Osteochondrosis

Overview

The term osteochondrosis refers to a group of disorders affecting patients with an immature skeleton. The etiology of joint pain in these individuals is frequently osteochondrosis, although traumatic, inflammatory, or viral causes should also be checked out. Osteochondrosis develops as a result of abnormal growth, injury, or overuse of the growth plate and surrounding ossification centers.

Overall, boys are more impacted, and symptoms often occur between the ages of 10 and 14 years. Boys are considered to be more typically impacted because they are more vulnerable to childhood trauma and overuse injuries. The majority of patients arrive with pain and impairment. The hip, knee, foot, elbow, and back are the most often afflicted areas of the body.

Osteochondrosis definition

Osteochondrosis refers to a set of illnesses that damage the developing skeleton. These conditions are caused by aberrant development, damage, or overuse of the growing growth plate and its accompanying ossification centers. Although the specific causation of these illnesses is unknown, hereditary factors, recurrent stress, vascular abnormalities, mechanical issues, and hormone imbalances may all play a part. The hip problem Legg-Calve-Perthes disease produces hip discomfort, an atraumatic limp, and knee pain.

The disorders Osgood-Schlatter and Sinding-Larsen–Johannson are common causes of anterior knee discomfort that is worsened by leaping and kneeling. Severe illness produces heel discomfort, which is aggravated by activity and the usage of cleats. It is sometimes mistaken for Achilles tendonitis and is treated with activity and shoe changes, heel cups, and calf stretches. Freiberg disease and Köhler bone disease, both of which affect the metatarsal head and navicular bone, are common causes of foot discomfort.

In both illnesses, radiographs show sclerosis, flattening, and fragmentation of bone. Medial epicondyle apophysitis or Panner disease can cause elbow discomfort. Tossing cessation and acetaminophen or nonsteroidal anti-inflammatory medicines are used to treat medial epicondyle apophysitis, which is aggravated by repeated throwing.

Panner disease is the leading cause of lateral-sided elbow discomfort in children under the age of ten. It may or may not be related to frequent tossing, and it resolves on its own. Back discomfort and a humpback deformity are symptoms of Scheuermann disease, which is caused by vertebral bone anterior wedging.

Osteochondrosis refers to a set of conditions that affect different parts of the body. This classification is based mostly on the morphologic and evolutionary similarities of the sites involved, as visible on radiographs. Osteochondroses are a diverse set of unrelated lesions that share the following characteristics:

• Predilection for affecting the immature skeleton
• Involvement of the epiphysis
• Apophysis or epiphysioid bone
• Radiographic picture dominated by fragmentation, collapse, sclerosis, and reossification of osseous centers

Almost all of the epiphyses can be impacted. Many of the characteristics of ischemia necrosis can be seen in involved areas, both radiologically and histologically.

It is preferable to use the term necrosis rather than avascular necrosis since, despite the presence of ischemia, arteries are present. The vascular theory is contentious since conditions such as Blount disease and Scheuermann disease do not induce ischemia alterations, and trauma has been suggested as a mechanism for a variety of diseases. However, the ischemia idea should not be dismissed just yet, because research has led to a fresh focus on numerous coagulation-related variables and vascular involvement as the principal causes.

The nomenclature used to describe osteochondroses has gotten more complicated. The term syndrome may be preferable to the term disease in general because it arguably encompasses both radiographic patterns and clinical manifestations. Some of these disorders, such as Sever disease and Van Neck disease, may be better described as phenomena.

Although some doctors classify osteochondritis dissecans as an osteochondrose, this classification is debatable. Osteochondritis dissecans is not primarily a disease process affecting growth centers, and it affects both adults and children. Only the juvenile version of this disease should be regarded an osteochondrosis since it may show localized ischemia involvement.

The inclusion of posttraumatic osteonecrosis and normal ossification variations in an extended taxonomy of osteochondroses has also been debated. It has been possible to establish the etiologic roots of various disorders as our understanding of them has expanded. The authors believe that morphologically comparable but etiologically unrelated illnesses should not be grouped together.

Nonsurgical and surgical therapies are the two broad categories of osteochondrosis therapy. The mainstay of treatment for osteochondroses is medical and supportive treatments. Surgery is only advised for certain goals, such as replacing failed conservative therapy, symptom relief, or minimizing late handicap. Although the course of osteochondrosis is lengthy, it is usually self-limiting. As a result, it is prudent to give the patient's reparative processes enough time to work.

