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Biomedical subjects

H M Frost

Publications and source records attributed to H M Frost.

At least 55 records · Page 3Linked to original sources
PubMed1998

A brief review for orthopedic surgeons: fatigue damage (microdamage) in bone (its determinants and clinical implications).

Bone modeling can slowly strengthen bones to keep their strains below bone's microdamage (MDx) threshold. When that condition is satisfied the slow basic multicellular unit (BMU)-based remodeling can usually repair the little MDx that occurs anyway, and some always does. While this arrangement minimizes fatigue fractures of whole bones or trabeculae, they can still happen if: (A) drugs, disease, or dead bone impair MDx repair; (B) if bone loads increase faster than the sluggish modeling can strengthen bone to meet the new loads, and/or faster than remodeling can repair the increased MDx; (C) if a cyst, tumor, or surgery removes enough bone to let strains in the remaining bone reach or exceed the MDx threshold; (D) if abnormal properties of bone as a material cause too much MDx to repair; (E) if altered modeling and remodeling thresholds cause an osteopenia that lets normal activities cause bone strains in or above the MDx threshold range; (F) or if strains in the bone supporting a load-bearing implant reach or exceed bone's MDx threshold.

Biomechanical Phenomena↗
PubMed1998

Estrogen and bone-muscle strength and mass relationships.

The largest voluntary loads on bones come from muscles. To adapt bone strength and mass to them, special strain threshold ranges determine where modeling adds and strengthens bone, and where remodeling conserves or removes it, just as different thermostat settings control the heating and cooling systems in a house. If estrogen lowers the remodeling threshold, two things should occur. First, at puberty in girls, bone mass should begin to increase more than in boys with similar muscle strengths, owing to reduced remodeling-dependent bone losses, while gains from longitudinal bone growth and bone modeling continue normally. That increase in bone mass in girls should plateau when their muscle strength stops increasing, since their stronger bones could then reduce bone strains enough to turn modeling off, but could let remodeling keep conserving existing bone. Second, decreased estrogen secretion [or a related factor(s)], as during menopause, should raise the remodeling threshold and make remodeling begin removing that extra bone. That removal should also tend to plateau after the remaining and weaker bone lets bone strains rise to the higher threshold. Postmenopausal bone loss shows the second effects. Previously unremarked relationships in the data of a 1995 Argentine study showed the first effects. This supports the idea that estrogen can affect human bone strength and mass by lowering the remodeling threshold, and loss of estrogen would raise the threshold and help cause postmenopausal bone loss even if other factors help to do it. The Argentine study also suggested ways to study those things and the roles of muscle strength and other factors in controlling bone strength and mass in children and adult humans. Those factors included, in part, hormones, vitamins, calcium, diet, sex, race, age, medications, cytokines, genetic errors, gene expression patterns, and disease.

Absorptiometry, Photon↗
PubMed1998

Could some biomechanical effects of growth hormone help to explain its effects on bone formation and resorption?

This article suggests that growth hormone effects on bone biomechanical factors help to cause changes in osteoblastic and osteoclastic activities in gigantism and growth-hormone-deficiency states. The suggestion stands partly on the following evidence. (1) In growing mammals, acute partial disuse decreases or stops longitudinal bone growth and periosteal bone formation and increases in outside bone diameter. Yet, in metaphyseal spongiosa, bone resorption and formation continue and net bone losses usually increase. (2) The same pattern of findings occurs in very young rats 5 weeks after hypophysectomy, accompanied by cessation of body and muscle growth and also by reduced physical activity. (3) Another study reduced muscle forces on hindlimb bones by suspending rats by the tail, and found that supplemental growth hormone for 80 days increased hindlimb muscle mass but not hindlimb periosteal bone formation. (4) Such facts support the previous suggestion, which might supplement other ideas about this hormone's modes of action on bone physiology. They include the possibility that the hormone can modulate the responsiveness of bone's biologic mechanisms to mechanical and other nonmechanical influences.

Animals↗
PubMed1998

On new opportunities for absorptiometry.

