Arthroplasty in veterans: Analysis of cartilage, bone, serum, and synovial fluid reveals differences and similarities in osteoarthritis with and without comorbid diabetes

Oren, Trevor W.; Botolin, Sergiu; Williams, Allison; Bucknell, Allan L.; King, Karen B.

doi:10.1682/jrrd.2010.09.0186

Cited by 52 publications

(41 citation statements)

References 74 publications

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“…Other major AGE crosslinks such as glucosepane are not yet readily measurable in bone [17]. Nonetheless, a diabetic increase in overall bone PE has been directly observed in one study to date [18]. In addition to hyperglycemia, oxidative stress enhances non-enzymatic glycation of collagen [19] as the AGE formation often requires an oxidative step.…”

Section: Introductionmentioning

confidence: 99%

Changes in the Fracture Resistance of Bone with the Progression of Type 2 Diabetes in the ZDSD Rat

et al. 2016

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Individuals with type 2 diabetes (T2D) have a higher fracture risk compared to non-diabetics, even though their areal bone mineral density is normal to high. Identifying the mechanisms whereby diabetes lower fracture resistance requires well-characterized rodent models of diabetic bone disease. Toward that end, we hypothesized that the bone toughness, more so than bone strength, decreases with the duration of diabetes in ZDSD rats. Bones were harvested from male CD(SD) control rats and male ZDSD rats at 16-wks (before the onset of hyperglycemia), at 22-wks (5–6 wks of hyperglycemia), and at 29-wks (12–13 wks of hyperglycemia). There were at least 12 rats per strain per age group. At 16-wks, there was no difference in either body weight or glucose levels between the 2 rat groups. Within 2 weeks of switching all rats to a diet with 48% of kcal from fat, only the ZDSD rats developed hyperglycemia (>250 mg/dl). They also began to lose body weight at 21-wks. CD(SD) rats remained normoglycemic (<110 mg/dl) on the high fat diet and became obese (>600 g). From micro-computed tomography (µCT) analysis of a lumbar vertebra and distal femur, trabecular bone volume did not vary with age among the non-diabetic rats but was lower at 29-wks than at 16-wks or at 22-wks for the diabetic rats. Consistent with that finding, µCT-derived intra-cortical porosity (femur diaphysis) was higher for ZDSD following ~12 wks of hyperglycemia than for age-matched CD(SD) rats. Despite an age-related increase in mineralization in both rat strains (µCT and Raman spectroscopy), material strength of cortical bone (from three-point bending testing) increased with age only in the non-diabetic CD(SD) rats. Moreover, two other material properties, toughness (radius) and fracture toughness (femur), significantly decreased with the duration of T2D in ZDSD rats. This was accompanied by the increase in the levels of the pentosidine (femur). However, pentosidine was not significantly higher in diabetic than in non-diabetic bone at any time point. The ZDSD rat, which has normal leptin signaling and becomes diabetic after skeletal maturity, provides a pre-clinical model of diabetic bone disease, but a decrease in body weight during prolonged diabetes and certain strain-related differences before the onset of hyperglycemia should be taken into consideration when interpreting diabetes-related differences.

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Section: Introductionmentioning

confidence: 99%

Changes in the Fracture Resistance of Bone with the Progression of Type 2 Diabetes in the ZDSD Rat

et al. 2016

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“…Candidate mechanisms include hyperglycemia leading to joint tissue changes, particularly in collagen [27], and obesity leading to (1) increased mechanical load to the joint [31]; and/or (2) nonbiomechanical factors such as metabolism from increased fat [8,14,20,22]. Obesity is a risk factor for diabetes [1,15,17,19,30] and osteoarthritis [8,13,20,22,26], and both factors are increasing rapidly in the US population [6,10].…”

