equals about 0.6 years in healthy human adults. When MDx production suddenly increases, the momentary MDx burden begins to increase too, and does so for a time equal to the repair period and in proportion to the increased MDx production. After the repair period elapses, the momentary MDx would tend to reach and stay at a maximum value as long as increased MDx production continued. Prolonging the repair period, preventing the creation of new remodeling units to repair MDx, or delaying mineralization of the new bone made by those units would also increase MDx burdens. Reducing MDx production or the repair period, or accelerating the creation of new modeling units would have the opposite effects on the momentary MDx burden but would also go through a transient phase before developing the new steady state conditions. Exploiting these relationships quantitatively and experimentally requires expressing them mathematically and using for the terms in any equations things one can define logically and measure practically. Accordingly, the article suggests a special definition of a unit amount of microdamage, how to measure it, and simple algebra and equations for calculating some effects of microdamage on the biologic system.

Epidemiology, radiology and histology of atypical femoral fractures

“…Physiologically formed microcracks can grow to one or several larger cracks (Frost 1989). When this crack reaches a critical size and penetrates the margin of the lateral cortex, micromovements can lead to thigh pain during weightbearing, by irritation of the periosteal envelope.…”

From Wolff's law to the Utah paradigm: Insights about bone physiology and its clinical applications

“…Normally remodeling BMUs replace the damaged bone with new bone, and strains below an operational MDx threshold range cause so little MDx that remodeling can repair it. When larger strains cause too much to repair, the resulting accumulated MDx causes or helps to cause all "spontaneous" and stress fractures (so "spontaneous" fractures are not really spontaneous) (Devas, 1975;Frost, 1989a;Markey, 1987), as well as pseudofractures in osteomalacia and pathologic fractures**. Such accumulations can also allow pull-outs or loosening of pedicle and other screws, or make a bone weak enough to let a minor incident (low energy trauma; Freeman et al, 1974;Greenspan et al, 1994) fracture it.…”

“…Antiremodeling agents like estrogen and the bisphosphonates depress disuse-mode remodeling (not just osteoclasts) and help to retard local and generalized bone losses (Fleisch, 1995;Frost, 1997a). Impaired microdamage repair by BMUs causes or helps to cause osteochondritis dissecans, aseptic necroses of bone, and spontaneous fractures of irradiated bone (Frost, 1986), as well as stress fractures in athletes and military trainees, pathologic fractures, pseudofractures in osteomalacia, and spontaneous fractures in true osteoporoses (Frost, 1989a)**. That impaired repair also helps to explain the loosening of some internal fixation implants and some load-bearing endoprostheses (Frost, 1992b).…”

Transphyseal linear ossific striations of the distal radius and ulna

“…Repetitive loading of a rigid or semi-rigid structure may cause microscopic cracks within it that tend to enlarge progressively with further loading cycles. Eventually, so little structure may remain uncracked that a final load much smaller than the structure's original fracture strength may cause a complete fracture [4]. Clinical and laboratory evidence show that such fatigue microfractures and the antecedent microdamage may occur in both healthy and diseased living bone…”

“…Microdamage as a materials fatigue phenomenon has become recognized as an event in viable bone, fibrous tissue and cartilage [1,4]. Repetitive loading of a rigid or semi-rigid structure may cause microscopic cracks within it that tend to enlarge progressively with further loading cycles.…”