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

2000 ◽  
Vol 18 (6) ◽  
pp. 305-316 ◽  
Author(s):  
Harold M. Frost
2001 ◽  
Vol 14 (04) ◽  
pp. 179-184 ◽  
Author(s):  
H. M. Frost

SummaryAn elegant design stratagem for an organ intended to carry loads for life without fracturing, rupturing or wearing out would make those loads determine the organ's strength. It seems load-bearing mammalian bones, joints, fascia, ligaments and tendons do exactly that. Physiologists begin to understand how they do it, and that led to the Utah paradigm of skeletal physiology. Those adaptations occur in two major steps. The first step creates the genetically predetermined newborn skeleton with its anatomical relationships and biologic machinery. The second step adds to the first one all postnatal adaptations to mechanical and other challenges that would affect an organ's strength, size, architecture and composition. During postnatal growth, increasing loads make tissue-level biologic mechanisms correspondingly increase the strength of such organs. Mechanical strain-dependent signals help to control that process, which muscle strength, muscle anatomy and neuromuscular physiology strongly influence. Its problems seem to cause or help to cause numerous skeletal and some extraskeletal disorders. A Table in the article lists examples of them.This article summarizes salient features of the Utah paradigm, which includes both facts and some meanings inferred from them. Other times and people must resolve any questions about those meanings and about the devils that can lie in the details. Parenthetically, instead of the accuracy of the facts on which that paradigm stands, the above questions usually concern the different meanings people can infer from facts, and whether particular facts and ideas would be relevant to a particular issue.


2016 ◽  
Vol 212 ◽  
pp. 341-348 ◽  
Author(s):  
Yu-Xin Liu ◽  
Da-Yong Zhou ◽  
Dong-Dong Ma ◽  
Yan-Fei Liu ◽  
Dong-Mei Li ◽  
...  

2020 ◽  
Vol 40 (10) ◽  
pp. 791-797
Author(s):  
Isabela M. Martins ◽  
Lygia M.M. Malvestio ◽  
Jair R. Engracia-Filho ◽  
Gustavo S. Claudiano ◽  
Flávio R. Moraes ◽  
...  

ABSTRACT: The Golden Retriever muscular dystrophy (GRMD) is one of the best models of Duchenne muscular dystrophy (DMD), with similar genotypic and phenotypic manifestations. Progressive proliferation of connective tissue in the endomysium of the muscle fibers occurs in parallel with the clinical course of the disease in GRMD animals. Previous studies suggest a relationship between mast cells and the deposition of fibrous tissue due to the release of mediators that recruit fibroblasts. The aim of this study was to evaluate the presence of mast cells and their relationship with muscle injury and fibrosis in GRMD dogs of different ages. Samples of muscle groups from six GRMD and four control dogs, aged 2 to 8 months, were collected and analyzed. The samples were processed and stained with HE, toluidine blue, and Azan trichrome. Our results showed that there was a significant increase in infiltration of mast cells in all muscle groups of GRMD dogs compared to the control group. The average number of mast cells, as well as the deposition of fibrous tissue, decreased with age in GRMD dogs. In the control group, all muscle types showed a significant increase in the amount of collagenous tissue. This suggests increased mast cell degranulation occurred in younger GRMD dogs, resulting in increased interstitial space and fibrous tissue in muscle, which then gradually decreased over time as the dogs aged. However, further studies are needed to clarify the role of mast cells in the pathogenesis of fibrosis.


2007 ◽  
Vol 86 (9) ◽  
pp. 908-911 ◽  
Author(s):  
S. Habelitz ◽  
B.J. Rodriguez ◽  
S.J. Marshall ◽  
G.W. Marshall ◽  
S.V. Kalinin ◽  
...  

