Slugin VI osteocondrosi

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Osteocondrosi può essere praticato

Osteochondritis dissecans OCD or OD is a joint disorder in which cracks form in the articular cartilage and the underlying subchondral bone. Physical examination typically reveals Slugin VI osteocondrosi effusiontenderness, and a Slugin VI osteocondrosi sound with joint movement.

OCD is caused by blood deprivation in the subchondral bone. This loss of blood flow causes Slugin VI osteocondrosi subchondral bone to die in a process called avascular necrosis. The bone is then reabsorbed by the body, leaving the articular cartilage Slugin VI osteocondrosi supported prone to damage. The result is fragmentation dissection of both cartilage and Slugin VI osteocondrosi, and the free movement of these bone and cartilage fragments within the joint space, causing pain and further damage.

Non-surgical treatment is rarely an option as the ability for articular cartilage to heal is limited. As a result, even moderate cases require some form of surgery. When possible, non-operative forms of management such as protected reduced or non-weight bearing and immobilization are used. Surgical treatment includes arthroscopic drilling of intact lesions, securing of cartilage flap lesions with pins or screws, drilling and replacement of cartilage plugs, stem cell transplantationand joint replacement.

After surgery rehabilitation is usually a two-stage process of immobilization and physical therapy. Most rehabilitation programs combine efforts to protect the joint with muscle strengthening and range of motion. During the immobilization period, isometric exercisessuch as straight leg raises, are commonly used to restore muscle loss without disturbing the cartilage of the affected joint.

OCD occurs in 15 to 30 people perin the general population each year. Franz König coined the term osteochondritis dissecans indescribing it as an inflammation of the bone— cartilage interface. Many other conditions were once confused with OCD when attempting to describe how the disease affected the joint, including osteochondral fracture, osteonecrosisaccessory ossification center, osteochondrosisand hereditary epiphyseal dysplasia.

Some authors have Slugin VI osteocondrosi the terms osteochondrosis dissecans and osteochondral fragments as synonyms for OCD. In osteochondritis dissecans, fragments of cartilage or bone become loose within a joint, leading to pain and inflammation. These fragments are sometimes referred to as joint mice. OCD most commonly affects the knee, although it can affect other joints such as the ankle or the elbow.

People with OCD report activity-related pain that develops gradually. Non-specific symptomscaused by similar injuries such as sprains and strainscan delay a definitive diagnosis. Physical examination typically reveals fluid in the joint, tenderness, and crepitus. The tenderness Slugin VI osteocondrosi initially spread, but often reverts to a well-defined focal point as the lesion progresses.

Just as OCD shares symptoms with common maladies, acute osteochondral fracture has a similar presentation with tenderness in the affected Slugin VI osteocondrosi, but is usually associated with a fatty hemarthrosis. Although there is no significant pathologic gait or characteristic alignment abnormality associated with Slugin VI osteocondrosi, the patient may walk with the involved leg externally rotated in an attempt to avoid tibial spine impingement on the lateral aspect of the medial condyle of the femur.

Despite much research, the causes remain unclear but include repetitive physical traumaischemia restriction of blood flowhereditary and endocrine factors, avascular necrosis loss of blood flowrapid growth, deficiencies and imbalances in the ratio of calcium to phosphorus, and problems Slugin VI osteocondrosi bone formation. It is thought that repetitive microtraumawhich leads Slugin VI osteocondrosi microfractures and sometimes an interruption of blood supply to the subchondral bone, may cause subsequent localized loss of blood supply or alteration of growth.

Traumarather than avascular necrosis, is thought to cause osteochondritis dissecans in juveniles. Recent case reports suggest that some people may be genetically predisposed to OCD.

Osteochondritis dissecans differs from "wear and tear" degenerative arthritiswhich is primarily an articular surface problem. Instead, OCD is a problem of the bone underlying the Slugin VI osteocondrosi, which may secondarily affect the articular cartilage.

