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  1. I. Bashkova1,2,
  2. I. Madyanov1,3,
  3. K. Misko1,
  4. E. Preobrazhenskaia4
  1. 1Chuvash State University named after I.N. Ulyanov, Department of Hospital Therapy, Cheboksary, Russian Federation
  2. 2Federal Center of Traumatology, Orthopedics and Endoprosthesis, Сonsultative polyclinic, Cheboksary, Russian Federation
  3. 3Republican Clinical Hospital, Department of Endocrinology, Cheboksary, Russian Federation
  4. 4Federal Center of Traumatology, Orthopedics and endoprosthesis, Scientific and Educational Department, Cheboksary, Russian Federation


Background: Genetic, biochemical, metabolic, hormonal (primarily imbalance of sex hormones) factors are involved in the progression of osteoarthritis (OA). Dehydroepiandrosterone and its metabolite, dehydroepiandrosterone sulfate (DHEA-S), have a stress-limiting, anti-atherogenic, anti-diabetic, antihypertensive, anti-infective, immunomodulatory effects. Heroprotective effect is not excluded. Experimental studies have identified a relationship between an age-related decrease in DHEA-S levels and various adverse effects of aging.

Objectives: To identify the contribution of DHEA-S to the pathogenesis of OA, it`s advisable to conduct a comparative analysis of connection of the adrenal hormones with clinical, laboratory, radiological signs of the course of OA.

Methods: Patients with primary OA with a lesion of the knee joints (n=90, including 22 men) were examined. The age of the patients - 29-69 years, the duration of the disease – 1.5-20 years. The control group (n=114, including 26 men) was formed by random sampling of the population from healthy people, it`s representative by gender and age. We investigated the serum levels of cortisol, DHEA-S, estradiol (in women), testosterone (in men) and carried out radiography of the knee joints. OA was diagnosed using R.D. Althman, the x-ray stage-according to the classification of Kellgren and Lawrence. Statistically determined the mean value, standard deviation. Differences between the samples were considered statistically significant at p<0.05. To create a model of OA pathogenesis, the method of principal components of factor analysis was used.

Results: The DHEA-S level in the blood of patients with OA was lower than that of the control group (2.40±1.20 vs 3.66±1.45 μg/ml, p=0.001),in women-was lower, than in men (2.25±1.17 vs 2.89±1.23 μg/ml, p=0.045). In the control group, gender differences were not statistically significant (p>0.05). All patients with OA showed an inverse correlation between age and DHEA-S (r=-0.511, p=0.0001, and r=-0.549, p=0.0001 respectively). For factor analysis the most important signs for the course of OA are ESR levels, C-reactive protein (CRP) in the blood (as markers of inflammatory component of OA, or factor 2) were selected, and the radiological stage of OA (degenerative component, or factor 1). In women, we regarded factor 1 as «degenerative», the maximum contribution to total dispersion was made by the «x-ray stage» (+0.72). This symptom was opposed by the «DHEA-S level» (-0.79) and «estradiol blood level» (-0.68), which suggests a link between degenerative and dystrophic processes in the knee joint in women with OA and a decrease in blood levels of DHEA-S and estradiol. Factor 2 we interpreted as «inflammatory». This was indicated by the values of «CRP» (+0.66) and «ESR» (+0.64). The «inflammatory» factor in women from hormonal indicators was opposed by the «blood cortisol content» (-0.31) and «DHEA-S level» (-0.26). Factor 1 in men accounted for 46% of the total variance. Since factor 1 in men included the most significant «CRP» (+0.85), «X-ray stage» (+0.77) and «ESR» (+0.72), we called it «antidegenerative anti-inflammatory factor». The maximum value (modulo) in factor 1 is for DHEA-S (-0.76) and the lower is for testosterone (-0.53). So, in men, a sufficient level of DHEA-S is closely related to the «antidegenerative-anti-inflammatory» factor of OA pathogenesis and DHEA-S counteracts 2 key pathogenetic processes simultaneously-degenerative and inflammatory.

Conclusion: In women, a decrease in DHEA-S is a risk factor for the predominantly degenerative component of OA, in men it`s a universal risk factor, predisposing both to the development of inflammation and degenerative changes in the joints

Disclosure of Interests: None declared.

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