Ключевые компоненты патогенеза асептической нестабильности эндопротезов суставов



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Аннотация

Данный литературный обзор посвящён комплексному анализу патогенетических механизмов асептической нестабильности (АН) эндопротезов суставов и связанного с ней перипротезного остеолиза. На основе систематизации современных научных данных рассмотрены ключевые факторы, определяющие развитие этих осложнений. Центральное место занимает анализ дебрис-индуцированного воспаления, при котором частицы износа материалов эндопротеза (металлы, полиэтилен, костный цемент) активируют макрофаги, что приводит к выбросу провоспалительных цитокинов (TNF-α, IL-1, IL-6). Эти медиаторы нарушают баланс костного ремоделирования путём стимуляции остеокластогенеза посредством активации сигнального пути RANKL/RANK/OPG и подавления функции остеобластов. Особое внимание уделено роли механических факторов: физиологической микроподвижности имплантата, которая при превышении порога толерантности (более 50–150 мкм) препятствует остеоинтеграции и способствует формированию фиброзной синовиальноподобной интерфейсной мембраны, а также явлению стресс-шилдинга, приводящего к резорбции кости из-за перераспределения нагрузки. Рассмотрено влияние жидкостных токов под давлением (до 150 мм рт. ст.), которые усиливают деструкцию костной ткани через прямое воздействие на остеоциты. Подробно проанализированы специфические иммунные реакции на компоненты эндопротеза: гаптенные свойства ионов металлов (Co, Cr, Ti) и костного цемента инициируют реакции гиперчувствительности замедленного типа с образованием неоантигенов и Т-клеточной активацией. Обсуждается локальное и системное токсическое действие металлических частиц, повреждающих ДНК, угнетающих пролиферацию остеобластов и мезенхимальных стволовых клеток. Отмечен вклад бактериальных эндотоксинов, сорбирующихся на частицах дебриса, которые потенцируют воспаление даже при отсутствии клинической инфекции. Подчёркивается, что АН является многофакторным процессом, в котором совокупное действие перечисленных механизмов смещает равновесие в сторону остеолиза. Рассмотрены перспективные направления для снижения риска АН, включая изучение генетической предрасположенности, разработку биосовместимых материалов с улучшенными трибологическими свойствами и таргетные стратегии подавления воспалительного каскада. Систематизация патогенеза создаёт основу для повышения долговечности эндопротезов и снижения частоты ревизионных вмешательств.

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Александр Дмитриевич Каменский

Федеральное государственное бюджетное образовательное учреждение высшего образования «Российский университет медицины» Министерства здравоохранения Российской Федерации

Автор, ответственный за переписку.
Email: alexkamenskiyvm@yandex.ru
ORCID iD: 0009-0007-3489-3555
SPIN-код: 9994-8149

Аспирант кафедры травматологии, ортопедии и медицины катастроф

Россия, 127006, Российская Федерация, г. Москва, улица Долгоруковская, дом 4

Юрий Вениаминович Парахин

Частное Учреждение Здравоохранения «Клиническая Больница «РЖД-Медицина» им. Н.А. Семашко, Москва, Россия

Email: parachinyuri@mail.ru
ORCID iD: 0009-0000-2591-0949
SPIN-код: 2524-0855

Руководитель Центра травматологии и ортопедии

Россия, 109386, Москва, Ставропольская улица, 23

Михаил Викторович Паршиков

Федеральное государственное бюджетное образовательное учреждение высшего образования «Российский университет медицины» Министерства здравоохранения Российской Федерации

Email: parshikovmikhail@gmail.com
ORCID iD: 0000-0003-4201-4577
SPIN-код: 5838-4366

Профессор кафедры травматологии, ортопедии и медицины катастроф

Россия, 127006, Российская Федерация, г. Москва, улица Долгоруковская, дом 4

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