Pathogenetic role of the impact of lipid peroxidation processes and the condition of antioxidant defense system to articular cartilage destruction and subchondral bone remodeling in patients with early primary and posttraumatic gonarthrosis

Abstract

The identification of the features of lipid peroxidation processes, the condition of antioxidant defense system (AOS) and their impact on metabolic processes in cartilage and bone tissues in patients with early signs of primary and post-traumatic gonarthrosis (GA) is necessary for the development of pathogenetically substantiated diagnostic and therapeutic strategies.

The objective is to study the features of LPO processes and the condition of AOP system, and to determine their impact to the articular cartilage destruction and subchondral bone remodeling in patients with early primary and post-traumatic gonarthrosis.

Materials and methods. We determined the systemic levels of primary (lipid hydroperoxides – LPO) and secondary (malondialdehyde – MDA),) lipid peroxidation products, SOD isoenzymes (SOD-2 and Cu-Zn SOD), SOD and catalase (Cat) activities, thiol (TC) and total antioxidant status (TAS) values. The correlations were found between the studied parameters and the products of articular cartilage destruction, as well as markers of bone tissue remodeling in 60 patients of the main group with early primary GA, 60 patients of the comparison group with post-traumatic GA, and in 50 healthy individuals of the control group.

Results. In the main group of patients, the following excesses of the normal values were found: LPO by 2.16, MDA by 1.98, SOD activity by 2.7, SOD-2 concentrations by 2.01, Cu-Zn SOD by 2.25 times along with the decreased Cat activity by 1.16, TC by 2.13, and OAS by 1.28 times. In individuals of the comparison group featured the excess of the normal LPO values by 1.98, MDA by 1.37 times, while Cu-Zn SOD concentration decreased by 1.21 times, TC by 1.25, and TAC by 1.31 times. In patients of both groups, we found direct correlation between the systemic increase in LPO product levels and cartilage destruction markers. In the main group of patients, positive correlation was found between the products of articular cartilage destruction and systemic levels of SOD-2, Cu-Zn SOD, Cat activity and TAS parameters, as well as between type I collagen fragments, Cat activity and SOD-2 serum concentrations. In the comparison group, negative correlations were found between the studied components of the antioxidant defense system and the products of cartilage tissue destruction.

Conclusions. Early signs of primary and post-traumatic GA feature the increased production of primary and secondary LPO products, positively associated with the intensification of cartilage matrix destruction. The pathogenetically significant mechanism of primary GA early manifestations is an imbalance in AOS, the components of which form positive correlations with the articular cartilage destruction markers and type I collagen fragments, a structural component of the bone matrix. The incipience of post-traumatic GA is accompanied by quantitative AOS imbalance; its components form pathogenetically significant negative correlations with cartilage matrix destruction products. This should be considered by those developing diagnostic and therapeutic strategies.