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H M Frost

Publications and source records attributed to H M Frost.

At least 37 records · Page 2Linked to original sources
PubMed2000

Does bone design intend to minimize fatigue failures? A case for the affirmative.

Threshold strain ranges help to control the ability of modeling to increase bone strength and "mass" and the ability of remodeling to conserve or decrease them. Whether expressed as strains or stresses, the probable remodeling threshold of bone (MESr) lies below its modeling threshold (MESm), which lies below its operational microdamage threshold (MESp), which lies well below its ultimate strength (Fx). Given normal modeling and remodeling potentials, that arrangement should tend to cause whole-bone strength and stiffness to keep typical peak bone strains ("E") from voluntary activities from exceeding bone's modeling threshold and therefore from reaching its microdamage threshold. Satisfying that laddered "MESr < "E" < MESm << MESp <<< Fx" arrangement should minimize fatigue failures of bones, which might be at least one purpose of normal bone design. That arrangement would have practical implications that include, in part, the following. (A) It could make healthy young adult bones about six times stronger than needed for the largest voluntary loads they usually carry. (B) It suggests a biomechanical pathogenesis for different kinds of osteoporosis. (C) It suggests design criteria that load-bearing bone implants and endoprostheses should satisfy to endure their voluntary mechanical usage. (D) It also suggests features that future models of mechanical loading effects on bone strength, architecture, and "mass" might incorporate.

Bone and Bones↗
PubMed2000

The Utah paradigm of skeletal physiology: an overview of its insights for bone, cartilage and collagenous tissue organs.

In a 1960 paradigm of skeletal physiology, effector cells (chondroblasts, fibroblasts, osteoblasts, osteoclasts, etc.) regulated by nonmechanical agents wholly determined the architecture, strength, and health of bones, joints, fascia, ligaments, and tendons. Biomechanical and tissue-level phenomena had no roles in that paradigm. Subsequent studies and evidence slowly revealed skeletal tissue-level mechanisms and their functions, including biomechanical ones, as well as "game rules" that seem to govern them. That slow discovery process found that effector cells are only parts of tissue-level mechanisms, as kidney cells are only parts of nephrons and wheels are only parts of cars. Normally all those things help to determine skeletal architecture, strength, and health, and adding them to the 1960 paradigm led to the still-evolving Utah paradigm of skeletal physiology that concerns, in part, how load-bearing skeletal organs adapt to the voluntary mechanical loads on them. That caused controversies this article does not try to resolve; instead, it describes some issues they concern. In that regard, controversy can depend on how one assesses the relevance of facts to a problem more than on their accuracy. If a paradigm added new facts to a former one and the new one's advocates viewed all those facts as relevant, but the former's advocates questioned the relevance of some of the new facts, their views about a problem could differ even though each view depended on accurate facts. Readers would make their own judgments about the bearing of those ideas on this article's content.

Bone and Bones↗
PubMed2000

Erect bipedal stance exercise partially prevents orchidectomy-induced bone loss in the lumbar vertebrae of rats.

This study investigates the responses of the fourth and fifth lumbar vertebral bodies of 6-month-old male Sprague-Dawley (SD) rats to orchidectomy (orx) and to erect bipedal stance for feeding for 12 weeks in specially designed raised cages (RC) for which the heights were raised from 20 cm to 35.5 cm. A total of 30 rats were divided into groups of: baseline; sham + housed in normal height cage (NC); orx + NC; sham + RC; and orx + RC. Bone histomorphometry was performed on the triple-labeled undecalcified fourth sagittal (LVL-4) and fifth transverse (LVX-5) sections. We found that orchidectomy induced high-turnover trabecular and cortical bone loss in the lumbar vertebrae. Forcing the rats to rise to erect stance for feeding reduced trabecular and cortical bone loss caused by orx. Apparently, depressing the elevated bone resorption next to the marrow induced by orx, and stimulating bone formation at the ventral periosteal surfaces, caused these effects. Orchidectomy and raised cage had similar effects on the two vertebrae except that the percentage of trabecular bone loss was greater in the LVL-4 than in LVX-5, and that bipedal stance exercise increased the total tissue area and mineral apposition rates (0-80 day interval) of ventral periosteal and dorsal endocortical surfaces of LVX-5 to a greater extent than it did in LVL-4. Such findings suggest that forcing rats to rise to an erect bipedal stance for feeding helps prevent loss of trabecular and cortical bone "mass," and presumably bone strength, in orchidectomized rats. This method also provides an inexpensive, noninvasive, reliable model to increase in vivo vertebral loading in rats that is similar in humans.