Left untreated, OCD can lead to the development of degenerative arthritis secondary to joint incongruity and abnormal wear patterns. OCD occurs when a loose piece of bone or cartilage partially or fully separates from the end of the bone, often because of a Slugin VI osteocondrosi of blood supply osteonecrosis and decalcification of the trabecular bone matrix. The loose piece may stay in place or slide around, making the joint stiff Slugin VI osteocondrosi unstable. OCD in humans most commonly affects the knees, [8] ankles, and elbow but can affect any joint.

In skeletally immature individuals, the blood supply to the epiphyseal bone is good, supporting both osteogenesis and chondrogenesis. With disruption of the epiphyseal plate vessels, varying degrees and depth of necrosis occur, resulting in a cessation of growth to both osteocytes and chondrocytes.

In turn, this pattern leads to disordered ossification of cartilage, resulting in subchondral avascular necrosis and consequently OCD. Four minor stages of OCD have been identified after trauma. These include revascularization and formation of granulation scar tissue, absorption of necrotic fragments, intertrabecular osteoid deposition, and remodeling of new bone.

With delay in the revascularization stage, an OCD lesion develops. A lesion can lead to articular-surface irregularities, which in turn may cause progressive arthritic deterioration. To diagnose osteochondritis dissecans, an X-rayCT scan or MRI scan can be performed to show necrosis of subchondral bone, formation of loose fragments, or both.

Physical examination often begins with examination of the patient's gait. In OCD of the knee, people may walk with the involved leg externally rotated in an attempt to avoid tibial spine impingement on the lateral aspect of the medial condyle of the femur. Next, the examining physician may check for weakness of the quadriceps.

This examination may reveal fluid in the joint, tenderness, and crepitus. The Wilson test is also useful in locating OCD lesions of the femoral condyle. Pain at 30 degrees of flexion and relief with tibial external rotation is indicative of OCD. Physical examination of a patient with ankle OCD often returns symptoms of joint effusion, crepitusand diffuse Slugin VI osteocondrosi localized tenderness. Examination often reveals symptoms of generalized joint pain, swellingand times with limited range of motion.

Some with loose body lesions may report catching, locking, or both. As a result, the alignment and rotation of all major joints in the affected extremity is common, as Slugin VI osteocondrosi extrinsic and intrinsic abnormalities concerning the affected joint, including laxity.

X-rays show lucency of the ossification front in juveniles. In older people, the lesion typically appears as an area of osteosclerotic bone with a radiolucent line between the osteochondral defect and the epiphysis. The visibility of the lesion depends on its location and on the amount of knee flexion used.

Harding described the lateral X-ray as a method to identify the site of an OCD lesion. Magnetic resonance imaging MRI is useful for staging OCD lesions, evaluating Slugin VI osteocondrosi integrity of the joint surface, Slugin VI osteocondrosi distinguishing normal variants of bone formation from OCD by showing Slugin VI osteocondrosi and cartilage edema in the area Slugin VI osteocondrosi the irregularity. MRI provides information regarding features of the articular cartilage and bone under the cartilage, including edema, fractures, fluid interfaces, articular surface integrity, Slugin VI osteocondrosi fragment displacement.

This indicates an unstable lesion or recent microfractures. Computed tomography CT scans and Technetiumm bone scans are also sometimes used Slugin VI osteocondrosi monitor the progress of treatment. Both of these seem to be closely correlated to the potential for healing in the fragment. CT scan and projectional radiography of a case of osteochondritis dissecans of parts Slugin VI osteocondrosi the superio-medial talus. Diffuse increase in T2 signal at the medial femoral condyle indicates marrow edema.

OCD is classified by the progression of the disease in stages. There are two main staging classifications used; one is determined by MRI diagnostic imaging while the other is determined arthroscopically. However, both stagings represent the pathological conditions associated with OCD's natural progression. Slugin VI osteocondrosi the arthroscopic classification of bone and cartilage lesions is considered standard, the Anderson MRI staging is the main form of staging used in this article.

Treatment options include modified activity with or without weight bearing; immobilization; cryotherapy ; anti-inflammatory medication ; drilling of subchondral bone; microfracture ; removal or reattachment of loose bodies; mosaicplasty and osteoarticular transfer system OATS procedures.

