Chondrocyte Intracellular Matrix Strain Fields of Articular Cartilage Surface in Hyperglycemia Model of Rat: Cellular Morphological Study

Abstract

Introduction:Chondrocyte is one cell in articular cartilage was products many proteins, molecules, and other factors. The external influence of cartilage, such as: hyperglycemia was entering joint capsule and impact to the chondrocytes and the cartilage. Hyperglycemia caused modification of heparan sulfate proteoglycan 2 (perlecan) proteins through glycation process.Aim:The aim of this study was to analyze morphological changing of chondrocytes pericellular matrix by the influence of hyperglycemia.Material and Methods:Eighteen adult male rats were divided into six groups: control, rat treated with sugar intake was 0.5 mg/kg, 0.75 mg/ kg, 1mg/kg, 1.5 g/kg and 2 mg/kg of body weight. The animal model was dislocated and left knee was taken to observe changing of chondrocytes pericellular matrix strain fields by Scanning Electron Microscope (SEM) from perpendicular to femoral condylus cartilage.Results:Changing of chondrocytes intracellular matrix strain fields as changing of cell diameters and cell distances at group control and group I to group V, which cell diameters was lower level and cell distances was the highest level at over diet 2. This changing of intracellular matrix strain fields was corresponding to changing chondrocytes morphology in hyperglycemia condition, due to hypertrophic stage as adaptive responses. This research as based on next research for accomplish of hyperglycemia influence to morphology articular cartilage changing to prevent degeneration of cartilage towards osteoarthritis.Conclusions:Present study concludes that hyperglycemia influence to chondrocyte intracellular matrix strain fields changing.

Hyperglycemia Duration Impact On Anatomical Damage Level Of Osteoarthritic Articular Cartilage In Rat Models With Diabetes Mellitus Type 1

“…By analyzing a superficial layer of the articular cartilage, the results of the DMT-1 groups revealed that DMT-1 increased the severity of OA disease [5], which had a more in-depth and branched fissure. This condition was caused by reducing the matrix integrity due to changing the chondrocyte phase from proliferating and hypertrophic phases to the hypertrophic phase; therefore, the chondrocyte size was increased in the DMT-1 groups, especially in the DMT-1.3 group, which had the longest duration.…”

“…Previous research concluded that hyperglycemia causes the hypertrophy phase of chondrocytes [4]. This condition starts at the superficial layer of the cartilage with a change in the chondrocytes' diagonal diameter and the distances between chondrocytes [5].…”

Osteoarthritis and type 2 diabetes: From pathogenetic factors to therapeutic intervention

“…Moreover, synovial inflammation upregulates the local production of catabolic enzymes and, consequently, cartilage degradation . Past animal studies have shown that high blood glucose levels in diabetic rats were associated with a decrease of collagen and proteoglycans in articular cartilage and tendons, as well as with the deposition of collagen within the synovial membrane …”

“…This leads to an increase in the oxidative stress promoting the secretion of prostaglandin E 2 (PGE 2 ), IL-1β, IL-6, IL-10, and TNF-α, potent pro-inflammatory mediators. 37 Collectively, the excess of glucose results in alterations of the cell metabolism and morphology, as well as in ECM structure, 38 due to the reduction in collagen synthesis and the increase of proteoglycan catabolism. 39 The consequent breakdown within the ECM promotes cartilage degradation and increases the release of several molecules in the synovial fluid, including the cartilage oligomeric matrix protein (COMP).…”

“…46 Past animal studies have shown that high blood glucose levels in diabetic rats were associated with a decrease of collagen and proteoglycans in articular cartilage and tendons, as well as with the deposition of collagen within the synovial membrane. 38,47,48 OA can be often initiated by a subchondral bone damage, which is then resorbed and may harm the overlying articular cartilage. It is known that diabetic patients generally present a lower bone remodelling capacity due to the local and systemic excess of proinflammatory cytokines.…”