For discussing the functions of different structures of all organisms.
12 posts • Page 1 of 1
I was just wondering what it is that controls bone remodelling. I know that this is carried out by osteoblasts/osteoclasts but I don't know what type of cell they are and what controls them. Does the brain release hormones that tell them exactly where to remove or add bone? And how do they know when a bone has been broken and needs repairal?
The information you wish to know is much to long and complex to give here. there are a lot of factors that contribue to this: hormones, vitamines, enzymes(phosphatases), your diet etc.
If you want to know it in detail i suggest you read a book about animal physiology
Nice suggestion, Andrew
Well, maybe this little information could help you a bit
by Rod Lakes from University of Wisconsin
The relationship between the mass and form of a bone to the forces applied to it was appreciated by Galileo (4.1.1), who is credited with being the first to understand the balance of forces in beam bending and with applying this understanding to the mechanical analysis of bone. Julius Wolff (4.1.2) published his seminal 1892 monograph on bone remodeling; the observation that bone is reshaped in response to the forces acting on it is presently referred to as Wolff's law. Many relevant observations regarding the phenomenology of bone remodeling have been compiled and analyzed by Frost (4.1.3,4.1.4). Salient points are as follows:
1. Remodelling is triggered not by principal stress but by 'flexure".
2. Repetitive dynamic loads on bone trigger remodelling; static loads do not.
3. Dynamic flexure causes all affected bone surfaces to drift towards the concavity which arises during the act of dynamic flexure.
These rules are essentially qualitative and they do not deal with underlying causes. A critique of these ideas has been presented by Currey (4). Additional aspects of bone remodeling may be found in the clinical literature. For example, after complete removal of a metacarpal and its replacement with graft consisting of a strut of tibial bone, the graft becomes remodelled to resemble a real metacarpal; the graft continues to function after 52 years (4.1.5). In the standards of the Swiss Association for Internal Fixation it is pointed out that severe osteoporosis can result from the use of two bone plates in the same region as a result of the greatly reduced stress in the bone (4.1.6). Pauwels (4.1.7) suggested that as a result of bending stresses the medial and lateral aspects of the femur should be stiffer and stronger than the anterior and posterior aspects. Such a difference has actually been observed (4.1.. Large cyclic stress causes more resorption than large static stress (4.1.9). Immobilization of humans causes loss of bone and excretion of calcium and phosphorus (4.1.10). Long spaceflights under zero gravity also cause loss of bone (4.1.11,4.1.12); hypergravity induced by centrifugation strengthens the bones of rats (4.1.13,4.1.14). Studies of stress-induced remodeling of living bone have been performed in vitro (4.1.15). Recently, in vivo studies in pigs (4.1.16) were conducted. In this study, strains were directly measured by strain gages before and after remodelling. Remodelling was induced by removing part of the pigs' ulna so that the radius bore all the load. Initially, the peak strain in the ulna approximately doubled. New bone was added until, after three months, the peak strain was about the same as on the normal leg bones. In vivo experiments conducted in sheep (4.1.17) have disclosed similar results. It is of interest to compare the response time noted in the above experiments with the rate of bone turnover in healthy humans. The life expectancy of an individual osteon in a normal 45 year old man is 15 years and it will have taken 100 days to produce it (4.1.18, 4.1.19).
Remodelling of Haversian bone seems to influence the quantity of bone but not its quality, i.e. Young's modulus, tensile strength, and composition(4.1.20). However the initial remodelling of primary bone to produce Haversian bone results in a reduction in strength (4). As for the influence of the rate of loading on bone remodelling, there is good evidence to suggest that intermittent deformation can produce a marked adaptive response in bone, whereas static deformation has little effect (4.1.16). Experiments (4.1.21) upon rabbit tibiae bear this out. In the dental field, by contrast, it is accepted that static forces of long duration move teeth in the jawbone. In this connection, (4.1.22) the direction (as well as the type) of stresses acting on the bone tissue should also be considered. Currey (4) points out that the response of different bones in the same skeleton to mechanical loads must differ, otherwise lightly loaded bones such as the top of the human skull, or the auditory ossicles, would be resorbed.
