References

pmj

Тихоокеанский медицинский журнал

Pacific Medical Journal

1609-1175

TGMU

10.17238/PmJ1609-1175.2017.1.27-35

pmj-107

Research Article

ОБЗОРЫ

REVIEWS

Аваскулярный некроз головки бедренной кости

Avascular necrosis of the femoral head

Мустафин

Р. Н.

Mustafin

R. N.

ruji79@mail.ru

Хуснутдинова

Э. К.

Khusnutdinova

E. K.

noemail@neicon.ru

Башкирский государственный университетРоссияBashkir State University (32 Zaki Validi St. UfaRussian Federation

Башкирский государственный университет; Институт биохимии и генетики Уфимского научного центра РАНРоссияInstitute of Biochemistry and Genetics, Ufa Research CenterRussian Federation

2017

28032017

012735

2017

Мустафин Р.Н., Хуснутдинова Э.К.

Mustafin R.N., Khusnutdinova E.K.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://www.tmj-vgmu.ru/jour/article/view/107

Аваскулярный некроз головки бедренной кости - мультифакториальное заболевание с прогрессирующим развитием тяжелого вторичного коксартроза. Различают вторичный и идиопатический остеонекроз. Патогенез болезни связан с местным нарушением кровообращения, коагулопатиями и ослаблением регенерации костной ткани. Гистологически пораженная кость характеризуется образованием пустых лакун с васкуляризированной фиброзной тканью вокруг, в субхондральной зоне и зоне некроза возрастает активность остеокластов, в то время как в зоне склероза усиливается активность остеобластов. Среди лабораторных показателей определяется значительное повышение уровней ингибитора-1 активатора плазминогена, фактора Виллебранда, ингибитора-1 активатора плазминогена, С-реактивного белка, интерлейкина-33, снижение уровней грелина, остеопротегерина, перекрестно-связанного N-концевого телопептида, С-концевого пептида проколлагена-1, фактора некроза опухоли-а, miR-17-5p. При генетических исследованиях выявляются мутации в гене COL2A1 и протромбина, ассоциации полиморфных локусов в генах фактора V Лейдена, метилентетрагидрофолатредуктазы, тканеспецифического активатора плазминогена, ингибитора-1 активатора плазминогена. Лечение включает оперативные вмешательства и коррекцию цитоактивности. Имеются данные о способности бисфосфонатов предотвращать коллапс головки бедра.

Avascular necrosis of the femoral head is a multifactorial disease with progressive development of severe secondary coxarthrosis. There are two types of necrosis - secondary and idiopathic. The pathogenesis of the disease is associated with the local blood circulation disorders, coagulopathies and violation of bone tissue regeneration. A bone with a histologic lesion is characterized by the formation of empty lacunae with vascularized fibrous tissue around it, and the osteoclast activity increases in the subchondral and necrosis zone, while in the sclerosis zone the osteoblast activity enhance. Among the laboratory parameters determined a significant increase in the levels of inhibitor 1 plasminogen activator, Willebrand factor, inhibitor 1 plasminogen activator, C-reactive protein, interleukin 33, a decrease of the ghrelin and osteoprotegerin levels, cross-linked N-terminal telopeptide, the C-terminal peptide of procollagen 1, tumor necrosis factor a, miR-17-5p. In genetic studies revealed mutations in the gene COL2AI and prothrombin, the association of polymorphic loci of genes for factor V Leiden, methylenetetrahydrofolate, tissue-specific plasminogen activator inhibitor 1, plasminogen activator. Treatment includes surgery and correction of the cytological activity. There is evidence for the ability of bisphosphonates to prevent the collapse of the femoral head.

остеонекрозпатогенезклиникадиагностика

osteonecrosispathogenesisclinicdiagnostics

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The authors declare that there are no conflicts of interest present.