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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">genort</journal-id><journal-title-group><journal-title xml:lang="ru">Гений ортопедии</journal-title><trans-title-group xml:lang="en"><trans-title>Genij Ortopedii</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1028-4427</issn><issn pub-type="epub">2542-131X</issn><publisher><publisher-name>ЦЕНТР ИЛИЗАРОВА</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18019/1028-4427-2025-31-6-773-779</article-id><article-id custom-type="elpub" pub-id-type="custom">genort-3378</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Оригинальные статьи</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Original articles</subject></subj-group></article-categories><title-group><article-title>Изучение связи между биомаркерами костного метаболизма и провоспалительными цитокинами у пациентов с остеоартрозом</article-title><trans-title-group xml:lang="en"><trans-title>Exploring the link between bone biomarkers and proinflammatory cytokines in patients with osteoarthritis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8796-9011</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Al-Mosawi</surname><given-names>R. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Al-Mosawi</surname><given-names>R. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Rabab Ali Al-Mosawi — Ph.D., Lecturer</p><p>Najaf</p></bio><bio xml:lang="en"><p>Rabab Ali Al-Mosawi — Ph.D., Lecturer</p><p>Najaf</p></bio><email xlink:type="simple">rababali.inj@atu.edu</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0004-6319-8314</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Abed Shubar</surname><given-names>S. N.</given-names></name><name name-style="western" xml:lang="en"><surname>Abed Shubar</surname><given-names>S. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Safa Nihad Abed Shubar — Ph.D., Lecturer</p><p>Mussaib</p></bio><bio xml:lang="en"><p>Safa Nihad Abed Shubar — Ph.D., Lecturer</p><p>Mussaib</p></bio><email xlink:type="simple">safa.abd@atu.edu.iq</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0002-4299-7577</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Aldin</surname><given-names>B. B.</given-names></name><name name-style="western" xml:lang="en"><surname>Aldin</surname><given-names>B. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Baraa Bahaa Aldin — Ph.D., Lecturer</p><p>Mussaib</p></bio><bio xml:lang="en"><p>Baraa Bahaa Aldin — Ph.D., Lecturer</p><p>Mussaib</p></bio><email xlink:type="simple">barra.ahmed.ims@atu.edu.iq</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0005-2108-1668</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Al-Fahham</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Al-Fahham</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ali A. Al-Fahham — Ph.D., Professor</p></bio><bio xml:lang="en"><p>Ali A. Al-Fahham — Ph.D., Professor</p><p>Iraq</p></bio><email xlink:type="simple">fahham925@gmail.com</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Al-Furat Al-Awsat Technical University</institution><country>Ирак</country></aff><aff xml:lang="en"><institution>Al-Furat Al-Awsat Technical University</institution><country>Iraq</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>University of Kufa</institution><country>Россия</country></aff><aff xml:lang="en"><institution>University of Kufa</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>19</day><month>12</month><year>2025</year></pub-date><volume>31</volume><issue>6</issue><fpage>773</fpage><lpage>779</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Al-Mosawi R.А., Abed Shubar S.N., Aldin B.B., Al-Fahham А.А., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Al-Mosawi R.А., Abed Shubar S.N., Aldin B.B., Al-Fahham А.А.</copyright-holder><copyright-holder xml:lang="en">Al-Mosawi R.A., Abed Shubar S.N., Aldin B.B., Al-Fahham A.A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.ilizarov-journal.com/jour/article/view/3378">https://www.ilizarov-journal.com/jour/article/view/3378</self-uri><abstract><p>Введение. Остеоартроз — многофакторное заболевание суставов, характеризующееся прогрессирующим разрушением суставного хряща, изменениями в субхондральной кости и хроническим воспалением синовиальной оболочки.Цель работы — измерить сывороточные уровни костных биомаркеров (остеокальцина и склеростина) у пациентов с остеоартрозом и сравнить их с уровнями у здоровых людей, а также выявить связь этих биомаркеров с провоспалительными цитокинами, включая IL-6, IL-17, IL-1β и TNF-α.Материалы и методы. Проведено контролируемое исследование с участием 65 пациентов с остеоартрозом и 35 здоровых людей. Образцы крови брали у участников после получения письменного информированного согласия. Уровень цитокинов и костных маркеров в сыворотке измеряли с помощью метода ИФА. Степень боли и ее интенсивность оценивали с помощью «Опросника оценки степени хронической боли».