Failure of bone remodeling to occur normally in certain disease states is of interest: for example, micropetrotic bone contains few if any viable osteocytes and usually contains a much larger number of microscopic cracks than adjacent living bone (4.1.23). This suggests that the osteocytes play a role in detecting and repairing the damage. In senile osteoporosis, bone tissue is removed by the body, often to such an extent that fractures occur during normal activities. Osteoporosis may be referred to as a remodelling error (4.1.4).
Some theoretical work, notably by Cowin and others (4.1.24), has dealt with the problem of formulating Wolff's law in a quantitative fashion. In this theory, constitutive equations are developed, which predict the remodelling response to a given stress. Stability considerations are invoked to obtain some constraints on the parameters in the constitutive equation.
Bone remodeling appears to be governed by a feedback system in which the bone cells sense the state of strain in the bone matrix around them and either add or remove bone as needed to maintain the strain within normal limits. The process or processes by which the cells are able to sense the strain and the important aspects of the strain field are presently unknown. Bassett and Becker (4.2.1) reported that bone is piezoelectric, i.e. that it generates electric fields in response to mechanical stress; they advanced the hypothesis that the piezoelectric effect is the part of the feedback loop by which the cells sense the strain field. This hypothesis obtained support from observations of osteogenesis in response to externally applied electric fields of the same order of magnitude as those generated naturally by stress via the piezoelectric effect. The study of bone bioelectricity has received impetus from observations that externally applied electric or electromagnetic fields stimulate bone growth (4.2.2). The electrical hypothesis, while favored by many, has not been proven. Indeed, other investigators have advanced competing hypotheses which involve other mechanisms by which the cells are informed of the state of stress around them.
For example, inhomogeneous deformation at the lamellae may impinge on osteocyte processes and thus trigger the osteocytes to initiate bone formation or remodelling (4.2.3). Motion at the cement lines was observed and it was suggested that such motion could act as a passive mechanism by which bone's symmetry axes may become aligned to the direction of time averaged principal stresses (2.9.9). Stress on bone may induce flow of fluid in channels, e.g. canaliculi, and such flow could play a role in the nutrition and waste elimination of osteocytes, which may be significant in bone remodeling (4.2.4). In a related vein, theoretical arguments have been presented in support of the hypothesis that bone cells are directly sensitive to hydrostatic pressure transmitted to them from the bone matrix via the tissue fluid (4.2.5). Although no experimental test of this direct pressure hypothesis has been published, we observe with interest that direct hydrostatic pressure has recently been observed to alter the swimming behavior of paramecia, possibly by means of action upon the cell membrane (4.2.6). Otter and Salman found that a hydrostatic pressure of 68 atm abolishes the reversing of direction of swimming, 170 atm stops swimming, and 400-500 atm irreversibly damages the cell. We observe that 100 atm corresponds to 1400 psi stress, or in bone, a strain of 0.07% which is in the normal range of bone strain. 500 atm corresponds to 7000 psi or a strain of 0.35%, well above the normal range of bone strain. Stress in bone also results in temperature differences between osteons (4.2.7); the cells may be sensitive to sudden temperature changes during human activity. A mechanochemical hypothesis has been advanced, in which the solubility of calcium may be affected by stress in the bone matrix (4.2.. Strain energy in bone might also influence the energetics of bone mineral nucleation (4.2.9). It has also been suggested that remodelling may be initiated in response to microcracks generated by mechanical fatigue of bone (4.2.10). In summary, many hypotheses have been proposed for the mechanism by which appropriate cells sense the state of strain in bone, but little or no experimental evidence is available to discriminate among them.
Cellular and biochemical aspects of bone remodelling
The adaptive response of bone to mechanical stimuli is mediated by living cells. A great deal is known concerning bone cell function and its control by ionic and hormonal factors, but little is known concerning the effect of mechanical strain in bone upon the biochemistry of its cells. Rasmussen and Bordier (4.3.1) have presented an extensive review of studies of bone cell physiology. Recently, the biochemical consequences of electrical stimulation of bone have been reported (4.3.2). Biochemical steps associated with cell activation are as yet poorly understood, but ion fluxes appear to play a role (4.3.3). Cyclic nucleotides mediate the effects of extracellular signals(4.3.4) and prostaglandins modulate them (4.3.4). Prostaglandin E 2 has been hypothesized to mediate bone resorption in trauma, malignancy, and periodontal disease. This prostaglandin, as well as the cellular constituents cyclic AMP and cyclic GMP, has been found in association with regions of bone stimulated electrically (4.3.2).
