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.
Recent realizations have begun to change how 'osteoporoses' are diagnosed, managed and studied. This article explains the nature and basis of some resulting controversies, chiefly for clinicians who manage such patients but do not participate in resolving those controversies. Currently the size of a bone 'mass' deficit serves to diagnose 'osteoporosis', but recently clarified physiology suggests at least three different kinds of osteoporosis could occur in people with identical bone 'mass' deficits. Indeed, they do occur. (a) In one kind, people have less bone than 'normal' but no bone problems unless they sustain injuries. Most of their resulting fractures, usually from falls, affect extremity bones. This condition can affect children, men and women. (b) In a second kind an osteopenia exists in which voluntary physical activities (not injuries) cause spontaneous fractures and/or bone pain, mainly in the spine, more often in women than men and seldom in children (osteogenesis imperfecta excepted). (c) A third kind combines features of the first two. As for the physiology involved in those affections, bone modeling can increase bone strength and 'mass', while BMU (Bone Multicellular Unit)-based bone remodeling can reduce them. Mainly bone strains control those two activities and muscles cause the largest strains, so muscle strength should strongly influence bone modeling, remodeling, strength and 'mass'. If so chronic muscle weakness should usually cause an osteopenia and weakened bones. Excessive amounts of fatigue damage or microdamage can also weaken bones. From that physiology one could argue that chiefly chronic muscle weakness instead of an intrinsic bone disorder would cause (a), while intrinsic but still enigmatic modeling and remodeling disorders would cause (b), and (c) could combine features of both conditions. If so, these ideas could have significant effects on the future criteria used to diagnose osteoporoses and osteopenias, on how they are studied in the clinic and laboratory, and on how they are prevented or, if they occur, are managed.
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