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Osteoarthritis (OA) is a widespread disease accompanied by persistent joint damage with obvious functional failure, which leads to early disability in patients. In OA, different groups of joints are involved in the pathological process. Hand joints are one of the classical sites of OA. The paper discusses the role of mechanical load, genetic factors, and sex hormone deficiency in the development of the disease. The treatment policy includes a set of non-pharmacological, pharmacological, and surgical methods.
The paper outlines the present view of the management tactics and treatment of chronic low back pain syndrome and the aspects of differential diagnosis of this condition.
Дегенерация межпозвонкового диска (МПД)-патологический процесс, возникающий вследствие взаимодействия генетических и средовых факторов, обусловливающих структурное и функциональное повреждение МПД и смежных структур, и являющийся начальным этапом дегенеративного каскада в позвоночно-двигательном сегменте. В инициации и прогрессировании дегенеративных процессов МПД традиционно обсуждается участие нескольких факторов: неадекватной механической нагрузки, снижения диффузии питательных веществ через замыкательные пластины и генетических факторов, которые вносят существенный вклад в развитие дегенеративных изменений. Выделяют 3 категории кандидатных генов, варианты кодирования которых ассоциированы с различными формами дегенеративных изменений МПД; разработана концептуальная модель генетических взаимодействий при дегенеративной болезни диска. Изучение вклада структурных нарушений в генез боли в спине, оценка влияния факторов риска позволяют оптимизировать тактику ведения больных и находить новые терапевтические решения, препятствующие прогрессированию болезни.
Spondyloarthritis (SpA) has extremely high social importance due to patient’s risk of early disability and a persistent decline in the quality of life. The last decade has brought important knowledge on its genetic mechanisms and pathophysiological aspects, as well as diagnosis and treatment. Axial spondyloarthritis (axSpA) is characterized by a pathological tissue response to immune and mechanical triggers, predominant lesion of the axial skeleton (spine, sacroiliac joints). It is divided into ankylosing spondylitis (AS) and non-radiological axSpA. Mechanical stress is proven to affect specific localization of inflammation and tissue damage in SpA. Areas of inflammation and erosion are limited to those having increased susceptibility and unique microanatomy. It is shown that a number of genes located outside the main histocompatibility complex significantly affect susceptibility to AS. A study of genes and polymorphisms not related to HLA-B27 revealed different pathogenesis mechanisms in various ethnic groups and formed a new understanding of AS pathogenesis and treatment. A family history of AS or anterior uveitis is useful to detect axSpA, as it is associated with the carrier of genetic marker HLA-B27. Researchers are strongly focused on studying AS patients» autoantibodies, where antibodies to CD74 are of the greatest diagnostic value. An imbalanced microbiome can trigger SpA development. Approximately 50 % of all SpA patients have microscopic signs of intestinal inflammation. The development and use of highly sensitive imaging methods in the future will lead to improved approaches for axSpA classification and more precise disease prognosis and therapeutic decisions. 18-fluorodeoxyglucose positron emission tomography is a sensitive method to determine syndesmophytes and sacroiliac joints in axSpA patients.
The paper presents the rheumatological aspects of the neck pain syndrome and the current view of the management and treatment of patients with cervicalgias.
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