Результаты. По сравнению с контрольной группой, у пациентов с остеоартрозом наблюдались значительно более высокие уровни IL-1β, TNF-α, IL-6, and IL-17 (P &lt; 0,0001). Уровень остеокальцина был значительно ниже в группе с остеоартрозом, чем в контрольной группе (среднее ± стандартное отклонение: 23,50 ± 19,30 нг/мл против 48,90 ± 5,20 нг/мл в контрольной группе), тогда как уровень склеростина был значительно выше (11,70 ± 1,10 нг/мл при остеоартрозе против 3,80 ± 0,90 нг/мл в контрольной группе, P &lt; 0,0001). Остеокальцин показал умеренную положительную корреляцию с IL-17, IL-6 и TNF-α; склеростин — отрицательную корреляцию с этими цитокинами.Обсуждение. Между остеокальцином и провоспалительными интерлейкинами существует сильная положительная корреляция. Снижение уровня склеростина при остеоартрите также происходит по общим механизмам с провоспалительными цитокинами, которые стимулируют экспрессию остеокальцина. Воспаление приводит к апоптозу остеоцитов или их дедифференцировке, что ещё больше снижает популяцию клеток, секретирующих склеростин, в субхондральной кости. Таким образом, объясняется обратная корреляция между уровнем склеростина и провоспалительными цитокинами при остеоартрите.Заключение. Результаты показывают выраженную связь «воспаление–кость» в патогенезе остеоартроза. Высокий уровень провоспалительных цитокинов может приводить к экспрессии остеокальцина, а также ингибировать склеростин, что способствует патологическим изменениям субхондральной кости. Эти биомаркеры отражают активность заболевания и, следовательно, могут быть использованы для раннего выявления, мониторинга и фенотипической стратификации остеоартроза.</p></abstract><trans-abstract xml:lang="en"><p>Background Osteoarthritis is multifactorial joint disorder marked by the progressive breakdown of articular cartilage, alterations in the underlying subchondral bone, and chronic inflammation of the synovial membrane.Objective To measure serum levels of bone biomarkers (osteocalcin and sclerostin) in osteoarthritis patients as compared to healthy controls and also to find out the link of these biomarkers with proinflammatory cytokines including IL-6, IL-17, IL-1β and TNF-α.Materials and methods A case-control study was implemented on 65 osteoarthritis patients and 35 healthy controls participants. Blood samples were taken from participants after obtaining written informed consent. Serum levels of cytokines and bone markers were measured using ELISA. Pain disability and intensity were measured using the "Chronic Pain Grade questionnaire".Results Compared to controls, patients with osteoarthritis had significantly higher levels of IL-1β, TNF-α, IL-6, and IL-17 (P &lt; 0.0001 for all). Osteocalcin levels were dramatically lower in the osteoarthritis group than the controls (mean ± SD: 23.50 ± 19.30 ng/mL vs. controls 48.90 ± 5.20 ng/mL), while sclerostin levels were much higher (11.70 ± 1.10 ng/mL in osteoarthritis vs. 3.80 ± 0.90 ng/mL in controls, P &lt; 0.0001). Osteocalcin showed a moderate positive correlation with IL-17, IL-6, and TNF-α; sclerostin showed a negative correlation with these cytokines.Discussion A strong positive correlation exists between osteocalcin and proinflammatory interleukins. The  downregulation of sclerostin in OA also shares common pathways with proinflammatory cytokines that drive expression of osteocalcin. Inflammation results in osteocyte apoptosis or their dedifferentiation, and  this further lowers the population of sclerostin-secreting cells in the subchondral bone. This is how the reverse correlation is explained between sclerostin and proinflammatory cytokines in OA.Conclusions Results show a robust inflammatory-bone axis in the pathogenesis of osteoarthritis. High proinflammatory cytokines might bring about osteocalcin expression and also inhibit sclerostin, leading to pathological subchondral bone alteration. These biomarkers reflect disease activity and therefore could be used for early detection as well as monitoring and phenotypic stratification of osteoarthritis.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>склеростин</kwd><kwd>остеокальцин</kwd><kwd>остеоартроз</kwd><kwd>IL-1β</kwd><kwd>TNF-α</kwd><kwd>IL-6</kwd><kwd>IL-17</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Sclerostin</kwd><kwd>Osteocalcin</kwd><kwd>Osteoarthritis</kwd><kwd>IL-1β</kwd><kwd>TNF-α</kwd><kwd>IL-6</kwd><kwd>IL-17</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Han Y, You X, Xing W, et al. Paracrine and endocrine actions of bone-the functions of secretory proteins from osteoblasts, osteocytes, and osteoclasts. Bone Res. 2018;6:16. doi: 10.1038/s41413-018-0019-6.</mixed-citation><mixed-citation xml:lang="en">Han Y, You X, Xing W, et al. 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