Hormonal influences on the muscle-bone feedback system: A perspective

Bone Research Group, UKK Institute, Tampere, Finland.
Journal of musculoskeletal & neuronal interactions (Impact Factor: 1.74). 07/2005; 5(3):255-61.
Source: PubMed


Hormones, muscle and bone tissues have co-existed virtually during the whole evolution of vertebrates, and it is obvious that they constitute a complex system able to cope with needs and challenges arising from a variety of physiological and locomotive needs. All body movements are produced by co-ordinated contractions of skeletal muscles, while consequent dynamic muscle work provides the fundamental source of mechanical loading to the skeleton. Mechanical competence of the skeleton is principally maintained by a mechanosensory feedback system that senses the loading-induced deformations within the bones and maintains the skeletal rigidity through structural adaptation. In contrast to the prevalent view suggesting a modulatory effect of hormones on the sensitivity of the mechanosensory system, a new conceptual scheme is proposed. In particular, it is argued that the mechanical and hormonal functions in the skeleton are fundamentally independent but can be seemingly interactive through hormonally-induced modifications in the bone structure, those basically forming a mineral reservoir for maintenance of physiological homeostasis. Whenever needed, utilization of this strategically placed reservoir would not essentially compromise the mechanical competence and locomotive capability of the skeleton. Although plausible, the present view is necessarily speculative and awaits corroborative experimental evidence.

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Available from: Harri Sievänen, Dec 26, 2013
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    • "Age-related differences can also be translated into biochemical and physico-chemical changes, critical to accurate interpretation of experimental factors. These changes in part could be due to the varying response of the mechanosensory system and/or hormonal influences, both of which alter the mechanical efficiency of muscle, bone, and their respective interfaces [27]. There is evidence supporting the loss of functional efficiency in a joint with age due to an innate decrease in metabolic rate of cells within mineralized and soft tissues, as well as the soft-hard and hard-hard tissue interfaces [28], [29], [30], [31], [32], [33]. "
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    ABSTRACT: Functional loads on an organ induce tissue adaptations by converting mechanical energy into chemical energy at a cell-level. The transducing capacity of cells alters physico-chemical properties of tissues, developing a positive feedback commonly recognized as the form-function relationship. In this study, organ and tissue adaptations were mapped in the bone-tooth complex by identifying and correlating biomolecular expressions to physico-chemical properties in rats from 1.5 to 15 months. However, future research using hard and soft chow over relevant age groups would decouple the function related effects from aging affects. Progressive curvature in the distal root with increased root resorption was observed using micro X-ray computed tomography. Resorption was correlated to the increased activity of multinucleated osteoclasts on the distal side of the molars until 6 months using tartrate resistant acid phosphatase (TRAP). Interestingly, mononucleated TRAP positive cells within PDL vasculature were observed in older rats. Higher levels of glycosaminoglycans were identified at PDL-bone and PDL-cementum entheses using alcian blue stain. Decreasing biochemical gradients from coronal to apical zones, specifically biomolecules that can induce osteogenic (biglycan) and fibrogenic (fibromodulin, decorin) phenotypes, and PDL-specific negative regulator of mineralization (asporin) were observed using immunohistochemistry. Heterogeneous distribution of Ca and P in alveolar bone, and relatively lower contents at the entheses, were observed using energy dispersive X-ray analysis. No correlation between age and microhardness of alveolar bone (0.7 ± 0.1 to 0.9 ± 0.2 GPa) and cementum (0.6 ± 0.1 to 0.8 ± 0.3 GPa) was observed using a microindenter. However, hardness of cementum and alveolar bone at any given age were significantly different (P<0.05). These observations should be taken into account as baseline parameters, during development (1.5 to 4 months), growth (4 to 10 months), followed by a senescent phase (10 to 15 months), from which deviations due to experimentally induced perturbations can be effectively investigated.
    PLoS ONE 04/2012; 7(4):e35980. DOI:10.1371/journal.pone.0035980 · 3.23 Impact Factor
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    • "There are a few potential ways of preventing bone fracture, i.e. strengthening bones and/or preventing falls (Ortiz-Luna et al., 2009; Stevens & Olson, 2000). In order to withstand prevalent loading without breaking; while remaining relatively light in weight to allow for locomotion, bones have the ability to adapt their structure to functional loading (Frost, 2000; 2003; Sievänen, 2005). It has been demonstrated that physical activity affects the weight bearing skeleton more than the non-weight bearing one (Mikkola et al., 2008), and it may therefore be argued that, the skeleton is loaded mainly by locomotory actions that impart strains on bones. "
    Theoretical Biomechanics, 11/2011; , ISBN: 978-953-307-851-9
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    • "Several hypotheses have been built to explain the association of MM on bone mass. Muscle strength gains are believed to induce periosteal aposition directly stimulating, via mechanic strength, osteocyte mechanoreceptors [14,15]. Additionally, bone and muscle share endocrine and genetic influences. "
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    ABSTRACT: After menopause, rapid bone mass loss occurs in response to hypoestrogenism. Several studies suggest that muscle mass and bone mineral density (BMD) are positively associated in postmenopausal women. Therefore, it may be assumed that postmenopausal low appendicular muscle mass (aMM) can increase BMD loss in a short period of time. The purpose of this study was to assess relationship of aMM with femoral neck BMD in postmenopausal women. Prospective, controlled clinical Trial including 64 women aged 45-70 years, who had not had their last menstruation for at least one year. Subjects were divided into two groups: low aMM (n = 32), and normal aMM (n-32). Femoral neck BMD and muscle mass were measured by DXA at baseline and after twelve months. Pairwise and independent t tests were used for data analysis. Baseline weight, BMI and muscle mass (total and appendicular) significantly differ between groups (p < 0.05). After twelve months, femoral neck BMD was significantly lower in the group with low aMM, whereas no significant difference was observed in the group with normal aMM (p < 0.05). In postmenopausal women, low appendicular muscle mass is associated negatively with femoral neck BMD in a short period of time.
    BMC Musculoskeletal Disorders 10/2011; 12(1):225. DOI:10.1186/1471-2474-12-225 · 1.72 Impact Factor
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