1. Hancox, N.M., Biology of Bone, Cambridge University Press, 1972.
2. Evans, F.G., The mechanical properties of bone, Thomas, Springfield, Ill, 1973.
3. Gordon, J. E. Structures, Penguin (1983)
4. Currey, J., The mechanical adaptations of bones, Princeton University Press, 1984.
5. Reilly, D.T. and Burstein, A. H., The mechanical properties of cortical bone, J. Bone Jnt. Surg., 56A, 1001-1022, 1974.
6. Currey, J.D., The mechanical properties of bone, Clin. Orthop. Rel. Res., 73, 210-231, 1970.
7. Phillips, R. W., Science of dental materials, W. B. Saunders, 1973.
4.1.1. Galilei, G., Discorsi E. Dimostrazioni Matematiche intorna a due nuove Scienze, pp. 158-172, 1638, Translated by H. Crew and A. deSalvio, Macmillan, NY, pp. 118-134, 1914.
4.1.2. Wolff, J., Das Gesetz der Transformation der Knochen , Hirschwald, Berlin, 1892.
4.1.3. Frost, H. M., Bone remodelling and its relation to metabolic bone diseases, C. Thomas, Springfield, IL, 1973.
4.1.4. Frost, H. M., Bone modelling and skeletal modelling errors , C. Thomas, Springfield, IL, 1973.
4.1.5. Nathan, P.A. and Fowler, A., Remodeling of a metacarpal bone graft in a child, J. Bone Jnt. Surg ., 58A,719-722, 1976.
4.1.6. Muller, M.E., Allgouer, M., Willeneger, H., Manual of Internal Fixation -Technique Recommended by the AO Group, Springer Verlag, 1970.
4.1.7. Pauwels, F., Die Bedeutung des Bauprinzipien des Stütz und Bewegensapparatens für die Beanspruchung der Rohrenknochen, Z. für Anat. und Entwicklungsgesch, 114:129-166, 1948.
4.1.8. Amtmann, E., The distribution of the breaking strength in the femur,
J. Biomech. 1, 271-277, 1968.
4.1.9. Seirig, A. and Kempko, W, Behavior of in vivo bone under cyclic loading, J. Biomech. , 2, 455-461, 1969.
4.1.10. Dietrick, J.E., Whedon, G., Shorr, E., Effects of immobilization upon various metabolic and physiological functions of bone, Am. Jnl. Med. 4, 3-36, 1948.
4.1.11. Mack, P.B., La Chance, P.L., Effects of recumbency and space flight on bone density, Am. J. Clin. Nutrition , 20,194-205, 1967.
4.1.12. Morey, E. R., and Baylink, D. K., Inhibition of bone formation during space flight, Science, 201, 1138-1141, 1978.
4.1.13. Wunder, C.C., Briney, S.R., Skangstad, C.A., Growth of mouse femurs during chronic centrifugation, Nature, 188, 151-152, 1960.
4.1.14. Wunder, C.C., Cook, R.M., Welch, R.C., Glade, R., Fleming, B.P., Femur bending properties as influenced by gravity: I. ultimate load and moment for 3-G rats, Aviat. Space Environ. Med. 48, 339-346, 1977.
4.1.15. Glucksmann, A., Studies of bone mechanics in vitro I-Influence of pressure on orientation of structure, Anat. Rec ., 72, 97-115,1938.
4.1.16. Goodship, A.E. , Lanyon, L.E., McFie, M., Functional adaptation of bone to increased stress, J. Bone Jnt. Surg. , 61A, 539-546, 1979.
4.1.17. Hall, B. K., Developmental and cellular skeletal biology , Academic Press, N.Y., 1978.
4.1.18. Sumner-Smith, G., Bone in clinical orthopaedics , W. B. Saunders, 1982.
4.1.19. Lanyon, L. E., Magee, P. T., and Bagott, D. G., The relationship of the functional stress and strain to the process of bone remodelling: an experimental study on the sheep radius, J. Biomech. 12, 593-600, 1979.
