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Biomedical subjects

H M Frost

Publications and source records attributed to H M Frost.

At least 19 recordsLinked to original sources
PubMed1994

Perspectives: a vital biomechanical model of synovial joint design.

Making a durable joint requires adapting the one present at birth to its subsequent mechanical usage and then maintaining it. The total loads on a joint's momentarily loaded area plus the size of that area determine the unit loads on its articular cartilage and subchondral bone. Given those facts, this model suggests the following. For adaptation: As is true for bone, a threshold range of unit loads that could turn cartilage modeling ON would lie below this tissue's microdamage threshold. When a joint's unit loads rose to that modeling threshold, chondral modeling would begin enlarging the momentarily loaded area to reduce and keep the unit loads on it below the microdamage thresholds of the bone and cartilage supporting that area. For maintenance: Maintenance activities would control the stiffness of cartilage and bone, which would also affect a joint's momentarily loaded area. These activities would usually repair whatever microdamage normally arises in those tissues, and could modify their microdamage thresholds too. In children, modeling and maintenance in bone and cartilage would function effectively. In adults chondral modeling becomes ineffective, but maintenance activities in bone and cartilage would remain effective, and likewise for modeling in the subchondral bone. This model assigns special importance in joint design to the stiffness of bone, cartilage, and ligament (as distinguished from their strength), to the typical largest unit loads applied to them by a subject's usual weekly physical activities, and to their microdamage.

Age Factors↗
PubMed1994

Perspectives: a biomechanical model of the pathogenesis of arthroses.

This model views the common, initiating cause of arthroses as excessive articular cartilage microdamage. If so, understanding it would become a central problem for understanding the pathogenesis of arthroses. The model proposes the microdamage can stem from: (1) Excessive total loads on normal joints; (2) underadaptations in a joint's size or shape that leave its momentarily loaded area too small for normal loads; (3) impaired microdamage repair in subchondral bone or articular cartilage; (4) abnormal composition or structure that makes a tissue develop excessive microdamage under normal loads. (5) (2)-(4) above could stem from changed set points or "lead times" for a joint's adaptations and maintenance, which in turn could stem from (6) genetic influences, some drugs, toxins, diseases, and "X," and (7) from combinations of the above. In the pathogenesis of arthroses this model assigns special importance to the stiffness of joint tissues (as distinguished from their strength), to the typical largest unit loads they carry as a result of a subject's usual physical activities, and to microdamage in those tissues.

Arthritis↗
PubMed1994

Perspectives: a vital biomechanical model of the endochondral ossification mechanism.

BACKGROUND: Mechanical usage effects could explain many features of endochondral ossification and related processes. Mineralization of growth plate cartilage could reduce its mechanical strains enough to make its resorption begin and to guide it in space. By removing most of its mineralized vertical septae, resorption could overload the remainder enough to increase woven bone formation on them and construct the primary spongiosa. After it finishes mineralizing, the primary spongiosa could become stiff enough to begin partial disuse in strain terms, so BMU-based remodeling would begin replacing it with lamellar bone. This would construct the secondary spongiosa. In transferring loads from the growth plate to the cortex, the central metaphyseal spongiosa becomes deloaded. This disuse would make remodeling remove it in the diaphyseal marrow space. METHODS: The slow growth of epiphyses and apophyses gives their spongiosas more time to adapt to their loads than the metaphyseal spongiosa beneath faster growing growth plates. Compared to metaphyseal trabeculae, this leads to fewer and thicker epiphyseal trabeculae that turn over more slowly and should persist for life because they carry loads for life. RESULTS: Rapid turnover of metaphyseal cortex in very young subjects could let it strain enough to form woven bone. Increased thickness and slower turnover of this cortex in older subjects could reduce its strains enough to make lamellar bone form there instead. This would compose this cortex mostly of woven bone in the very young and of lamellar bone in adults. CONCLUSIONS: This model assigns particular importance to the stiffness and strains of tissues (as distinguished from their strength and stresses), to the relative rates of some processes, and to responses of the skeleton's biologic mechanisms to a tissue's typical largest mechanical strains (as distinguished from their stresses).

Adult↗
PubMed1994

Perspectives: applications of a biomechanical model of the endochondral ossification mechanism.

