Abstract

BACKGROUND: Currently, OA is considered a polyetiological disease, where several phenotypes are distinguished based on the leading role of a specific risk factor. It is assumed that each clinical phenotype corresponds to its own fundamental changes in various organs and systems. Modern experimental evidence of chondro-osteogenic activity allows us to consider melatonin as a potential drug for various types of osteoarticular pathology.AIM: To study clinical and biochemical changes and effects of melatonin in the metabolic phenotype of OA and insomnia.MATERIALS AND METHODS: The study involved patients with a metabolic phenotype of OA and healthy volunteers. The subjects were collected complaints and anamnesis, as well as general clinical and orthopedic examination. In the blood serum, markers of bone and cartilage metabolism were determined. Patients were asked to answer the questions of clinical scales to assess the quality of sleep, the functional state of the joints and quality of life.RESULTS: The study involved 36 patients. Participants were divided into 3 groups: group health patients — patients without articular pathology, sleep quality disorders and normal body mass index; control group- patients with metabolic phenotype of OA, insomnia and basic treatment for 30 days; experimental group — patients with a metabolic phenotype of OA and insomnia, whose basic treatment included melatonin (Melaxen®) at a dosage of 3 mg for 30 days. Statistically significant differences were observed between the initial levels of acid phosphatase (AP), bone isoenzyme alkaline phosphatase (ALP) and calcium (Ca) in the control and experimental groups. According to the results of screening for the detection of insomnia among patients with the metabolic phenotype of, there were statistically significant insomnological disorders compared to the group health patients, as well as significant differences in terms of pain, symptoms, activity and quality of life in general according to the KOOS and SF-36 scales. Correlation analysis showed moderate correlations with biochemical parameters in patients with OA metabolic phenotype groups. After the treatment there was a certain increase in the level of Ca and a decrease in the activity of ALP and АP in patients of experimental group in comparison with patients of control groups. There was a positive trend in the range of criteria of the KOOS and SF-36 scale in experimental groups, pronounced decrease in pain syndrome (P), symptoms (S) and an increase in the levels of daily activity (A) and the total indicator (Sum) in comparison with patients of control groups. Also as improved sleep quality on all scales in comparison with the control group. In control group, problems with the quality and quantity of sleep remained at the same level.CONCLUSION: In patients with the most pronounced indicators of clinical manifestations of OA, more active processes of bone remodeling. The higher the level of bone resorption markers, the greater the severity of the clinical course in patients with osteoarthritis, and the worse the quality of sleep in general. The addition of melatonin to the treatment regimen was associated with a decrease in serum activity of the bone isoenzyme of alkaline phosphatase, acid phosphatase, an increase in calcium levels, as well as with an improvement in sleep and clinical symptoms ОА.

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