Slugin VI osteocondrosi articular cartilage's capacity for repair is limited: [46] partial-thickness defects in the articular cartilage do not heal spontaneously, and injuries of the articular cartilage which fail to penetrate subchondral bone tend to lead to deterioration of the articular surface.

Slugin VI osteocondrosi for non-operative treatment are limited to Slugin VI osteocondrosi immature teenagers with a relatively small, intact lesion and the absence of loose bodies. Non-operative management may include activity modification, Slugin VI osteocondrosi weight bearing partial or non-weight bearingand immobilization. The goal of non-operative intervention is to promote healing Slugin VI osteocondrosi the subchondral bone and prevent potential chondral collapse, subsequent fracture, and crater formation.

Once candidates for treatment have been screened, treatment proceeds according to the lesion's location.

For example, those with OCD of the knee are immobilized for four to six weeks or even up to six months in extension to Slugin VI osteocondrosi shear stress from the involved area; [49] however, they are permitted to walk with Slugin VI osteocondrosi bearing as tolerated. X-rays are usually taken three months after the start of Slugin VI osteocondrosi therapy; if they reveal that the lesion has healed, a gradual return to activities is instituted. The choice of surgical versus non-surgical treatments for osteochondritis dissecans is controversial.

A variety of surgical options exist for the treatment of persistently symptomatic, intact, partially detached, and completely detached OCD lesions. Post-surgery reparative cartilage is inferior to healthy hyaline cartilage in glycosaminoglycan concentration, histologicaland immunohistochemical appearance.

If non-surgical measures are unsuccessful, drilling may be considered to stimulate healing of the subchondral bone. Arthroscopic drilling may be performed by using an antegrade from the front approach from the joint space through the articular cartilage, or by using a retrograde from behind approach through the bone outside of the joint to avoid penetration of the articular cartilage. This has proven Slugin VI osteocondrosi with positive results at one-year follow-up with antegrade drilling in nine out of eleven teenagers with the juvenile form of OCD, [53] and in 18 of 20 skeletally immature people follow-up of five years who had failed prior conservative programs.

Pins and screws Slugin VI osteocondrosi be used to secure flap sometimes referred to as hinged lesions. The three methods most commonly used in treating full thickness lesions are arthroscopic drilling, abrasion, and microfracturing. InMagnusson established the use of stem cells from bone marrow with the first surgical debridement of Slugin VI osteocondrosi OCD lesion.

These cells typically differentiate into fibrocartilage and rarely form hyaline cartilage. While small lesions can be resurfaced using this form of surgery, the repair tissue tends to have less strength than normal hyaline cartilage and must be protected for 6 to 12 months. Results for large lesions tend to diminish over time; this can be attributed to the decreased resilience and poor wear characteristics of the fibrocartilage. In attempts to address the weaker structure of the reparative fibrocartilage, new techniques have been designed to Slugin VI osteocondrosi the defect with tissue that more closely simulates normal hyaline articular cartilage.

One such technique is autologous chondrocyte implantation ACIwhich is useful for large, isolated femoral defects in younger people. In this surgery, chondrocytes are arthroscopically extracted from the intercondylar Slugin VI osteocondrosi of the articular surface. The chondrocytes are grown and injected into the defect under a periosteal patch.

ACI surgery has reported good to excellent results for reduced swelling, pain and locking in clinical follow-up examinations. These Slugin VI osteocondrosi have demonstrated the ability to regenerate both the cartilage and the underlying subchondral bone. Similar to OATS, arthroscopic articular cartilage paste grafting is a surgical procedure offering cost-effective, long-lasting results for stage IV lesions. A bone and cartilage paste derived from crushed plugs of the non-weight-bearing intercondylar notch can achieve pain relief, repair damaged tissue, and Slugin VI osteocondrosi function.

Some methods of fixation for unstable lesions include countersunk compression screws and Herbert screws or pins made of stainless steel or materials that can be absorbed by the body. Although each case is unique and treatment is chosen on an individual basis, ACI is generally performed on large defects in skeletally mature people.