A biomechanical model of endochondral ossification (Frost and Jee, 1994. Anat. Rec., 240:435-446) can help to explain: (1) some differences in fracture patterns in children and adults, (2) increased fractures during the human adolescent growth spurt, (3) localization of stress fractures and pseudofractures to cortical instead of trabecular bone, (4) increased bone mass in adult-acquired and childhood obesity, (5) subchondral bone densification and osteopenia in some arthroses, (6) why and where mammals lose spongiosa with aging, (7) why, as percents of the original bone stock, metaphyseal trabecular bone losses with aging usually exceed cortical bone losses, (8) why osteochondritis dissecans and aseptic necroses of bone localize in epiphyses instead of metaphyses, (9) some features of growth plate histology in rickets and the chondrodystrophies, (10) why spontaneous fractures in osteoporotic patients affect vertebral more than metaphyseal spongiosa, (11) why osteopenias develop in most chronic, debilitating diseases, and (12) why histomorphometric values can differ in iliac bone biopsies obtained by the "vertical" Jamshidi and "horizontal" Bordier-Meunier techniques.

Adolescent↗
PubMed1994

Wolff's Law and bone's structural adaptations to mechanical usage: an overview for clinicians.

Basic Multicellular Unit-based bone remodeling can lead to the removal or conservation of bone, but cannot add to it. Decreased mechanical usage (MU) and acute disuse result in loss of bone next to marrow; normal and hypervigorous MU result in bone conservation. Bone modeling by resorption and formation drifts can add bone and reshape the trabeculae and cortex to strengthen them but collectively they do not remove bone. Hypervigorous MU turns this modeling on, and its architectural effects then lower typical peak bone strains caused by future loads of the same kind to a threshold range. Decreased and normal MU leave this modeling off. Where typical peak bone strains stay below a 50 microstrain region (the MESr) the largest disuse effects on remodeling occur. Larger strains depress it and make it conserve existing bone. Strains above a 1500 microstrain region (the MESm) tend to turn lamellar bone modeling drifts on. By adding to, reshaping and strengthening bone, those drifts reduce future strains under the same mechanical loads towards that strain region. Strains above a 3000 microstrain region (the MESp) can turn woven bone drifts on to suppress local lamellar drifts but can strengthen bone faster than lamellar drifts can. Such strains also increase bone microdamage and the remodeling that normally repairs it. Those values compare to bone's fracture strain of about 25,000 microstrain.

Adaptation, Physiological↗
PubMed1993

Wolff's law: an 'MGS' derivation of Gamma in the Three-Way Rule for mechanically controlled lamellar bone modeling drifts.

The Gamma function in a model called the Three-Way Rule can predict qualitatively some responses of lamellar bone modeling drifts to defined longitudinal bone strain patterns. The derivation of Gamma in this article suggests a way to define it from in vivo longitudinal bond strain measurements. It depends on three operators called M, G and S. Let M equal +1 on any part of a bone surface (the 'study surface') where the local Magnitude of the longitudinal mechanical strains exceeds a threshold that can turn adaptive modeling drifts ON; otherwise let it equal zero. For the cross section of a bone or trabecula that intersects the study surface, let G equal +1 when the Greatest strain over the whole cross section is in tension, but -1 if it is in compression. On a study surface where M = +1, let S equal G in uniaxial loading, but +1 if the Subsurface strain gradient emerging from inside the bone to this study surface is positive, and -1 if this gradient is negative. Then the product of M x G x S yields gamma as +1, 0 or -1, and those are its only permitted values. The values would mean a mechanically induced formation drift, or no drift, or a resorption drift, respectively should begin on that study surface. Gamma can predict the drift patterns in five basic or 'principal' structural adaptations of trabeculae, cortex and whole bones to defined mechanical challenges and bone strain patterns.

Animals↗
PubMed1992

The role of changes in mechanical usage set points in the pathogenesis of osteoporosis.

Mechanical usage (MU) effects on modeling drifts and BMU-based remodeling affect bone mass in defined ways. Decreased MU stops additions of bone by modeling and increases removal of bone next to marrow by remodeling. The latter effect thins cortices and reduces trabecular number, thickness, and connectivity. Return to normal MU makes remodeling begin conserving existing bone and leaves modeling still off. Hypervigorous MU can make modeling increase bone mass during growth and makes remodeling keep conserving it in children and adults. These effects can be said to begin when typical bone strains rise through two threshold ranges, one for remodeling and a higher one for modeling. Raising the thresholds while normal MU continues should give bone a spurious disuse message, whereupon disuse effects would begin. The bone anatomic and tissue dynamic patterns in acute and chronic disuse resemble those seen in developing and acquired postmenopausal osteoporosis and in other forms of osteoporosis, too. If some hormones, drugs, and other agents increase those thresholds, this could explain such similarities.

Biomechanical Phenomena↗
PubMed1992

On the rat model of human osteopenias and osteoporoses.

