Showing posts with label Dissecans. Show all posts
Showing posts with label Dissecans. Show all posts

Wednesday, February 12, 2014

Knee Osteochondritis Dissecans

Background

Osteochondritis dissecans (OCD), by definition, is a disorder of one or more ossification centers, characterized by sequential degeneration or aseptic necrosis and recalcification. OCD lesions involve both bone and cartilage. These lesions differ from acute traumatic osteochondral fractures; however, they may manifest in a similar fashion. OCD lesions also must be differentiated from meniscal pathology. OCD causes 50% of loose bodies in the knee. The etiology of these lesions is multifactorial, including trauma, ischemia, abnormal ossification centers, genetic predisposition, or some combination of these factors. Little agreement exists among researchers regarding the etiology of OCD.

Images of osteochondritis dissecans of the knee are provided below:

Anteroposterior and lateral radiographs of medial Anteroposterior and lateral radiographs of medial femoral condyle osteochondritis dissecans. Anteroposterior radiograph of medial femoral condyAnteroposterior radiograph of medial femoral condyle osteochondritis dissecans. Arthroscopic view of medial femoral condyle osteocArthroscopic view of medial femoral condyle osteochondritis dissecans, hinged medially. Note the large size and thickness of the fragment. Arthroscopic view of osteochondritis dissecans of Arthroscopic view of osteochondritis dissecans of the medial femoral condyle. The osteochondral fragment has been elevated from the crater. Note the sclerotic crater with an interposed fibrocartilaginous layer. This lesion has been previously treated with drilling; an old drill hole can be seen faintly at the upper aspect of the crater. Arthroscopic debridement of the osteochondritis diArthroscopic debridement of the osteochondritis dissecans bed to bleeding bone. Replacement of the fragment and temporary KirschneReplacement of the fragment and temporary Kirschner wire stabilization. Completed osteochondritis dissecans stabilization Completed osteochondritis dissecans stabilization with 2 Herbert screws. On initial examination, the most lateral defect was comminuted and removed; the larger weight-bearing surface was maintained and stabilized.

In 1558, Ambroïse Paré removed loose bodies from a knee joint. In 1870, Paget described quiet necrosis within the knee. In 1888, König coined the term "osteochondritis dissecans." He proposed this condition was caused by spontaneous necrosis due to trauma.

With the advent of roentgenography, osteochondrotic conditions in other joints, primarily the hip, were recognized. In 1910, Legg, Calvé, and Perthes independently identified a condition of the hip joint in children, which is now known as Legg-Calvé-Perthes disease. In 1921, Waldenström introduced the term coxa plana (ie, disintegration of capital femoral epiphysis.)

Since the introduction of radiography, 50 additional anatomic sites within the body where OCD can occur have been identified.

Recent studies

Tabaddor et al evaluated the efficacy and safety of poly 96L/4D-lactide bioabsorbable copolymer fixation for unstable OCD in 24 adolescents (mean age, 14.4 y). Plain films at an average of 19.2 months after surgery showed interval healing in 9 patients, no significant change in 1, complete healing in 13, and loose bodies with no interval healing in 1. MRIs showed interval healing in 16 of 17 knees at a mean follow-up of 22.4 months.[1]

Pascual-Garrido et al examined the outcomes of surgical procedures for osteochondritis dissecans in 46 adult patients (48 knees), with patients ranging in age from 20 to 49 years. Patients who were treated with surgical cartilage procedures showed durable function and symptomatic improvement at a mean of 4 years follow-up. Patients treated with arthroscopic reduction and internal fixation and loose-body removal had greater improvement in outcome scores than those treated with an osteochondral allograft. Seven knees required revision procedures at a mean follow-up of 14 months.[2]

Adachi et al evaluated the functional and radiographic outcome of retroarticular drilling without bone grafting in 12 patients with juvenile osteochondritis dissecans after 6 months of unsuccessful nonoperative treatment. The mean Lysholm score significantly improved postoperatively (from 72.3 to 95.8). All lesions except 1 healed after retroarticular drilling, and healing was achieved at a mean of 4.4 months on plain radiographs and 7.6 months on magnetic resonance imaging.[3]

Kijowski et al retrospectively compared the sensitivity and specificity of previously described magnetic resonance imaging criteria for the detection of instability in patients with juvenile or adult osteochondritis dissecans of the knee, with arthroscopic findings as the reference standard. Separately, previously described MR imaging criteria for detection of OCD instability were 0-88% sensitive and 21-100% specific for juvenile OCD lesions and 27-54% sensitive and 100% specific for adult OCD lesions. When used together, the criteria were 100% sensitive and 11% specific for instability in juvenile OCD lesions and 100% sensitive and 100% specific for instability in adult OCD lesions. The authors concluded from their findings that previously described MR imaging criteria for OCD instability have high specificity for adult but not juvenile lesions of the knee.[4]

NextEpidemiologyFrequencyUnited StatesThe average age at presentation is 10-20 years, but osteochondritis dissecans may occur in persons of any age group.The male-to-female ratio is 2-3:1.Bilateral involvement is noted in 30-40% of cases.In 85% of cases, lesions are observed on the medial femoral condyle (MFC) of the knee; 15% of cases are observed on the lateral femoral condyle. Of the MFC lesions, 70% occur in the posterolateral aspect. Of patients with OCD, 21-40% have some history of trauma.International

In Sweden, prevalence is reported at the following levels:

In skeletally immature patients, 150 cases per 250,000 people are reported.In skeletally immature female patients, 18 cases per 100,000 people are reported.In skeletally immature male patients, 29 cases per 100,000 people are reported.PreviousNextFunctional Anatomy

In skeletally immature individuals, the vascularity to epiphyseal bone is very good, supporting both osteogenesis and chondrogenesis. With disruption of the epiphyseal 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 nonspecific changes that produce disordered enchondral ossification, resulting in subchondral avascular necrosis or OCD.