Pathophysiology

Although the first events in the pathophysiology of osteochondrosis are unknown, clinical and radiologic evidence suggests to ischemia necrosis of the ossification core. This process might be caused by a main vascular event, a specific traumatic experience, or a combination of additive traumas.

The osteochondrotic process is essentially epiphyseal osseous nucleus degradation. This is very definitely the result of either

1. Interference with the blood supply, which leads to necrosis of the cartilage-canal vessels in the subchondral bone and adjacent epiphysis, or 
2. failure of the bony centrum to enlarge and disordered proliferation of the cartilaginous cells in the epiphysis.

The illness process might be sequential or concurrent. It can affect a single epiphysis (isolated illness) or numerous (multiple-site disease), and the sesamoids are not immune (as in Sinding-Larsen syndrome and involvement of first metatarsal sesamoids). The basic mechanisms appear to be the same for isolated and multi-site illness. However, depending on the pressures and strains to which the epiphyses have been exposed, the presentations may vary. The long-term clinical outcome of a patient is determined by the effectiveness of regeneration and repair.

There is little long-term harm done with full recovery. However, incomplete healing or inability to heal can lead to persistent pain and impairment later in life. As a result, the physician must be cautious to avoid missing an osteochondrosis in a young patient.

Ponseti proposed that the following features are common to all osteochondroses:

• Uncertain etiology
• Clinical pattern of progression
• Radiologic appearance of ischemic necrosis

The following models for the development of osteochondroses:

• Normal epiphysis subjected to extreme trauma (eg, pitcher’s elbow with osteochondritis dissecans of the capitellum)
• Mildly dyschondrotic epiphysis subjected to more stress than usual (eg, Perthes disease)
• Severely affected dyschondrotic epiphysis subjected to normal stress (eg, the capital femoral epiphysis in Gaucher disease)

Classification of Osteochondrosis

Previously, osteochondroses were classified as pressure, traction, and atavistic (Burrows' classification) or compression, tension, and atavistic (Goff's classification). These systems were deficient. Siffer suggested a categorization of osteochondroses into articular, nonarticular, and physeal forms, which is still widely used today.

Articular osteochondroses exhibit the following characteristics:

• Primary involvement of the articular and epiphyseal cartilage and a subjacent endochondral ossification center – Freiberg disease 
• Secondary involvement of the articular and epiphyseal cartilage as a consequence of ischemic necrosis of subjacent bone – Perthes disease, Köhler disease, osteochondritis dissecans

Nonarticular osteochondroses occur at the following locations:

• Tendinous attachments - Osgood-Schlatter syndrome, Monde-Felix disease
• Ligamentous attachments - Vertebral ring
• Impact sites - Sever disease

Physeal osteochondroses involve the following:

• Long bones – Tibia vara ( Blount disease)
• Scheuermann disease

Etiology

Osteochondroses should be considered syndromes rather than illnesses since they might be caused by a variety of factors, some of which are unknown. As a result, the etiology is mostly speculative. The primary goal is to discover any identifiable pathologic condition that may be managed or perhaps treated with appropriate therapy.

Probable causes

Several probable causes of osteochondroses have been postulated. Social deprivation, food inadequacy, and passive smoking are the oldest, most contentious, and hence least universally acknowledged of these (an unknown industrial factor). The research that claimed these elements as causes were geographically limited, and their findings might have been skewed by the etiologic fallacy.

The following factors have been widely accepted as the most likely causes of osteochondrosis, either alone or in various combinations:

• Genetic predisposition 
• Environmental factors
• Thrombotic predisposition
• Acute or repeated trauma
• Embolism
• Copper (trace element) deficiency
• Infection
• Mechanical factors

Blount disease is known to be inherited in an autosomal dominant pattern; however, the inheritance patterns of other possibly inheritable illnesses (e.g., Scheuermann disease) remain unknown.

Animal studies have suggested that trace element deficiencies (for example, copper and zinc) are likely causes. Infection, which was formerly thought to be universally dismissed as a cause of osteochondrosis, has recently been demonstrated to initiate or accelerate the disease process. Its effect might be direct or indirect, depending on whether it is associated to autoimmune pathways.

Individual mechanical factors, such as Osgood-Schlatter disease and Sinding-Larsen-Johansson disease, may be linked to the development of specific diseases. A long patella (Grelsamer type II) and extensor apparatus, as well as external tibial torsion, are examples of such factors. Several writers have proposed that Osgood-Schlatter syndrome is traumatic in nature and does not include ischemia necrosis.

