Peripatellar finger tenderness
Introduction
Introduction Common in patellofemoral joint cartilage injury. Articular cartilage damage is very common in sports injuries, but it is difficult to diagnose, especially early diagnosis is almost impossible in routine examinations, so it is often ignored and not treated in time. However, no matter what kind of cartilage damage, it may eventually lead to degeneration and necrosis of chondrocytes and permanent damage, so it has attracted attention in recent years.
Cause
Cause
1. Acute or chronic trauma: It may directly hit the cartilage and destroy the collagen fiber mesh arch structure in the cartilage. It can also directly cause tangential fracture of cartilage. Chrisman has studied the relationship between trauma and tibial rickets in a biochemical perspective for many years. He found that within 2 hours after cartilage injury, the concentration of free arachidonic acid in cartilage can be increased by 4 times. Arachidonic acid is a precursor of prostaglandins, a major component of phospholipid membranes. Its product is converted into prostaglandin E2, which stimulates AMP circulation, releases tissue protein kinase, destroys the chain of chondroitin sulfate and protein binding in cartilage matrix, and causes cartilage matrix to be lost. It causes the cartilage to soften the metabolites into the synovial fluid, causing inflammation of the synovial inflammatory reaction, and stimulates the synovial membrane to release a large amount of enzymes to further destroy the cartilage, causing a vicious circle.
2. Strain of the patellofemoral joint: long-term abnormal friction and compression of the tibial cartilage, especially in the knee flexion position, repeated jumps, weights, and torsions can cause excessive stress between the patellofemoral or Uneven stress distribution makes the tibial cartilage prone to damage, and suffers from tibial rickets.
3. patellofemoral joint instability: common unstable factors such as high or low tibia, knee Q angle abnormality, humeral tilt, humeral torsion deformity, humerus or femoral condyle dysplasia, due to abnormal position of the humerus or abnormal line alignment, or The contact surface stress between the patellofemoral joints is abnormal, which causes the tibial rickets. Many scholars have done a lot of work on the stress distribution and stress test of the patellofemoral joints. There are high contact pressure theory, low contact pressure theory, and pressure division. The theory of unevenness and the theory of increased intraosseous pressure in the tibia have experimental support, but whether the pressure is too high or the pressure is not uniform, as long as the pressure exceeds or does not reach the normal range of the tibial cartilage, it may lead to cartilage. transsexual.
4. Pathological changes: The main pathological changes of tibial rickets are manifested as softening of the tibial cartilage, formation of yellow fissure and exfoliation, and increased secretion of synovial inflammation. Periorbital fasciitis supports inflammatory changes and hyperplasia or contracture. The exfoliated cartilage pieces may be detached into the joint mouse in the joint cavity, causing the knee joint to interlock.
The lesions of the athlete's tibia cartilage were most common in the medial plane, followed by the central zone (60° contact zone) and the medial zone. However, Ficat reported the highest incidence in the lateral area.
Rijnds divides the cartilage lesions of the tibial chondroma into four degrees. The degree I is the soft and mild swelling and yellowing of the cartilage in the subfracture area of the cartilage surface, which is roughly equivalent to the first layer (stationary layer) of chondrocytes, and the second degree is cartilage. 2 layers (transition layer) and 3rd layer (mast cell layer) are damaged, there are shallow cracks visible to the naked eye, III degree is cartilage layer 4 (calcification layer) damage, deep cracks, local subchondral bone, cartilage fragments Exfoliation from the surface layer, IV degree damage to the subchondral bone, ulcer formation, local cartilage destruction. There is often a gradual erosion of healthy cartilage around the lesion adjacent to the cartilage, often with varying degrees of degeneration.
Examine
an examination
Related inspection
Magnetic and magnetic resonance imaging (MRI) of the bones and joints of the extremities
(1) X-ray findings: taking ordinary X-ray film does not make much sense for diagnosis, but choose to take the axial position of the humerus with different knee angles. You can observe the shape of the tibia and the degree of hardening of the subchondral bone of the humerus. For example, the tibia angle tibia depth index tibia index groove angle, overlap angle and other lateral knee X-ray films can detect the abnormal humerus position when the tibia length (P) is equal to the patellar ligament length (PT). When PT exceeds 15% of P, Or more than 1cm, it is a high tibia.
(2) MRI examination: exfoliation and ulceration of the tibial cartilage can be found.
Diagnosis
Differential diagnosis
diagnosis:
1. Clinical features
When the patient is active, complaining of soreness after sputum, symptoms such as aggravation of pain when going up and down the floor or half a squat, such as sacral squeaking, sputum sputum, squeaky sputum, single-legged semi-salary pain, sputum and tenderness, etc., can be roughly diagnosed as the disease.
2. Imaging examination
(1) X-ray findings: taking ordinary X-ray film does not make much sense for diagnosis, but choose to take the axial position of the humerus with different knee angles. You can observe the shape of the tibia and the degree of hardening of the subchondral bone of the humerus. For example, the tibia angle tibia depth index tibia index groove angle, overlap angle and other lateral knee X-ray films can detect the abnormal humerus position when the tibia length (P) is equal to the patellar ligament length (PT). When PT exceeds 15% of P, Or more than 1cm, it is a high tibia.
(2) MRI examination: exfoliation and ulceration of the tibial cartilage can be found.
3. The final diagnosis basis
Diagnosis depends on arthroscopic surgery or MR.