4.1.20. Woo, S. L. Y., Kuei, S. C., Amiel, D., Gomez, M. A., Hayes, W. C., White, F. C., and Akeson, W. H., The effect of prolonged physical training on the properties of long bone: a study of Wolff's law, J. Bone Jnt. Surg. , 63A, 780-787, 1981.
4.1.21. Liskova, M. and Hert, J., Reaction of bone to mechanical stimuli, part 2, periosteal and endosteal reaction of the tibial diaphysis in rabbit to intermittent loading, Folia Morphologica 19, 310-317, 1971.
4.1.22. Wright, K.W.J. and Yettram, A.L., An analytical investigation into possible mechanical causes of bone remodelling, J. Biomed. Eng ., (England) 1, 41-49, 1979.
4.1.23. Frost, H. M., Osteocyte death in vivo, J. Bone Jnt. Surg. , 42A, 138-143, 1960.
4.1.24. Cowin, S. C. and Hegedus, D. H., Bone Remodeling I: Theory of adaptive elasticity, Journal of Elasticity , 6, 313-326, 1976.
I like the picture. Didn't have time to read the article. Saved it and will read it when i have time...
Check my signature. I hate most teachers!! I like mine, though...
BTW, Dave, no offense, but your teacher seems not interested in teaching you biology...
well, i partly blame the fact that he's old(read forgetful), and he seems the "old school" type of teacher: read and memorize this or get a beating. He can't do that now obviously so his teaching system is kinda weak without it...
I hear he's retiring next year. Too late for me and my class .
Living one day at a time;
Enjoying one moment at a time;
Accepting hardships as the pathway to peace;
The skeleton is a metabolically active organ that undergoes continuous remodeling throughout life. Bone remodeling involves the removal of mineralized bone by osteoclasts followed by the formation of bone matrix through the osteoblasts that subsequently become mineralized. The remodeling cycle consists of three consecutive phases: resorption, during which osteoclasts digest old bone; reversal, when mononuclear cells appear on the bone surface; and formation, when osteoblasts lay down new bone until the resorbed bone is completely replaced. Bone remodeling serves to adjust bone architecture to meet changing mechanical needs and it helps to repair microdamages in bone matrix preventing the accumulation of old bone. It also plays an important role in maintaining plasma calcium homeostasis. The regulation of bone remodeling is both systemic and local. The major systemic regulators include parathyroid hormone (PTH), calcitriol, and other hormones such as growth hormone, glucocorticoids, thyroid hormones, and sex hormones. Factors such as insulin-like growth factors (IGFs), prostaglandins, tumor growth factor-beta (TGF-beta), bone morphogenetic proteins (BMP), and cytokines are involved as well. As far as local regulation of bone remodeling is concerned, a large number of cytokines and growth factors that affect bone cell functions have been recently identified. Furthermore, through the RANK/receptor activator of NF-kappa B ligand (RANKL)/osteoprotegerin (OPG) system the processes of bone resorption and formation are tightly coupled allowing a wave of bone formation to follow each cycle of bone resorption, thus maintaining skeletal integrity.
http://www.iofbonehealth.org/health-pro ... ology.html
I am working on a project where I have to simulate bone remodelling using abaqus and UMAT.
In my input file I start with a lower young's modulus and this is the value UMAT takes at the first iteration to calculate stresses.
Then it saves this as a state variable and pass it on to input file, where one has to use *DEPVAR in order to accept this value and at next iteration this is given back to the UMAT to continue with the stresses calculation and material properties calculation.
My problem is how should I ensure that the program terminates when the EMOD is equal to the final EMOD as there is no error signal from the above control equation any more. I can use a condition here to observe whether the average strain is equal to expected strain or whether EMODS are equal and that EMOD should stay the same, but is this the way one should do it or is there a better way to do the same. If I give a condition at what range I should say that the error signal is zero.
12 posts • Page 1 of 1
Who is online
Users browsing this forum: No registered users and 0 guests