Section: Discussionmentioning

confidence: 99%

Veterans With Diabetes Receive Arthroplasty More Frequently and at a Younger Age

King

Findley

Williams

et al. 2013

Clinical Orthopaedics &Amp; Related Research

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Background A future increase in total joint arthroplasties in patients with diabetes seems likely considering the prevalence of osteoarthritis and diabetes mellitus are increasing. However, the rates of arthroplasty in the population of patients with diabetes are unclear. Questions/purposes We sought to determine whether lower extremity arthroplasties in a veteran population with diabetes is different from a similar population without diabetes. The following specific questions were asked: (1) Is the rate of TKA in veterans with diabetes higher than in those without diabetes? (2) Is the rate of THA in veterans with diabetes higher than in those without diabetes? (3) Are arthroplasty revision rates greater in veterans with diabetes than in veterans without diabetes?Methods The US Department of Veterans Affairs Health administrative data from fiscal year 2000 was used to identify persons with primary or secondary TKA or THA. The rate of surgeries among a diabetic population was compared with that among a nondiabetic population. Results The diabetic cohort received total joint arthroplasties at a higher rate than the nondiabetic cohort at all ages younger than 66 years, with a range of odd ratios from 1.3 to 3.4. In answer to our specific questions, (1) the rate of TKA (95% CI, 2.1-3.7), (2) the rate of THA (95% CI, 1.0-2.6), and (3) the rates of arthroplasty revision (95% CI, 0.9-5.8 TKA and 0.7-6.8 THA) were higher in veterans with diabetes. Furthermore, those with diabetes in the youngest age group studied received total joint arthroplasties and revision surgeries at approximately double the rates of those without diabetes.

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“…bovine versus human), making it difficult to compare results. Furthermore, the clinical relevance of the in vitro induced AGE levels is difficult to deduce as these values cannot be compared to glycation content in diabetic human bone, as the only study that measured glycation in diabetic bone assessed pentosidine content but not total fluorescent AGEs [52]. …”

Section: Effect Of Ages On Bone's Biomechanical Behaviormentioning

confidence: 99%

“…These values are higher than that observed in human bone even after only ~7 days of the total 38-day incubation. Further, the in vitro induced quantities are difficult to compare to that in diabetic human bone because the single study that assessed glycation in diabetic human bone measured only pentosidine, but not total fluorescent AGEs [52]. Given the weak relationship between pentosidine and total fluorescent AGEs [31], it is difficult to extrapolate and compare the extent of glycation across these studies.…”

Section: Comparison Of Age Levels In Bone Specimens Exposed To Inmentioning

confidence: 99%

“…The other assessed pentosidine in cortical bone, which reported ~23-fold lower pentosidine content than that measured in diabetic human bone [52, 64]. Furthermore, in the study on diabetic human bone specimens, findings are difficult to interpret as it is unclear whether the specimens were cortical or cancellous bone or a mixture of both.…”

Section: Comparison Of Age Levels In Bone Specimens Exposed To Inmentioning

confidence: 99%

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Effect of type 2 diabetes-related non-enzymatic glycation on bone biomechanical properties

Karim

Bouxsein

2016

Bone

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There is clear evidence that patients with type 2 diabetes mellitus (T2D) have increased fracture risk, despite having high bone mineral density (BMD) and body mass index (BMI). Thus, poor bone quality has been implicated as a mechanism contributing to diabetic skeletal fragility. Poor bone quality in T2D may result from the accumulation of advanced glycation end-products (AGEs), which are post-translational modifications of collagen resulting from a spontaneous reaction between extracellular sugars and amino acid residues on collagen fibers. This review discusses what is known and what is not known regarding AGE accumulation and diabetic skeletal fragility, examining evidence from in vitro experiments to simulate a diabetic state, ex vivo studies in normal and diabetic human bone, and diabetic animal models. Key findings in the literature are that AGEs increase with age, affect bone cell behavior, and are altered with changes in bone turnover. Further, they affect bone mechanical properties and microdamage accumulation, and can be inhibited in vitro by various inhibitors and breakers (e.g. aminoguanidine, N-Phenacylthiazolium Bromide, vitamin B6). While a few studies report higher AGEs in diabetic animal models, there is little evidence of AGE accumulation in bone from diabetic patients. There are several limitations and inconsistencies in the literature that should be noted and studied in greater depth including understanding the discrepancies between glycation levels across reported studies, clarifying differences in AGEs in cortical versus cancellous bone, and improving the very limited data available regarding glycation content in diabetic animal and human bone, and its corresponding effect on bone material properties in T2D.

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Arthroplasty in veterans: Analysis of cartilage, bone, serum, and synovial fluid reveals differences and similarities in osteoarthritis with and without comorbid diabetes

Cited by 52 publications

References 74 publications

Changes in the Fracture Resistance of Bone with the Progression of Type 2 Diabetes in the ZDSD Rat

Changes in the Fracture Resistance of Bone with the Progression of Type 2 Diabetes in the ZDSD Rat

Veterans With Diabetes Receive Arthroplasty More Frequently and at a Younger Age

Effect of type 2 diabetes-related non-enzymatic glycation on bone biomechanical properties

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