Finite Element Modeling of Chondrolabral Lesions in Pincer-Type Femoroacetabular Impingement.

Background: The prevalence of chondrolabral lesions due to femoroacetabular impingement (FAI) is 93% in cadaveric material. As a biomechanically determined factor, it can lead to hip destruction and early osteoarthritis in pincer-type impingement. The aim of this work was to study the biomechanism and stress-strain behavior of chondrolabral lesions in pincer-type impingement during daily activity-associated movements.

CHANGES IN ARTICULAR CARTILAGE OF THE HIP JOINT INDUCED BY ACETABULAR LABRUM DAMAGE.

Objective: The aim: Histological studies of hip joint cartilage after articular labrum resection.

Patients And Methods: Materials and methods: Articular labrum of hip joint was excised in adult rabbits. In 1,5 and 4 months, the histology of the joint was studied.

[Orthopedic treatment of the shoulder joint impairment in patients with rheumatoid arthritis].

Brachial joint affection in patients, suffering rheumatoid arthritis, occupies a third place after such of the elbow and the hand. Due to significant reduction of a freedom degree, caused by inflammation, the upper extremity looses function of active instrument for the items transposition. Volume of surgical treatment of such patients depends on stage of the process.

[Lesions of the radio-carpal joint in patients with rheumatoid arthritis and its surgical treatment].

Affection of radio-carpal joint is most frequently revealed in patients, suffering rheumatoid arthritis. While the disease progressing in almost 75% of patients the inflammatory changes in radio-carpal joint occur. An acute and chronic synovitis, damage of a cartilage constitute a cause of a typical erosion of bones inside a joint, weakening of a tendo-ligamentous apparatus and its further deformity.

Arginase inhibitor in the pharmacological correction of endothelial dysfunction.

THIS PAPER IS ABOUT A WAY OF CORRECTION OF ENDOTHELIAL DYSFUNCTION WITH THE INHIBITOR OF ARGINASE: L-norvaline. There is an imbalance between vasoconstriction and vasodilatation factors of endothelium on the basis of endothelial dysfunction. Among vasodilatation agents, nitrogen oxide plays the basic role.