PubMed · 692929
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J C Renier. 1978-09-08. [Coxarthrosis].. https://pubmed.ncbi.nlm.nih.gov/692929/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Based on the experience gained with the surgical treatment of over 900 patients with different forms of degenerative dystrophic diseases of the hip joint the current principles of the choice of different types of surgical interventions were defined. As far as the patients with aseptic necrosis of the head of the femur are concerned, the main problem in this case lies in the early diagnosis of osteonecrosis. The surgical treatment is specified by the leading factor of the pathogenesis at every stage of the development of the process (vascular disorders, changes in the biomechanism of the joint). The planning of operations in patients with dysplastic coxarthrosis rests on the consideration of 8 basic factors that influence the disease by means of factorial analysis and determination of the prognostic estimations of the treatment efficacy.
Ischemic or avascular necrosis of the hip is a serious complication of the treatment of developmental hip dysplasia. The degree of ischemic insult can be classified based on an understanding of the vascularity of the proximal femur. Physeal involvement and subsequent growth disturbance, producing late deformity of the proximal femur, can compromise long-term results. Early recognition of ischemic necrosis patterns can be helpful in planning further treatment.
Eicosanoids, including prostaglandins and leukotrienes, are important mediators of inflammation. To observe inflammation after necrosis, the histology and the changes of eicosanoid levels were compared in the subchondral cortex and spongy bone of femoral head of sixteen patients with Ficat III or IV idiopathic avascular necrosis (AVN). Neither inflammatory cells nor elevation of eicosanoid levels were observed in the necrotic subchondral cortex or osteochondral junction, whereas infiltration of lymphocytes and plasma cells, fibrosis, and fat emboli were present in the reparative front of necrotic spongy bone. Biochemical analysis in this region revealed significant increases of prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2 (TXB2), leukotriene B4 (LTB4), and LTC4. The increased eicosanoids due to initial necrosis become aggravating factors by increasing vascular permeability, which leads to marrow edema and intraosseous hypertension; it ultimately develops into a cycle of inflammation and AVN.