Mechanical loads cause bone strains; and muscle forces, not body weight, cause the largest strains. The strains help to control the effects of bone modeling and remodeling on bone strength and "mass." When strains exceed a threshold range, modeling increases bone strength and "mass." When strains stay below a smaller threshold range, remodeling begins removing bone next to marrow. As a result, increasing muscle strength increases bone strength and "mass," and decreasing muscle strength decreases bone strength and "mass." Estrogen apparently lowers the remodeling threshold, which reduces bone losses. Loss of estrogen raises that threshold to cause losses of bone next to marrow. Such facts help to explain: 1. Bone loss in aging adults. 2. An increase in bone "mass" in girls at menarche. 3. The loss of bone during menopause. 4. The greater bone "mass" in obese than in slender subjects, and in weightlifters than in marathon runners. 5. And the pathogenesis of physiologic osteopenias and true osteoporoses. Thus new standards are needed for the relationships between bone and muscle strengths, and as functions of sex, age, race, disease, endocrine status, nutrition, vitamin and mineral intakes, medications, puberty, and menopause. Obtaining those standards and studying such relationships provide many new opportunities for studies that involve dual energy X-ray absorptiometry (DXA) and peripheral quantitative computer tomography (pQCT) and, perhaps some day, ultrasound and magnetic resonance imaging (MRI) techniques.

Journal Article↗
PubMed1997

Indirect way to estimate peak joint loads in life and in skeletal remains (insights from a new paradigm).

BACKGROUND: Bone adapts its strength and cross-sectional amount to the loads on it in now partly known ways. This makes it possible to estimate the unit loads on joint surfaces by an indirect method. METHODS: In essence, multiply the usual largest allowed compression load on a unit cross section area of epiphyseal trabecular bone (now approximately known), by the cross sectional amount of that bone that supports a unit area of the joint surface (partly known and readily measured by histomorphometry). This would equal the usual largest compression unit load on both the joint surface and the articular cartilage supported by that trabecular bone. RESULTS: Suggested typical peak unit loads on synovial joint surfaces in different joints and/or parts of joints could range from approximately 2 up to approximately 50 megapascals. CONCLUSIONS: Besides its use in studies of joint development, physiology and osteoarthritis in living subjects, this method could estimate muscle strength and joint loads from skeletal remains in anatomical, anthropologic, forensic-pathological, and even paleontologic studies.

Anthropology↗
PubMed1997

Defining osteopenias and osteoporoses: another view (with insights from a new paradigm).

This article suggests classifying "osteoporoses" by their biomechanical pathogenesis instead of by their severity or their accompanying medical conditions. (A) In a "true osteoporosis," bone fragility would increase to such an extent that normal physical activity would cause spontaneous fractures and/or a bone pain syndrome, mainly affecting the spine; however, falls could also cause extremity bone fractures. (B) In a "physiologic osteopenia," reduced bone strength and "mass" would fit correspondingly reduced physical activities and muscle strength so well that fractures would not happen without falls or other injuries. Those fractures would affect extremity bones more than the spine. (C) In "combination states," features of (A) and (B) would combine variably. (D) "Transient osteopenias" would occur while serious injuries heal. After healing, transient osteopenias usually resolve without treatment, and fractures occur only from injuries. While an osteopenia's severity usually affects the risk of fracture, its pathogenesis could strongly affect the treatment needed for prevention or cure.

Biomechanical Phenomena↗
PubMed1997

On our age-related bone loss: insights from a new paradigm.

Bone strength and "mass" normally adapt to the largest voluntary loads on bones. The loads come from muscles, not body weight. Bone modeling can increase bone strength and "mass," bone remodeling can conserve or reduce them, and each can turn ON and OFF in response to its own threshold range of bone strains. During growth, the loads on bones from body weight and muscle forces increase, and modeling correspondingly increases bone strength and "mass." In young adults those loads usually plateau, so bone strength can "catch up" and modeling can turn OFF. Meanwhile remodeling keeps existing bone. After about 30 years of age, muscle strength usually decreases. In aging adults this would put bones that had adapted to stronger young-adult muscles into partial disuse and make remodeling begin to reduce their strength and "mass," as disuse regularly does in experimental situations in other mammals, both growing and adult. Those changes associate strongly with the size of the bone strains caused by the loads on bone. While nonmechanical effects associated with aging should contribute to that age-related bone loss too, a new skeletal paradigm suggests the above mechanical influences would dominate control of the process in time and anatomical space.

