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H M Frost

Publications and source records attributed to H M Frost.

At least 91 records · Page 5Linked to original sources
PubMed1989

Transient-steady state phenomena in microdamage physiology: a proposed algorithm for lamellar bone.

This algorithm suggests that in steady states the momentary burden of unrepaired microdamage (MDx) in lamellar bone equals the rate of creation of new MDx multiplied by the time taken to repair a locus of MDx completely in the biomechanical sense. That "repair period" equals about 0.6 years in healthy human adults. When MDx production suddenly increases, the momentary MDx burden begins to increase too, and does so for a time equal to the repair period and in proportion to the increased MDx production. After the repair period elapses, the momentary MDx would tend to reach and stay at a maximum value as long as increased MDx production continued. Prolonging the repair period, preventing the creation of new remodeling units to repair MDx, or delaying mineralization of the new bone made by those units would also increase MDx burdens. Reducing MDx production or the repair period, or accelerating the creation of new modeling units would have the opposite effects on the momentary MDx burden but would also go through a transient phase before developing the new steady state conditions. Exploiting these relationships quantitatively and experimentally requires expressing them mathematically and using for the terms in any equations things one can define logically and measure practically. Accordingly, the article suggests a special definition of a unit amount of microdamage, how to measure it, and simple algebra and equations for calculating some effects of microdamage on the biologic system.

Algorithms↗
PubMed1989

Some effects of basic multicellular unit-based remodelling on photon absorptiometry of trabecular bone.

This article offers algorithms and an algebra for estimating effects of bone turnover, remodelling space, undermineralized bone and trabecular surface-to-volume ratio effects on trabecular bone mass estimation by photon absorptiometry. From published histomorphometric data and other evidence the algorithms suggest the amount of mineral in a given bone sample can suggest to absorptiometry an amount of bone that differs from the truth by over 40% in the extreme, and more commonly by 5-15%. They suggest that by reducing a bone's global mineral content high bone turnover causes underestimation of true bone mass. They suggest that by letting mineral return to the remodelling space and undermineralized bone, reduced bone turnover causes apparent gains in bone mass. The commonly suggested 5-15% magnitude of such errors exceeds those assumed in the past. The algorithms suggest that after a challenge to remodelling those bone mineral changes can take from 6 months to over 3 years to reach steady states. Those features could explain why many osteoporosis treatments judged effective from initial absorptiometric evidence failed when used for long periods in patients. Finally the algorithms suggest that a real increase in ideal bone volume can even appear to absorptiometry as no gain or an initial loss, which has already happened in two human experiments.

Bone Development↗
PubMed1989

The biology of fracture healing. An overview for clinicians. Part I.

The bone healing process normally unites fractures, arthrodeses, osteotomies, and bone grafting operations. The process normally proceeds in successive stages named the fracture, granulation, and modeling/remodeling stages. A separate regional acceleratory phenomenon speeds up each of the other stages. The osteoclast and osteoblast cells that make intercellular substances of each stage do not exist in sufficient numbers to heal the bone at the moment of fracture or operation. They are made by local multicellular mediator mechanisms that contain precursor and supporting cells, capillaries, lymph, and innervation, plus local autocrine and paracrine regulation. Under the influences of local and systemic agents, these mediator mechanisms determine whether new local osteoclasts and osteoblasts will appear, in addition to when, where, how many, what kind, and for how long. Errors in those functions can then lead to several kinds of retarded or otherwise abnormal bone healing that will be discussed in Part II of this work.

Fractures, Bone↗
PubMed1989

The biology of fracture healing. An overview for clinicians. Part II.

Bone healing problems can be divided into: technical failures, when treatment problems have impaired normal biologic potential; biologic failures, when biologic malfunctions have made the correct treatment ineffective; and combinations of the two. Biologic failures include inadequate callus formation or lack of a normal regional acceleratory phenomenon (RAP), normal modeling or remodeling, or maldifferentiation of the healing tissues, plus combinations. The most common biologic failures involve the inability to form callus and/or a normal RAP. When an inadequate RAP combines with inadequate callus production, then chronic infection, nonunion, multiple failed bone grafts and fixation procedures, and even amputation can ensue. Accumulating evidence suggests that most biologic failures stem from problems attributable to mitogens, differentiating and priming agents, growth factors, and other labile biochemical and biophysical messengers and signals in the region of the fracture itself. The ability of bone to heal can differ in different parts of the bony skeleton at a given moment. Until the basic causes of such problems can be corrected, present-day clinicians must manage them by presently available treatments while conducting research that might resolve them. The causes of most biologic failures probably act within the first weeks after the fracture, although it may take months for clinical roentgenograms to show their effects.

