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JFSF, Journal of Frailty, Sarcopenia and Falls, 2016; 1(1): 4-7

Human Musculoskeletal Models of Disuse

Year: 2016

Dionyssiotis Y., Kapsokoulou A., Samlidi E., Iatridou G.
1 Physical Medicine & Rehabilitation Department, European Interbalkan Medical Center, Thessaloniki, Greece 2 Medical School of Patras, Rio, Patras, Greece 3 Medical School of Thessaly, Larissa, Greece 4 Physical Therapy Unit “Physiospot”, Athens, Greec


According to Frost’s mechanostat theory when the bone receives strains of about 800 to 1600 micro-strain retains its strength; increased strains promote formation (remodeling)
up to a fracture point, and when bone is a low loading status receiving strains below 800 micro-strains starts remodeling moves to the opposite direction of resorption1,2. The picture
(Figure 1) shows the substantially variable bone response dependent upon the degree of deformation (strain)3. The theory is developed in the “musculoskeletal unit” with the
employment of real bone mineral density measurement technology i.e. peripheral quantitative computed tomography, pQCT (Figure 2). An increase in muscle area (i.e. muscle) is not positively correlated with trabecular bone mineral density, but this is not the case with the bone mineral content which is increased. Increased bone mineral content is leading to increased bone strength.
The final development of this theory was called “Utah Paradigm of Skeletal Physiology”: Exercise causes an increase in bone mass and strength more in children than
adults, and is marginally effective in increasing bone mass in the elderly. The reduced effectiveness of exercise in the frame of the elderly can be attributed to decreased
sensitivity of this aging skeleton to mechanical stimuli. One way to overcome this poor response to the aged frame could be the use of promising non-mechanical factors to
overcome the decreased anabolic sensitivity and increase bone mass and strength. We already know that estrogen modify the set points of the mechanostat. As long as
estrogens, for example in a woman, are within a normal range, common loading (daily activities) maintains a relatively stable state in the bone. Estrogen deficiency in
menopause, therefore, results in a situation that a common load cannot maintain the bone any more. Bone receives a disuse signal because the set point of the mechanostat
is moving towards resorption direction in the presence of loading strains of the former common loading activities and the absence of the prophylactic action of estrogen.
Similar modification of the set point can be done with other interventions such as anabolic drugs i.e. teriparatide towards formation (remodeling with positive formation/
resorption balance)

GID: 4133; Last update: 11.04.2016
More information: Original Article