Aging↗
PubMed1997

Biomechanical control of knee alignment: some insights from a new paradigm.

A chondral growth force response curve suggests how longitudinal bone growth at growth plates responds to compression loads. Between zero load and some limit, increasing loads increase growth. Above that limit, further increases in compression can decrease growth, and large enough compression loads can stop it. In the valgus-varus sense, in a child's knee these responses would tend to make its growth plates and the joint align perpendicularly to the time-averaged compression loads on them and tend to correct small malalignments but make large malalignments become worse. Combined with effects of the regional acceleratory phenomenon, in children these responses can also explain some cases of postfracture knee valgus and its subsequent spontaneous correction.

Biomechanical Phenomena↗
PubMed1997

Osteoporosis treatment: quo vadis? (A brief overview).

What we formerly called osteoporosis includes four conditions with an osteopenia: A) osteopenias usually due to mechanical disuse, where injuries cause fractures, and in limb bones more than the spine; B) osteopenias with such fragile bone that normal activities instead of injuries can cause fractures and/or bone pain, and in the spine more than limb bones; C) a group that combines features of (A) and (B); D) temporary osteopenias while major fractures, burns or other injures heal. If belatedly, we now realize our past failure to view those conditions as separate entities compromised many past studies of the prevalence, diagnosis and ways to prevent and cure each of them. That failure also compromised many past explanations of the nature, pathogenesis and natural course of "osteoporosis", and much of the related research. This caused some confusion as well as controversies about illusory instead of genuine issues. Controlling existing osteoblasts and osteoclasts with drugs has not prevented or cured those conditions. That will require controlling the modeling drifts and remodeling BMUs that create those cells. Modeling can increase bone mass and strength, remodeling can conserve or reduce them, and neither can provide the other's functions. During normal mechanical usage modeling is OFF and remodeling works in its "conservation mode" to keep existing bone. In disuse, modeling stays OFF while remodeling works in its "disuse mode" to remove bone and cause an osteopenia. Most natural nonmechanical agents (Table 1) can help or hinder those mechanical responses, but cannot duplicate or override them. Wrist and hip fractures from falls cause the most serious problems associated with these conditions. Those fractures begin in the cortex of epiphyseal-metaphyseal regions of limb bones. They never begin in trabecular bone and rarely in the shafts of long bones. They never begin in the trabecular bone and rarely in the shafts of long bones. Since a bone's strength depends on its shape and size (architecture) as well as on the amount of bone in it (bone mineral "density" and content), treatments intended to prevent or cure these conditions should strengthen the above cortex, and absorptiometric studies should begin to account for both bone architecture and bone tissue content. "Bone anabolic" agents (parathyroid hormone and some prostaglandins) can make modeling add bone to normal and osteopenic skeletons, but when the treatment stops remodeling begins removing that bone. "Antiremodeling agents" (including estrogen and many bisphosphonates) can make remodeling tend to keep existing bone, but when such treatments stop remodeling usually resumes removing bone. Combining anabolic agents with antiremodeling agents offers an exceptionally promising prospect of effective prevention and cure of the above osteopenias. Practical problems make this approach not yet ready for human use, but it soon could be.

Adult↗
PubMed1996

Perspectives: a proposed general model of the "mechanostat" (suggestions from a new skeletal-biologic paradigm).

This provisional general model for the skeleton's mechanostat spans the biologic "distance" between the organ and macromolecule. It could apply to bone, cartilage and fibrous tissue, and to bones, joints, ligaments and other organs made wholly or in part from the basic tissues. It suggests where small things such as a cytokine effect on some cell should fit in the overall scheme of skeletal physiology. It proposes that interlocking negative feedback loops provide mechanical-usage-dedicated message traffic routes on which nonmechanical agents could act to optimize or impair postnatal skeletal adaptations to varied mechanical and nonmechanical challenges, and treatments of disease too. It suggests that future research must try to understand the mechanostat's cell- and molecular-biologic roots.

Animals↗
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↗