The idea that rats cannot model human osteopenias errs. The same mechanisms control gains in bone mass (longitudinal bone growth and modeling drifts) and losses (BMU-based remodeling), in young and aged rats and humans. Furthermore, they respond similarly in rats and man to mechanical influences, hormones, drugs and other agents.

Adult↗
PubMed1992

Perspectives: bone's mechanical usage windows.

As mechanical usage (MU) of a bone changes from complete disuse towards maximal vigor, the biologic mechanisms that can adapt it to its MU tend to react predictably. Acute disuse can increase BMU (Basic Multicellular Unit, the remodeling 'packet') creations but reduces how much bone they form, to increase bone loss next to marrow. Normal usage reduces those creations to normal and tends to equalize their resorption and formation; this conserves bone. In mild overloading, BMUs still conserve existing bone, while modeling drifts can begin adding to and/or reshaping it. Severe overloading can increase microdamage alarmingly, its repair by BMUs too, and can cause woven bone formation, anarchic resorption and a regional acceleratory phenomenon. Those ranges of MU vigor can define four 'windows'. An adapted window should apply to healthy, normally active adult mammals, and a mild overload window to healthy, normally active growing ammals. The biologic responses in the pathologic window could explain among other things some total joint and internal fixation failures, some pathologic fractures and some bone healing and sports medicine problems.

Adaptation, Physiological↗
PubMed1991

A new direction for osteoporosis research: a review and proposal.

This article suggests why drugs that only reduce the activity of existing osteoclasts or enhance the activity of existing osteoblasts probably cannot cure the osteopenias associated with most osteoporoses. Instead they should add only limited amounts of bone, which should begin to disappear after treatment stops. That behavior depends on these facts. Different threshold ranges of mechanical bone strains control gains and losses of bone mass. One threshold controls gains by modeling drifts, and a lower one controls losses by remodeling BMUs. A drug that does not change those thresholds should limit gains (or losses) of bone during indefinitely continued treatment. Success in curing those osteopenias should require learning how to change the thresholds.

Biomechanical Phenomena↗
PubMed1990

Skeletal structural adaptations to mechanical usage (SATMU): 1. Redefining Wolff's law: the bone modeling problem.

From the nature of a bone's endload and its local surface strains, the theory computes a modeling operator, Gamma (gamma), that predicts whether mechanical factors will cause lamellar bone modeling drifts, and where and of what kind. A given mechanical bone strain history then provides a separate modeling rate function, M, to specify the rate of such modeling drifts as fractions of the largest possible ones. Multiplying the two functions, e.g., gamma.M, then predicts mechanically controlled bone modeling responses for cortical and trabecular bone, both quantitatively and qualitatively. The theory correctly predicts each of the 6 known "principal adaptations" of lamellar bone, which provide a critical test of any such theory for this organ. The theory accounts for biologic, biomechanical, and clinical-pathologic knowledge not available in Wolff's time nor accounted for by most biomechanicians since. Existing proven methods can provide all numerical data needed to satisfy the theory's mathematical equations and already suggest provisional values for most of them. Its originator views the theory as the kernel of more and better theories to come rather than a finished work, a kernel that suggests a new and in some respects novel logical framework for analysing the problems, and a kernel that invites critique, refinement, and/or exploitation by others.

Adaptation, Physiological↗
PubMed1990

Skeletal structural adaptations to mechanical usage (SATMU): 2. Redefining Wolff's law: the remodeling problem.

Basic multicellular unit (BMU)-based remodeling of lamellar bone causes bone turnover, net gains and losses of bone on some bone surfaces or "envelopes," and a remodeling space comprising bone temporarily absent due to evolving resorption spaces and incomplete refilling of them by new bone. Those features depend a) on how many new BMU arise annually, b) on how much bone each BMU has resorbed and c) formed upon its completion, and d) on how long the typical BMU takes to become completed. Because a, b, and c have limiting or maximal values in life that direct and/or indirect effects of mechanical usage of the skeleton can change, the theory presented here derives mechanical usage functions that express what fractions of those maxima a given mechanical usage history allows to happen. The theory predicts some changes in bone formation, resorption, balance, turnover, and remodeling space that depend on how remodeling responds to the vigor of a subject's mechanical usage. The theory can predict specific effects of specific mechanical challenges that experiments can test, and it fits abundant published evidence. As the kernel of a new approach to the problem it awaits critique and refinement by others. It plus the 3-way rule can redefine Wolff's law conceptually and also in mathematical and quantifiable form.

Adaptation, Physiological↗