Animals↗
PubMed2000

Muscle, bone, and the Utah paradigm: a 1999 overview.

The still-evolving Utah paradigm of skeletal physiology supplements former ideas about the control of postnatal bone strength and "mass" in health and disease, on earth and in orbit, and as functions of physical activities including sports. In its view, peak muscle forces on bone dominate control of the biologic mechanisms that control changes in our postnatal whole-bone strength and mass. This contrasts with former ideas that chiefly nonmechanical factors dominate that control and mechanical factors have little influence on it. The newer view begs the question of how such a bone-muscle relationship would work, and the Utah paradigm offers plausible explanations for that. Whereas many biomechanicians, orthopedists, and sports medicine experts might find the newer view sensible, some people in other disciplines may not. This article summarizes some evidence that support the Utah paradigm and the above-stated view and explores some of the paradigm's features and implications.

Bone Diseases, Metabolic↗
PubMed2000

Growth hormone and osteoporosis: an overview of endocrinological and pharmacological insights from the Utah paradigm of skeletal physiology.

Multidisciplinary advances in skeletal physiology offer a new paradigm for the effects of growth hormone (GH) and other agents on bone and osteoporosis. The still-evolving Utah paradigm of skeletal physiology supplements earlier ideas with later discovered roles of the skeleton's tissue-level 'nephron equivalents' and muscle strength in skeletal development, physiology and disorders. This article summarizes how these factors could influence the effects of GH on bone strength and bone 'mass', and the use of GH in the treatment of osteoporoses. Although the cellular and molecular biological mechanisms involved remain obscure, the associated cascades of cellular, genetic and biochemical processes and molecules should offer many opportunities to find or design agents that have medically useful effects on bone and muscle without giving rise to unwanted side-effects.

Biomechanical Phenomena↗
PubMed2000

Making rats rise to erect bipedal stance for feeding partially prevented orchidectomy-induced bone loss and added bone to intact rats.

The objectives of this study were to investigate the different effects on muscle mass and cancellous (proximal tibial metaphysis [PTM]) and cortical (tibial shaft [TX]) bone mass of sham-operated and orchidectomized (ORX) male rats by making rats rise to erect bipedal stance for feeding. Specially designed raised cages (RC) were used so that the rats had to rise to erect bipedal stance to eat and drink for 12 weeks. Dual-energy X-ray absorptiometry (DEXA) and peripheral quantitative computerized tomography (pQCT) were used to estimate the lean leg mass and bone mineral. Static and dynamic histomorphometry were performed on the triple-labeled undecalcified sections. We found that making the intact rats rise to erect bipedal stance for feeding increased muscle mass, cortical bone volume, and periosteal bone formation. Orchidectomy increased net losses of bone next to the marrow by increasing bone turnover. Making the ORX rats rise to erect bipedal stance increased muscle mass, partially prevented cancellous bone loss in the PTM, and prevented net cortical bone loss in TX induced by ORX by depressing cancellous and endocortical high bone turnover and stimulating periosteal bone formation. The bone-anabolic effects were achieved mainly in the first 4 weeks in the PTM and by 8 weeks in the TX. These findings suggested that making the rats rise to erect bipedal stance for feeding helped to increase muscle mass and cortical bone mass in the tibias of intact rats, increase muscle mass, and partially prevented cancellous and net cortical bone loss in ORX rats.

Animals↗
PubMed2000

The "muscle-bone unit" in children and adolescents: a 2000 overview.

In former views hormones, calcium, vitamin D and other humoral and nonmechanical agents dominated control of postnatal bone strength (and "mass") in children and adolescents. However later evidence that led to the Utah paradigm of skeletal physiology revealed that this control depends strongly on the largest mechanical loads on bones. Trauma excepted, muscles cause the largest loads and the largest bone strains, and these strains help to control the biological mechanisms that determine whole-bone strength. That makes the strength of children's load-bearing bones depend strongly on growing muscle strength and how bones respond to it. Most hormones and other nonmechanical agents that affect bone strength can help or hinder that "bone strength-muscle strength" relationship but cannot replace it. In addition some agents long thought to exert bone effects by acting directly on bone cells, affect muscle strength too. In that way they could affect bone strength indirectly. Such agents include growth hormone, adrenalcorticosteroid analogs, androgens, calcium, genes, vitamin D and its metabolites, etc. Thus bone and muscle do form a kind of operational unit. It is part of the Utah paradigm that supplements earlier views with later evidence and concepts. The paradigm explains how the "bone strength-muscle strength" relationship works. This article provides an overview of that physiology, and some of its implications for pediatric endocrinologists.