Four stages of OCD have been identified, including revascularization and formation of granulation tissue, osteoclasis of necrotic fragments, intertrabecular osteoid deposition, and remodeling of new bone. With delay in the revascularization stage, an osteochondritis dissecans lesion develops. OCD lesions may lead to articular-surface irregularities, which can cause degenerative arthritic changes.

PreviousNextSport Specific Biomechanics

A proposed cause of OCD is an anatomic variation allowing the lateral aspect of the femoral condyle to abut the tibial spine, leading to repetitive localized epiphyseal microtrauma with osteochondral separation and subsequent OCD. This pattern may lead the patient to walk with the tibia externally rotated to avoid this abutment.

PreviousProceed to Clinical Presentation , Knee Osteochondritis Dissecans

Friday, January 31, 2014

Humeral Capitellum Osteochondritis Dissecans

Background

In 1889, Francis Konig described osteochondritis dissecans as a subchondral inflammatory process of the knee resulting in a loose fragment of cartilage from the femoral condyle. Although no inflammatory cells have been identified on histologic sections of excised fragments, the term osteochondritis dissecans has persisted and since been broadened to describe a similar process occurring in many other joints, including the knee, hip, ankle, elbow, and metatarsophalangeal joints.[1, 2, 3, 4, 5, 6]

Humeral capitellum osteochondritis dissecans occurs after the capitellum has ossified and is the result of "injury" to the subchondral bone. The initial histologic appearance is consistent with avascular necrosis. The avascular necrosis of subchondral bone leads to loss of support for adjacent cartilaginous structures. The natural history of some osteochondritis dissecans lesions is the separation of these structures from the capitellum, leading to the development of an osteochondral fragment of articular cartilage on the underlying bone at the superficial surface of the diarthrodial joint.[7, 8, 9, 10]

For excellent patient education resources, see eMedicineHealth's patient education article Tennis Elbow.

Related Medscape Reference topics:

Elbow and Forearm Overuse Injuries

Lateral Epicondylitis

Medial Epicondylitis

Overuse Injury

Related Medscape resources:

Resource CenterExercise and Sports Medicine

Specialty SiteOrthopaedics

Specialty SitePathology & Lab Medicine

American Orthopaedic Society for Sports Medicine 31st Annual Meeting-Competing Tennis Elbow Surgeries Both Deemed Successful

Deep transverse friction massage for treating tendinitis

Physical Therapy and Brace Therapy for Tennis Elbow

NextEpidemiologyFrequencyUnited States

Humeral capitellum osteochondritis dissecans comprises 6% of all osteochondritis dissecans cases.

In the United States, humeral capitellum osteochondritis dissecans most commonly occurs in the second decade of life and is rare in individuals younger than 10 years or older than 50 years. Humeral capitellum osteochondritis dissecans is primarily observed in children aged 10-15 years.

Approximately 85% of osteochondritis dissecans cases involve males, with a large proportion of these being Little League pitchers. Humeral capitellum osteochondritis dissecans is believed to affect 4.1 of every 1000 males. Among male relatives of affected males, the prevalence rate is 14.6%. Osteochondritis dissecans also occurs in females, most notably gymnasts. Finally, it also commonly occurs in persons who participate in racquet sports and in weight lifting.

Humeral capitellum osteochondritis dissecans usually occurs in the dominant arm. In up to 20% of cases, it occurs bilaterally.

PreviousNextFunctional Anatomy

While the trochlea of the distal humerus articulates with the sigmoid fossa of the proximal ulna, the capitellum of the distal humerus articulates with the head of the radius. These articulations, in conjunction with the radioulnar articulation, compose the elbow joint. The articulation of the radial head and humeral capitellum provides mobility for a wide range of supination and pronation, as well as flexion and extension. This area is thus particularly susceptible to the rotary, compressive, axial, and angular forces associated with activities such as throwing.

The radiocapitellar articulation is supported laterally by the radiocollateral, the accessory collateral, the lateral ulnar collateral, and the annular ligaments. These ligaments function to stabilize the elbow throughout the motions of pronation, supination, flexion, and extension.

PreviousNextSport-Specific Biomechanics

The exact etiology of osteochondritis dissecans is unclear.[1, 4, 5, 11, 12, 13] In overhead throwing, articular forces at the radiocapitellar articulation are significant. Progressive pronation, compression, and rotation occur on the anteromedial radial head and the inferior and medial aspects of the capitellum as the elbow is extended.

These forces are believed to lead to fibrillation on the articular surface and subchondral osseous changes, with the possible production of osteocartilaginous fragments and the development of humeral capitellum osteochondritis dissecans. The valgus orientation of the elbow contributes to these compressive loads. Excessive axial loading to the elbow is also believed to be the primary cause of injury in gymnasts and weight lifters.[14, 15]

PreviousProceed to Clinical Presentation , Humeral Capitellum Osteochondritis Dissecans