Dentin is a mesenchymal tissue, and, as such, is based on a collagenous matrix that is reinforced by apatite mineral. Collagen fibrils show piezoelectricity, a phenomenon that is used by piezoresponse force microscopy (PFM) to obtain high-resolution images. We applied PFM to image human dentin with 10-nm resolution, and to test the hypothesis that zones of piezoactivity, indicating the presence of collagen fibrils, can be distinguished in dentin. Piezoelectricity was observed by PFM in the dentin intertubular matrix, while the peritubular dentin remained without response. High-resolution imaging of chemically treated intertubular dentin attributed the piezoelectric effect to individual collagen fibrils that differed in the signal strength, depending on the fibril orientation. This study supports the hypothesis that peritubular dentin is a non-collagenous tissue and is thus an exception among mineralized tissues that derive from the mesenchyme.


2016 ◽  
Vol 3 (11) ◽  
pp. 2825-2831 ◽  
Author(s):  
Sheng-Lin Lee ◽  
Yang-Fang Chen ◽  
Chen-Yuan Dong

Author(s):  
Bhawan B. Bhende

Alkaptonuria (AKU) is a rare disorder of autosomal recessive inheritance. It is caused by a mutation in a gene that results in the accumulation of homogentisic acid (HGA). Characteristically, the excess HGA means sufferers pass dark urine, which upon standing turns black. This is a feature present from birth. Over time patients develop other manifestations of AKU, due to deposition of HGA in collagenous tissue namely ochronosis and ochronotic osteoarthropathy. Although this condition does not reduce life expectancy, it significantly affects quality of life. The natural history of this condition is becoming better understood, despite gaps in knowledge. Clinical assessment of the condition has also improved along with the development of a potentially disease-modifying therapy. Furthermore, recent developments in AKU research have led to new understanding of the disease, and further study of the AKU arthropathy has the potential to influence therapy in the management of osteoarthritis.


2016 ◽  
Vol 5 (6) ◽  
pp. 676-687 ◽  
Author(s):  
Sophia P. Pilipchuk ◽  
Alberto Monje ◽  
Yizu Jiao ◽  
Jie Hao ◽  
Laura Kruger ◽  
...  

Surgery Today ◽  
2019 ◽  
Vol 49 (11) ◽  
pp. 958-964
Author(s):  
Satoshi Umeda ◽  
Yasuhide Nakayama ◽  
Takeshi Terazawa ◽  
Ryosuke Iwai ◽  
Shohei Hiwatashi ◽  
...  

2000 ◽  
Vol 04 (02) ◽  
pp. 67-84 ◽  
Author(s):  
Harold M. Frost

As age, experience and common sense look at biomechanical, hormonal, genetic and other roles in bone physiology and its disorders, two questions can arise: (a) How did we fail? (b) How could we make it better? The acerbic Sam Johnson said that to teach new things, we should use examples of already known ones. If so, an analogy might help to clarify this article's message for people who work with bones and their disorders. Assume this: (a) Mythical physiologists were taught that renal physiology depends on "kidney cells" but were taught nothing about nephrons; (b) so they explained renal health and disorders in those terms. (c) For many decades, they "knew" that view was correct (as the ancients "knew" the world was flat). (d) But then others described nephrons and some errors their properties revealed in those views about renal physiology; (e) so controversies began. Today, an analogous situation confronts real biomechanicians and physiologists. (i) Most of them were taught that osteoblasts and osteoclasts (bone's "effector cells") explain bone physiology without "nephron-equivalent" input, so they explained bone disorders and mechanical effects in those terms. (ii) Yet nephron-equivalent mechanisms and functions, including biomechanical ones, in bones have the same operational relationship to their cells, health and disorders as nephrons and their functions do to renal cells, health and disorders. (iii) Adding that knowledge to former views led to the Utah paradigm of skeletal physiology. It also revealed errors in many former views about bone physiology; (iv) so real controversies have begun. Biomechanicians, physiologists, clinicians and pharmacologists from whom poor interdisciplinary communication hid that paradigm could think the view in (i) above remains valid, and keep analyzing data and designing studies within its constraints. Like Wegner's idea of plate tectonics in geology, the Utah paradigm came before its field was ready, so others fought it. But while the plate-tectonics war was won, it has just begun for the Utah paradigm. This article reviews how such things could apply to bone and some of their implications. Its conclusion offers succinct answers to the italicized questions above.


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