Adolescent↗
PubMed2000

The Frozen Shoulder syndrome plus other evidence and the Utah Paradigm suggest the syndrome's pathogenesis and new targets for collagenous tissue research.

Sometimes naturally occurring disorders combined with other evidence can provide a "virtual laboratory" exercise that answers old questions and reveals new problems and questions that need appropriately "targeted" research. This article provides an example that involves the frozen shoulder syndrome, for which varied evidence and insights of the still-evolving Utah paradigm of skeletal physiology suggest a plausible pathogenesis. It involves organ- and tissue-level vital-biomechanical features of collagenous tissues that need systematic study. The features include diametric modeling, irreversible creep, a creep compensation mechanism, the regional acceleratory phenomenon, and the signals and thresholds that can help to determine how and where those things act in anatomical space. Such features participate in many extraskeletal as well as skeletal disorders, so the frozen shoulder syndrome can provide an instructive model of them. As an aside, in over 120 consecutive cases managed by me since 1956 this syndrome resolved completely in six or less months without treatment. That shows this untreated syndrome is usually if not always self limited. While I respect the doubts of colleagues who do not agree yet, that experience shows the conclusion is correct.

Journal Article↗
PubMed2000

Why the ISMNI and the Utah paradigm? Their role in skeletal and extraskeletal disorders.

Besides bringing problems, aging can let the mind's eye see more clearly than before, and it can let us express ourselves better. As age, experience and common sense examine today's skeletal medicine and surgery two questions keep popping up: A) How did we fail?; B) How to make it better? The Utah paradigm of skeletal physiology and the seminal ISMNI offer some answers, but exploiting them faces problems. Problem #1: By 1960 all clinicians and physiologists 'knew' (as the ancients 'knew' this world is flat) that effector cells controlled solely by nonmechanical agents explain all skeletal physiology and disorders ('effector cells' include osteoblasts, osteoclasts, chondroblasts and fibro-blasts). Or, nonmechanical agents -->cell level -->organ and intact subject. Adding later-discovered information to that 1960 view led to the Utah paradigm, which reveals the formerly hidden tissue-level 'dimension' of skeletal physiology. It builds on this idea: (mechanical + nonmechanical agents) -->(tissue level + cell level) --> organ and intact subject. The paradigm assigns great influence of neuromuscular physiology and physical activities on skeletal architecture, strength and mechanical competence. It also exposes flaws in many older views so controversies arise. Problem #2: The Utah paradigm and Wegner's concept of plate tectonics in geology seem alike in that each is valid but came before its time, so others fought it. They differ in this: The fight about Wegner's idea is over, but for the Utah paradigm and the ISMNI it just began. Hence more controversies. Nevertheless: A growing minority realizes that paradigm provides a far better base to build on than its antecedents, and since it keeps evolving as more evidence comes in it could endure for some decades. Yet very few realize this: It and the ISMNI have important implications for fields besides biomechanics and orthopaedics. Examples include anatomy, cardiovascular disease, dentistry, endocrinology, family medicine, gastroenterology, general surgery, genetics, gerontology, gynecology, maxillofacial surgery, neurology, neurosurgery, nutrition, ophthalmology, pathology, pediatrics, physical medicine and rehabilitation, plastic surgery, radiology, rheumatology, space and sports medicine, and urology. Quite a list! For the italicized questions above this article offers answers, of which its conclusion distills an essence.

Journal Article↗
PubMed1999

Joint anatomy, design, and arthroses: insights of the Utah paradigm.