Bony Callus↗
PubMed1987

Bone "mass" and the "mechanostat": a proposal.

The observed fit of bone mass to a healthy animal's typical mechanical usage indicates some mechanism or mechanisms monitor that usage and control the three longitudinal growth, bone modeling, and BMU-based remodeling activities that directly determine bone mass. That mechanism could be named a mechanostat. Accumulated evidence suggests it includes the bone itself, plus mechanisms that transform its mechanical usage into appropriate signals, plus other mechanisms that detect those signals and then direct the above three biologic activities. In vivo studies have shown that bone strains in or above the 1500-3000 microstrain range cause bone modelling to increase cortical bone mass, while strains below the 100-300 microstrain range release BMU-based remodeling which then removes existing cortical-endosteal and trabecular bone. That arrangement provides a dual system in which bone modeling would adapt bone mass to gross overloading, while BMU-based remodeling would adapt bone mass to gross underloading, and the above strain ranges would be the approximate "setpoints" of those responses. The anatomical distribution of those mechanical usage effects are well known. If circulating agents or disease changed the effective setpoints of those responses their bone mass effects should copy the anatomical distribution of the mechanical usage effects. That seems to be the case for many agents and diseases, and several examples are discussed, including postmenopausal osteoporosis, fluoride effects, bone loss in orbit, and osteogenesis imperfecta. The mechanostat proposal is a seminal idea which fits diverse evidence but it requires critique and experimental study.

Animals↗
PubMed1987

Osteogenesis imperfecta. The set point proposal (a possible causative mechanism).

The minimum effective strain (MES) constitutes a threshold that separates biomechanically acceptable from unacceptable strains on growing bone and fibrous tissues. Strains above that threshold affect modeling and remodeling activities in ways that change the size and configuration of growing bones, tendons, ligaments, and fascia to fit their new mechanical usage and return their strains to the threshold level. Were that threshold set too high from birth, the effects of normal function on remodeling and modeling should lead to thin fibrous tissue structures, to slender, osteopenic diaphyses and spongiosa, and to increased fragility. Those and other predictable set point effects fit so precisely many of the known hard and soft tissue abnormalities of osteogenesis imperfecta patients, that an elevated MES set point may be a heretofore unrecognized basic pathogenetic factor in that disease.

Animals↗
PubMed1985

The pathomechanics of osteoporoses.

The disease osteoporosis is a manifestation of osteopenia and mechanical incompetence. The osteopenia (reduced bone tissue volume) can follow insufficient bone accumulation during growth, secondary to abnormalities in cortical bone modeling and/or remodeling of spongiosa. Or it can follow pathologic bone losses due to altered activation of bone remodeling units and to the special bone-balance-determining delta B X BMU function. Combinations of the above can occur. Mechanical incompetence (fracture and/or bone pain during normal mechanical usage) is due partly to the osteopenia, which reduces bone strength to 90% to occasionally 40% of normal. However, even 40% of normal strength should leave bones with approximately five times the strength needed to withstand maximum normal mechanical loads. Further weakening of osteoporotic bone to 10% of normal or less is due to accumulations of mechanical microdamage, which increase when less bone still carries normal loads. Microdamage also accumulates because malfunctions of the remodeling mechanism that normally repairs it occur consistently in most osteoporoses. Thus microdamage physiology emerges as a major feature of the pathophysiology of the osteoporoses. Future research must find what controls it in life and how to reduce it for medical needs.

Biomechanical Phenomena↗
PubMed1983

The skeletal intermediary organization.

This review offers a synthesis of the intermediary organization (IO) of the skeleton. The multicellular units of its lowest level have a common plan, appropriate variations of which then create simple bony, chondral, dental, and fibrous tissues. The more complex higher IO entities then cause those tissues to grow, organize, and model into organs and then maintain the physiological and mechanical competence of those organs. The varied IO units have indivisible quantum properties which isolated cells lack but which, when summed in bulk at the organ level, effectively mimic continuous functions and create most of the known features of skeletal physiology, anatomy, and disease. Those quantum properties also permit the prediction of previously unperceived and unforeseen states and behavior, both normal and abnormal, many of which have been verified.

Bone Development↗