Compounding factors

Compounding variables linked to osteochondrosis have also been discovered. These include, among other things, hormonal imbalance (hypothyroidism), sickle cell anemia, Gaucher disease and mucopolysaccharidoses, tetany owing to magnesium insufficiency, and cystic fibrosis. All of these illnesses, however, are now well-established diseases in their own right and, in the authors' opinion, should not be associated with osteochondroses.

Osteochondritis Dissecans

Osteochondritis dissecans (OCD), commonly known as an osteochondral lesion, is a poorly understood condition with a multifactorial origin. OCD is an idiopathic disorder that can develop from infancy through adulthood, with the majority of individuals presenting in early adolescence. The severity of osteochondral lesions ranges from asymptomatic to mild discomfort, with advanced instances exhibiting indications of joint instability and locking.

Lesions can develop from stability to disintegration of the overlaying cartilage, resulting in the creation of a loose body in the afflicted joint region. Early-onset osteoarthritic alterations of the joint can occur at any level of severity if not recognized and managed properly; hence, early detection and therapy are critical to achieving positive long-term results.

Etiology

Although the pathogenesis of osteochondritis dissecans is unknown, it is thought to be multifactorial in nature. Genetic susceptibility, inflammation, spontaneous avascular necrosis, and recurrent microtrauma are all proposed etiologies. Multiple studies have failed to prove inflammation as the underlying cause of osteochondritis, which was originally thought to be related to osseous inflammation

According to the idea, spontaneous osteonecrosis occurs during the growth of the underlying cartilage throughout adolescence. The vascular supply to the subchondral bone switches from a juvenile perichondrial supply to a mature supply from the medullary cavity at this point. It is assumed that the epiphyseal bone is prone to avascular necrosis during this transition phase.

The greater frequency of OCD in young athletes supports a microtrauma etiology. These ideas have been researched with varied degrees of success in determining the cause, but the most widely recognized etiology is that of recurrent microtrauma, with or without an inciting incident, resulting in the patient's first presentation.

Epidemiology

Osteochondritis dissecans affects 15 to 29 people out of every 100,000. Although it can develop at any age from infancy to adulthood, the majority of patients are between the ages of 10 and 20. Males are afflicted twice as frequently as females, with a greater frequency among young athletes. The knee, particularly the lateral side of the medial femoral condyle, is the most afflicted joint, however the elbow (capitellum) and ankle (talus) are also impacted to varying degrees.

Pathophysiology

Osteochondritis dissecans is an idiopathic localized joint condition affecting the subchondral bone, regardless of cause. Fragmentation of a tiny focus of subchondral bone generates a gap between the osteochondral lesion and the parent bone, resulting in diminished vascularization and fragment osteonecrosis.

Stable pieces are those that are maintained in place by intact articular cartilage above them. The defect may progress to include the underlying cartilage, resulting in fragment instability. Lesions that become unstable may remain in place or shift from the parent site and create a loose body within the joint. Early-onset osteoarthritis develops in a substantial percentage of these individuals due to the changed articular surface induced by the osteochondral lesion.

Symptoms

The appearance and location of osteochondral lesions vary. Patients with accidental detection at imaging may be asymptomatic. This is true for people who have always been asymptomatic or who never presented for examination but recall remote persistent mild discomfort that vanished without treatment. Other individuals report with persistent mild discomfort in the afflicted joint, with or without an acute injury. These patients usually visit many months to a year after their symptoms first appear. When a patient has a loose fragment, the symptoms are usually more severe, with significant joint pain, locking, edema, and joint instability.

These individuals may have palpable soreness, a limited or painful range of motion in the affected joint, and effusion or edema on physical examination. Other types of injuries, such as fractures and ligamentous tears, should be ruled out.

Diagnosis 

Imaging plays an important role in the assessment and therapy of these individuals. The initial imaging acquired is routine radiography of the afflicted joint. On radiographs, there is an oval lucency affecting the subchondral bone, with subjacent sclerotic bone. The bone fragment is occasionally seen within the subchondral defect or, if displaced, somewhere within the joint. Radiographs cannot assess the integrity of the osseous fragment and overestimate the extent of the lesion.

When an aberration on radiographs is discovered, MRI is often utilized to confirm the diagnosis by separating a developmental ossification variant from OCD and to aid in treatment planning by determining if the lesion is likely to be stable at the time of arthroscopy. Because MRI is very sensitive and specific in assessing fragment stability, it is indicated for individuals whose stability is a clinical issue.

