Abstract
Introduction: Non-enzymatic protein glycosylation in diabetic patients leads to stiffening of collagen-containing tissues affecting joint mobility. Motor dysfunction in diabetic patients can be detected as muscle weakness or atrophy.Objective: To determine the presence of muscles weakness and limited joint mobility at ankle (AJ), subtalar (SJ) and first metatarsophalangeal joint (I MTP) in diabetic patients and to determine impact of diabetes duration on those changes.Patients and Methods: A cross-sectional study was conducted among 100 diabetic patients in “Primary Health Care Centre Banjaluka” in 2014. Function of ten foot and ankle muscles has been evaluated by manual muscle testing. Muscle strength was scored by semiquantitative grading system used in the Michigan Diabetic Neuropathy Score. Range of motion (ROM) at the AJ, SJ and I MTP was measured with goniometer.Results: The average patients age was 61.91±10.74 and diabetes duration 12.25±8.60 years. The average strength of foot and ankle muscles expressed by muscle score was 11.56±5.08. The average ROM at AJ (47.85°) was significantly decreased compared to the reference value that is 65° (t =-15.378, P=000). The average ROM at SJ (35.10°) was significantly decreased compared to the reference value that is 50° (t =-15.378, P=000). The average ROM at the I MTP (72.70°) was significantly decreased compared to the reference value that is 120° (t =-15.378, P = ,000).Conclusion: Patients with diabetes have decreased foot and ankle muscle strength, and the average values of the range of motion at AJ, SJ and I MTP, but the duration of the diabetes does not correlate significantly with those changes.
Highlights
Non-enzymatic protein glycosylation in diabetic patients leads to stiffening of collagen-containing tissues affecting joint mobility
The average strength of foot and ankle muscles expressed by muscle score was 11.56±5.08
The average muscle strength of the foot and ankle muscles expressed by muscle score (MS) was 11.56±5.08
Summary
Non-enzymatic protein glycosylation in diabetic patients leads to stiffening of collagen-containing tissues affecting joint mobility. Diabetes mellitus (DM), or diabetes is the global epidemic of the 21st century and it is the fourth leading cause of death in most developed countries.[1] Diabetes complications in the lower extremities are a major cause of morbidity, disability, emotional and physical suffering in people with DM2 generating at the same time huge economic costs for patients, their families and the entire society.[3] Non-enzymatic glycosylation of the protein caused by long standing hyperglycemic state during longer DM duration leads to stiffening of collagen containing tissues,[4,5,6] which reflects joint structure decreasing elasticity of cartilage, ligaments, and joint capsule.[5,6,7] A key factor of the tissue damage in patients with DM is gradually and excessive accumulation of advanced glycation end products (AGEs) that produce abnormal covalent cross-links within collagen fibers and other proteins. Once formed, AGEs can be decomposed only when the protein they are incorporated into is degraded.[8] coupled with a longer period of time spent in support phase in DN patients contributes to the susceptibility for skin damage through a prolonged mechanical load on tissue leading to skin breakdown and ulceration.[15]
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