This model of joint design argues 1) that excessive fatigue damage (MDx) in articular cartilage collagen can be the "final cause" of an arthrosis; 2) that known responses of a growing joint's anatomy and geometry, and modeling and maintenance activities, to mechanical loads minimize that cause and thus arthroses; 3) and many biomechanical, biochemical, cell-biologic, genetic and traumatic "first causes" of arthroses could lead to that final cause. The model depends partly on the following facts (marked by a single asterisk) and ideas (marked by a double asterisk). A) During growth a joint's total loads can increase over 20 times without causing an arthrosis, yet in adults an equal loading increase would cause one. B) Fatigue damage (MDx) occurs in joint tissues, larger strains increase it, and minimizing strains reduces it. C) Bone can repair amounts of MDx below an "MDx threshold," but larger amounts can escape repair and accumulate. The model assumes articular cartilage has similar features. D) Bone modeling makes bones strong enough to keep their strains below bone's MDx threshold and minimize MDx. Chondral modeling shapes and sizes joints during growth; that would keep articular cartilage strains below the chondral MDx threshold to minimize chondral MDx and arthroses. Normal chondral modeling nearly stops in adults, which might explain point A above. E) Throughout life maintenance activities preserve optimal physical, chemical and biologic properties of a joint's tissues. To past emphases on the biochemical, genetic, cellular and molecular biologic features of adult joint physiology, this model adds organ-level, tissue-level and vital-biomechanical features of growing joints that invite study and understanding at lower levels of biologic organization.

Animals↗
PubMed1999

Changing views about 'Osteoporoses' (a 1998 overview).

Recent realizations have begun to change how 'osteoporoses' are diagnosed, managed and studied. This article explains the nature and basis of some resulting controversies, chiefly for clinicians who manage such patients but do not participate in resolving those controversies. Currently the size of a bone 'mass' deficit serves to diagnose 'osteoporosis', but recently clarified physiology suggests at least three different kinds of osteoporosis could occur in people with identical bone 'mass' deficits. Indeed, they do occur. (a) In one kind, people have less bone than 'normal' but no bone problems unless they sustain injuries. Most of their resulting fractures, usually from falls, affect extremity bones. This condition can affect children, men and women. (b) In a second kind an osteopenia exists in which voluntary physical activities (not injuries) cause spontaneous fractures and/or bone pain, mainly in the spine, more often in women than men and seldom in children (osteogenesis imperfecta excepted). (c) A third kind combines features of the first two. As for the physiology involved in those affections, bone modeling can increase bone strength and 'mass', while BMU (Bone Multicellular Unit)-based bone remodeling can reduce them. Mainly bone strains control those two activities and muscles cause the largest strains, so muscle strength should strongly influence bone modeling, remodeling, strength and 'mass'. If so chronic muscle weakness should usually cause an osteopenia and weakened bones. Excessive amounts of fatigue damage or microdamage can also weaken bones. From that physiology one could argue that chiefly chronic muscle weakness instead of an intrinsic bone disorder would cause (a), while intrinsic but still enigmatic modeling and remodeling disorders would cause (b), and (c) could combine features of both conditions. If so, these ideas could have significant effects on the future criteria used to diagnose osteoporoses and osteopenias, on how they are studied in the clinic and laboratory, and on how they are prevented or, if they occur, are managed.

Adolescent↗
PubMed1999

Why do bone strength and "mass" in aging adults become unresponsive to vigorous exercise? Insights of the Utah paradigm.

Trauma excepted, muscle forces cause the largest loads on bones and the largest bone strains. In children, steadily increasing muscle strength increases bone loads and strains above a modeling threshold, which allows modeling to increase bone strength and "mass" and conservation-mode remodeling to retain existing bone. As a result, bone strength and "mass" both increase. In young adults, muscle strength plateaus, so bone strength can increase enough to reduce strains below the modeling threshold, turn modeling off, and also plateau. Those strains still exceed the lower remodeling threshold, so conservation-mode remodeling retains existing bone. Most aging adults lose momentary muscle strength, so their bone strains fall toward the remodeling threshold. That drop leaves modeling off and switches remodeling to its disuse mode to begin removing bone next to marrow, contributing to the well-known age-related loss of bone. Although "vigorous" exercise by aging adults can raise strains above the remodeling threshold to turn conservation-mode remodeling back on and reduce or stop further bone losses, causing the much larger strains needed to reach or exceed the modeling threshold would require larger increases in momentary muscle strength and muscle mass than most such adults could achieve. Thus, exercises that can readily increase bone strength and "mass" in children and adolescents (in whom modeling is already turned on) only seem to reduce bone loss in aging adults. This difference makes their bones seem partly unresponsive to physical exercise. This effect would occur in addition to possible nonbiomechanical explanations that others have suggested for the phenomenon.

