Effect of type 2 diabetes on bone cell behavior

Vaidya, Rachana; Church, Anna E.; Karim, Lamya

doi:10.1016/b978-0-12-821070-3.00001-5

Cited by 3 publications

(4 citation statements)

References 99 publications

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“…As cortical porosity is intimately linked to the bone remodeling and fracture toughness of bone ( Tang and Vashishth, 2011 ; Granke et al, 2016 ), elevated levels of CML might play a role in altering bone remodeling with a consequent effect on cortical porosity, however since the cortical porosity in our ribose and control group was not significantly different, we don't observe much differences in the fracture toughness between these groups. Studies have reported changes in the function of osteoblasts and osteocytes in the presence of AGEs to indicate an altered bone remodeling ( Vaidya et al, 2021 ; Tanaka et al, 2015 ; Suzuki et al, 2020 ), yet the role of CML in bone remodeling remains unknown. As we utilized cadaver bones devoid of live cells, we could not assess CML's role in turnover, and further work assessing CML's impact directly on the turnover process is needed to evaluate this scenario.…”

Section: Discussionmentioning

confidence: 99%

“…Unlike cortical bone, CML did not relate with fAGEs, or any mechanical properties assessed by compression tests in trabecular bone. Trabecular bone is highly porous, heterogeneous, has a high surface area to volume ratio, and thus has more active bone remodeling than cortical bone ( Vaidya et al, 2021 ; Eriksen, 2010 ). Since the effect of CML on active remodeling cannot be tested on cadaver bones, future studies on bone cells and organ culture could help elucidate the effect of CML on bone's mechanical behavior.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Accumulation of fluorescent advanced glycation end products and carboxymethyl-lysine in human cortical and trabecular bone

Vaidya¹,

Rezaee²,

Edwards³

et al. 2022

Bone Reports

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Accumulation of fluorescent advanced glycation end products and carboxymethyl-lysine in human cortical and trabecular bone

Vaidya¹,

Rezaee²,

Edwards³

et al. 2022

Bone Reports

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“…84,85 Hyperglycemic conditions have been shown to induce the formation of AGEs, which is not only limited to crosslinking of collagen in the ECM but extends to altered cellular function via the signaling role of AGEs. 86,87 Specifically, AGEs are associated with several signaling cascades within many cell types by virtue of their interaction with the receptor for AGE (RAGE). [88][89][90] Activation of AGE-RAGE can induce apoptosis, 91 regulate the expression of pro-inflammatory markers, 89,[92][93][94][95][96][97][98][99] and lead to degradation of the ECM 100 (Figure 1).…”

Section: Effects Of Hyperglycemia and Ages On Tendon Cell Behaviormentioning

confidence: 99%

Effect of Diabetes on Tendon Structure and Function: Not Limited to Collagen Crosslinking

Vaidya

Lake

Zellers

2022

J Diabetes Sci Technol

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Diabetes mellitus (DM) is associated with musculoskeletal complications—including tendon dysfunction and injury. Patients with DM show altered foot and ankle mechanics that have been attributed to tendon dysfunction as well as impaired recovery post-tendon injury. Despite the problem of DM-related tendon complications, treatment guidelines specific to this population of individuals are lacking. DM impairs tendon structure, function, and healing capacity in tendons throughout the body, but the Achilles tendon is of particular concern and most studied in the diabetic foot. At macroscopic levels, asymptomatic, diabetic Achilles tendons may show morphological abnormalities such as thickening, collagen disorganization, and/or calcific changes at the tendon enthesis. At smaller length scales, DM affects collagen sliding and discrete plasticity due to glycation of collagen. However, how these alterations translate to mechanical deficits observed at larger length scales is an area of continued investigation. In addition to dysfunction of the extracellular matrix, tendon cells such as tenocytes and tendon stem/progenitor cells show significant abnormalities in proliferation, apoptosis, and remodeling capacity in the presence of hyperglycemia and advanced glycation end-products, thus contributing to the disruption of tendon homeostasis and healing. Improving our understanding of the effects of DM on tendons—from molecular pathways to patients—will progress toward targeted therapies in this group at high risk of foot and ankle morbidity.

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“…Гомеостаз кісткової тканини залежить від резорбційної дії остеокластів та кісткоутворюючої дії остеобластів. Відтак, механізми, що регулюють зв'язок між остеокластами та остеобластами, мають вирішальне значення для гомеостазу кісткової тканини, а їх порушення є важливою складовою патогенезу цукрового діабету [7].…”

Section: Introduction / вступunclassified

Structural and Functional Changes in Osteogenic Cells and Biomarkers of Bone Remodeling in Chronic Hyperglycemia

Ponyrko,

Bumeister,

Korenkov

et al. 2023

EUMJ

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Analysis of the results of experimental studies on skeletal bone structure disorders in the setting of hyperglycemia discovered a lack of information on the peculiarities of the remodeling process and structural and functional changes of osteogenic cells in long tubular bones depending on the duration of diabetes mellitus. Objective. Therefore, the aim of our experimental study was to determine the peculiarities of the effect of hyperglycemia on bone remodeling and structural and functional changes in osteogenic cells of long tubular bones of mature rats. Methods and Materials. Methods used to study the structure of femurs: 1) transmission electron microscopy, 2) immunohistochemical. In the study of osteoblasts, special attention was paid to the integrity of cellular structures and membrane organelles, the presence of cytoplasmic vacuolization. Results. Analysis of the osteogenic activity in the bone tissue of the experimental group showed that an increase in blood glucose leads to a change in the concentration of osteopontin, which directly affects the formation of bone tissue. The immunohistochemical study of osteogenic cells revealed a significant disruption of the structure of organelles, which leads to a disruption of the normal functioning of these cells, which is manifested in a decrease in osteopontin levels and a gradual increase in RANKL. Conclusions. It can be noted that under hyperglycemia conditions, structural disorders of osteoblasts occur already on the 30th day of the experiment: significant hypertrophy of the granular endoplasmic reticulum (GER), increasing destruction of membrane organelles with further progression in accordance with the increase in the duration of chronic hyperglycemia.

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Effect of type 2 diabetes on bone cell behavior

Cited by 3 publications

References 99 publications

Accumulation of fluorescent advanced glycation end products and carboxymethyl-lysine in human cortical and trabecular bone

Accumulation of fluorescent advanced glycation end products and carboxymethyl-lysine in human cortical and trabecular bone

Effect of Diabetes on Tendon Structure and Function: Not Limited to Collagen Crosslinking

Structural and Functional Changes in Osteogenic Cells and Biomarkers of Bone Remodeling in Chronic Hyperglycemia

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