The following four MRI indications are related with OCD lesion instability, as first identified by De Smet with regard to the knee on T2 weighted imaging of the knee:

1. Line of hyperintense signal equal to the fluid at the fragment bone interface measuring 5 mm or more in length,
2. A discrete round focus of hyperintense signal deep to the OCD lesion measuring 5 mm or more,
3. Focal defect in the overlying cartilage measuring 5 mm or more, and
4. The fluid that passes the articular cartilage and subchondral bone and extends to the lesion is represented by a hyperintense signal. The same data may be used to assess the stability of any joint with an OCD lesion. These parameters have a high sensitivity and specificity in determining the stability of OCD lesions. In challenging circumstances, MRI arthrography can be useful. When MRI is not an option, CT arthrography, however less sensitive, can be performed on the patient.

MRI is also beneficial in monitoring the therapy of these individuals after diagnosis, whether conservative or surgical treatment is selected. The suggested time interval for doing an MRI to assess healing is determined by institutional guideline and is surgeon dependant.

Following conservative management, MRI findings that suggest healing include: a decrease or resolution of the surrounding bone marrow edema pattern, a decrease in lesion size, a decrease or resolution of the hyperintense T2 signal rim or cyst-like foci, and ingrowth of bone within the bed of the OCD lesion with osseous bridging. Following surgery, MRI enables for noninvasive assessment of articular surface and bone cartilage interface healing.

Treatment of Osteochondrosis

Treatment will be determined by the patient's age, timing of manifestation, intensity of symptoms, and the stability of the lesion. Several classification systems for lesions have been developed, with the degree of overlying cartilage involvement and mobility of the lesion fragment being the most important features. Conservative therapy with immobilization and protected weight-bearing for a period of time, depending on which joint is afflicted, is favored in stable lesions.

Drilling techniques may be used to treat patients with stable lesions who have failed conservative therapy (retroarticular or transarticular drilling). Healing rates and symptom improvement ranged from 92 percent to 100 percent for these procedures, with transarticular drilling having slightly higher success rates. When lesions become unstable or displaced, surgical intervention is required, which is usually done arthroscopically.

The knee is the most common site for surgery, accounting for 58 percent of all treatments for OCD lesions. Fixation, debridement, microfracture, and cartilage grafting/transplantation are some of the modalities and procedures available. Lesions can be fixed in place using a variety of metallic screws, bioabsorbable implants, or osteochondral plugs.

When the extent of the OCD lesion allows for the use of metallic fixation screws, effective healing rates range from 84% to 100%. The downside of metallic screws is the requirement for a second treatment to remove the screw 6 to 12 weeks after initial fixation. Bioabsorbable implants do not require a second treatment to remove and have a success rate of about 90%; nevertheless, these implants have a greater incidence of problems.

Osteochondral autograft or allograft plugs can also be employed, with clinical results ranging from "good to excellent" in 72 percent of allograft plug recipients. The general objective of surgery is to promote cartilage reformation and/or articular surface repair in order to prevent early-onset osteoarthritis.

Prognosis

Stable osteochondral lesions have a better prognosis than unstable lesions. When stable lesions are treated only with conservative measures, spontaneous healing usually occurs. There is currently no one universal grading scale for surgically treated lesions. However, depending on the approach used, unstable lesions receiving surgery or those that fail conservative care and subsequently receive surgical treatment have a success rate ranging from 30% to 100%.

However, the vast majority of surgically treated individuals will acquire early-onset osteoarthritis. Patients who seek therapy throughout their adolescent have a better prognosis than adult patients.

Conclusion 

An interprofessional team including a radiologist, orthopedic surgeon, physical therapist, nurse practitioner, and main caregiver diagnoses and manages osteochondritis dessecans. Treatment will be determined by the patient's age, timing of manifestation, intensity of symptoms, and the stability of the lesion. Several classification methods for lesions have been created, with the degree of underlying cartilage involvement and mobility of the lesion fragment being the most essential features.

Conservative therapy with immobilization and protected weight-bearing for a period of time, depending on which joint is afflicted, is favored in stable lesions. Drilling techniques may be used to treat patients with stable lesions who have failed conservative therapy (retroarticular or transarticular drilling). Healing rates and symptom relief ranged from 92 percent to 100 percent for these treatments, with transarticular drilling having somewhat higher success rates.

When lesions become unstable or displaced, surgical intervention is required, which is usually done arthroscopically. In general, stable lesions have better results than unstable lesions.