Adaptation, Physiological↗
PubMed1999

On the trabecular "thickness"-number problem.

The decrease in trabecular number with aging and in osteoporosis seems to be naturally irreversible. In one view the resulting loss of bone strength would be irreversible too, but in another view the remaining trabeculae could increase their strength, chiefly by thickening. Whether that can occur has become important for osteoporosis research and management as well as for some biomechanical issues. This article reviews evidence and ideas that concern that matter. It suggests why the second view could be correct although previous studies did not detect it. However, that view still needs the kind of proof the general skeletal science community could accept.

Aging↗
PubMed1999

On the estrogen-bone relationship and postmenopausal bone loss: A new model.

In this model of estrogen effects on bone, a postulated mediator mechanism in marrow would affect modeling and remodeling only of bone next to or close to it. That mediator mechanism could sense estrogen. In response to that hormone, it would let remodeling of bone next to marrow proceed in its conservation mode. This would minimize losses of that bone and tend to prevent an osteopenia. But acute estrogen deficiency would make that mechanism switch remodeling of bone next to marrow to its disuse mode. Meanwhile, conservation-mode remodeling would continue for haversian and subperiosteal bone. The resulting losses of bone next to marrow would expand marrow cavities, thin cortices, and reduce trabecular bone "mass," but would not reduce outside bone diameters. That scheme could explain the osteopenia that follows natural or experimental estrogen deficiency in mammalian females. If so, as estrogen secretion rises in girls at puberty they should begin accumulating more bone next to marrow. They do. Also if so, at menopause women should begin to lose that bone. They do. Those effects would exist in addition to known effects of estrogen on existing osteoclasts and osteoblasts.

Adolescent↗
PubMed1998

Personal experience in managing acute compression fractures, their aftermath, and the bone pain syndrome, in osteoporosis.

Recovery from acute symptomatic vertebral compression fractures in osteoporosis patients can be said to occur in three broad stages. For over three decades the author managed them in the following way. In the 3-week-long acute stage after the fracture, the patient usually stayed in bed for 4-8 days until able to turn easily from side to side. Then a back support was provided and the patient was allowed up for frequent but brief intervals. In the following approximately 10-week-long healing stage, the patient lay down for 20 min every 2 h (the Intermittent Horizontal Rest Regimen or IHRR). Patients who developed a subsequent lordotic low back pain stage did the IHRR for a further 10 weeks. In the uncommon bone pain syndrome, doing the IHRR for 10 weeks, or occasionally longer, also relieved pain. When the IHRR failed to provide early pain relief in a compliant patient, other causes of the pain were sought and were usually found.

Acute Disease↗
PubMed1998

Osteoporoses: a rationale for further definitions?

Bone's biologic mechanisms adapt it to meet the needs of its mechanical usage and muscle strength. Modeling by drifts can increase bone strength and "mass," BMU-based remodeling can conserve or reduce them, and neither can do the other's work. Under increasing forces on bone, modeling increases bone strength and "mass" and remodeling maintains the extra bone. In disuse, modeling turns OFF and remodeling reduces bone strength and "mass" to cause osteopenia. Osteopenia increases bone fragility as does bone microdamage, and they can coexist. Too little bone for one's mechanical usage and muscle strength can cause spontaneous fractures and/or bone pain. The bone-loss and tissue-dynamic patterns in acute and chronic disuse strongly copy the patterns in developing and established osteopenias in known medical conditions. Such things suggest that at least three osteoporosis variants can occur: (1) in physiologic osteopenias, bone strength and "mass" would decrease to correspond to reduced muscle strength and physical activity so that spontaneous fractures and bone pain would not occur. An intrinsic bone disorder would not cause this osteopenia, and fractures would only follow injuries, usually of extremity bones. (2) In "true osteoporosis," bone strength and "mass" could not meet the needs of muscle strength and physical activities, so that spontaneous fractures and/or bone pain would occur, mainly in the spine. An intrinsic bone disorder would cause this affection. Of course, injuries could fracture extremity bones too. (3) Features of (1) and (2) could combine variably in "combination states." These proposals have implications for the diagnosis, management, and study of the osteoporoses.

Animals↗