The Cellular Basis of Metabolic Bone Disease

Rasmussen, Howard; Bordier, P

doi:10.1056/nejm197307052890107

Cited by 170 publications

(133 citation statements)

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“…The reduction of the PTH secretion and the increased or normal CT level should modify the properties of the bone cells. According to Rasmussen and Bordier (1973), the sideration of the parathyroid function, although the C cells function remain normal, might diminish the resorption activity of the osteoclasts and accelerate the differ entiation of osteoclasts into osteoblasts. The osteoblastic activation should permit the repair of the bone resorption.…”

Section: Discussionmentioning

confidence: 99%

Actual concept of osteoporosis in paraplegia

Chantraine

1978

Spinal Cord

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Abstract.The osteoporosis which appears in paraplegics below the neurological lesion has been studied in 100 patients with the following parameters: quantitative X-rays, urinary hydroxyproline excretion, kinetic study of calcium metabolism by 45Ca, serum phosphorus and calcium, parathormone and calcitonin radio-immunoassay, quantitative histology, density fractionation of bone and amino-acid composition of fractionated bone analysis.All our results show that the important bone resorption occurring very early in the paraplegia is immediately followed by an increase of the bone repair. This osteoporosis below the neurological lesion in paraplegia represents an unbalance between the synthesis and the resorption of bone which possesses a large degree of activity. Furthermore, we demonstrated that the collagen of this bone is underhydroxylated. Following the quanti tative X-rays and intraosseous phlebography results we have considered the aetiopatho genesis of this osteoporosis. It seems that vascular modifications due to the lesion of the autonomic nervous system play an important role and furthermore we believe that immobilisation represents only a minor factor in the aetiology of this osteoporosis.IN paraplegia an osteoporosis appears very early after the spinal cord lesion and is located below this lesion.The aetiopathogenesis of this osteoporosis is not known although the disuse factor has been advanced. On the other hand, the angiographic investigations made by Galibert (1959) and Rossier et al. (1973) have shown that modifications existed below the spinal lesion since the beginning of the paraplegia. Benassy et al. (1963) reported changes in the arterial and venous blood gases (02 saturation, pH, pC02, pOz) consisting in a marked arterialisation of lower limb venous blood. Thus, these modifications evolve in the same direction as the angiographic ones. These blood flow modifications could play a role in the pathogenesis of this porosis. Vasomotor paralysis, a consequence of the orthosympathic system damage, provokes a slowdown of the intraosseous circulation. Arterio-venous shunts also give an increase of the venous pressure. This situation leads to an increase of the intraosseous medullary pressure. Trueta (I964, 1968) and Dhem (1973) have shown the consequence of intraosseous circulation decrease on the cellular differentiation.Stimulated by these data and the fact that the autonomic nervous system CANS) might play a role in this osteoporosis, we have reviewed the problem and investigated the following parameters: X-rays; intramedullary pressure of bone; urinary hydroxyproline excretion; kinetic study of calcium metabolism by 45Ca; urine calcium; serum calcium and phosphorus; serum calcitonin and parathormone; quantitative histological study; density fractionation of bone and amino-acid composition of fractionated bone analysis.We will briefly summarise the methods and the results of those investigations which have been reported elsewhere.

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Section: Discussionmentioning

confidence: 99%

Actual concept of osteoporosis in paraplegia

Chantraine

1978

Spinal Cord

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“…In early views, the responses of osteoclasts and BMUs to parathyroid hormone, calcitonin, and other humoral agents were viewed as essential for calcium homeostasis (Albright and Reifenstein, 1948;Barzel, 1970;Favus, 1999;Rasmussen and Bordier, 1974;Snapper, 1957). Some people even viewed that as their chief function.…”

Section: Homeostasis and Bonementioning

confidence: 99%

From Wolff's law to the Utah paradigm: Insights about bone physiology and its clinical applications

2001

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Efforts to understand our anatomy and physiology can involve four often overlapping phases. We study what occurs, then how, then ask why, and then seek clinical applications. In that regard, in 1960 views, bone's effector cells (osteoblasts and osteoclasts) worked chiefly to maintain homeostasis under the control of nonmechanical agents, and that physiology had little to do with anatomy, biomechanics, tissue-level things, muscle, and other clinical applications. But it seems later-discovered tissue-level mechanisms and functions (including biomechanical ones, plus muscle) are the true key players in bone physiology, and homeostasis ranks below the mechanical functions. Adding that information to earlier views led to the Utah paradigm of skeletal physiology that combines varied anatomical, clinical, pathological, and basic science evidence and ideas. While it explains in a general way how strong muscles make strong bones and chronically weak muscles make weak ones, and while many anatomists know about the physiology that fact depends on, poor interdisciplinary communication left people in many other specialties unaware of it and its applications. Those applications concern 1.) healing of fractures, osteotomies, and arthrodeses; 2.) criteria that distinguish mechanically competent from incompetent bones; 3.) design criteria that should let load-bearing implants endure; 4.) how to increase bone strength during growth, and how to maintain it afterwards on earth and in microgravity situations in space; 5.) how and why healthy women only lose bone next to marrow during menopause; 6.) why normal bone functions can cause osteopenias; 7.) why whole-bone strength and bone health are different matters; 8.) why falls can cause metaphyseal and diaphyseal fractures of the radius in children, but mainly metaphyseal fractures of that bone in aged adults; 9.) which methods could best evaluate whole-bone strength, "osteopenias" and "osteoporoses"; 10.) and why most "osteoporoses" should not have bone-genetic causes and some could have extraosseous genetic causes. Clinical specialties that currently require this information include orthopaedics, endocrinology, radiology, rheumatology, pediatrics, neurology, nutrition, dentistry, and physical, space and sports medicine. Basic science specialties include absorptiometry, anatomy, anthropology, biochemistry, biomechanics, biophysics, genetics, histology, pathology, pharmacology, and cell and molecular biology. This article reviews our present general understanding of this new bone physiology and some of its clinical applications and implications. It must leave to other times, places, and people the resolution of questions about that new physiology, and to understand the many devils that should lie in its details. (Thompson D'Arcy, 1917). Anat Rec 262: 2001.

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“…The proclivity to sarcomatous transformation, the variability of osteoblasts (size, shape, and staining), the peculiarity of osteoclasts (size and number of nuclei, up to 100, seen also in giant-cell tumors), and control of the disease by antimitotic agents such as plicamycin (also known as mithramycin) suggest that the disease may be a benign neoplasm of the mesenchymal osteoprogenitor cell, as was hypothesized by Rasmussen and Bordier in 1973 [125].…”

Section: Etiologymentioning

confidence: 89%