A recent evidence-based review found that most patients with
Scheuermann disease do not need surgical intervention, which should
be reserved only for patients with mature skeletons who have a curve
greater than 75 degrees, pain, a rigid deformity, and unacceptable
appearance.47 Bracing is indicated in patients who have an immature
skeleton with an increasing curve. Orthopedic Referral Patients with
osteochondrosis should be referred to an orthopedic surgeon for
further evaluation if nonoperative treatment has not been effective.
Patients with Osgood-Schlatter disease, Sinding-Larsen–Johannson
disease, or Sever disease who have mature skeletons and disabling
symptoms should be referred. Those with Freiberg disease and loose
joint fragments should be referred for possible joint debridement.
Patients suspected of having Köhler bone disease who have had recent
trauma, illness, or elevated inflammatory markers should be referred to
rule out infection or occult fracture. Referral is also indicated in those
with medial epicondyle apophysitis or Panner disease who have acute
trauma, pain despite several weeks of rest, or loose joint fragments.
Any patient suspected of having Legg-Calvé-Perthes disease or
Scheuermann disease should be referred for further evaluation. A
summary of diagnostic, treatment, and referral indications for each
osteochondrosis disorder is provided in Table 1.
Osteochondrosis is a family of orthopedic diseases of the joint that
occur in children, adolescents and rapidly growing animals, particularly
pigs, horses, dogs, and broiler chickens. They are characterized by
interruption of the blood supply of a bone, in particular to the
epiphysis,[1] followed by localized bony necrosis,[2] and later, regrowth
of the bone.[3] This disorder is defined as a focal disturbance of
endochondral ossification and is regarded as having a multifactorial
cause, so no one thing accounts for all aspects of this disease.[1]
Osteochondrosis Specialty Rheumatology, orthopedic surgery
Osteochondrosis is a developmental disease. It usually occurs in an
early stage of life. It has personified features as focal chondronecrosis
and confinement of growth cartilage due to a failing of endochondral
ossification. Fissures can develop from lesions over the top articular
cartilage and form a cartilage flap and an osteochondral fragment. It is
diagnosed as osteochondritis dissecans.[4]
In dogs osteochondrosis is seen in elbow, shoulder, knee, and ankle
joints. Elbow osteochondrosis is also known as "elbow dysplasia". There
are three types of elbow dysplasia: fragmented medial coronoid
process, ununited anconeal process and Osteochondritis dissecans of
the medial humeral condyle. Breeds that have the predisposition to
these are Basset Hound, Labrador, Golden Retriever, and Rottweiler.
Other breeds can also be diagnosed with this condition but it is not
common.[5] One of the leading factors to some elbow osteochondrosis
is that the radius and ulna are growing at different rates. In this
situation, the stress to the joint surface is not even and can cause some
form of osteochondrosis in the elbow when the puppy grows or make
already existing elbow dysplasia even worse. Some of the breeds that
are susceptible to that are for example Dachshunds, Corgis, Pugs,
Bulldogs, and Beagles.[4]
These conditions nearly all present with an insidious onset of pain
referred to the location of the bony damage. Some, notably Kienbock's
disease of the wrist, may involve considerable swelling,[6] and LeggCalvé-Perthes disease of the hip causes the victim to limp.[7] The spinal
form, Scheuermann's disease, may cause bending, or kyphosis of the
upper spine, giving a "hunch-back" appearance.[8] Symptoms in
animals Edit The most common symptoms are lameness and pain in the
affected joints. Animals may try to ease the pain and walk differently
and the pain can be noticed by the change in animals walking style. The
condition affects both sides (right and left leg). On most occasions, the
other leg is worse. This can result that the dog starts encumbering the
other leg and the healthier leg becomes more strained.[5] Sometimes
the symptoms are so mild or there are no symptoms which can make it
hard to detect that there is something wrong with that dog.[9]
The ultimate cause for these conditions is unknown, but the most
commonly cited cause factors are rapid growth, heredity, trauma (or
overuse), anatomic conformation, and dietary imbalances; however,
only anatomic conformation and heredity are well supported by
scientific literature. The way that the disease is initiated has been
debated. Although failure of chondrocyte differentiation, formation of
a fragile cartilage, failure of blood supply to the growth cartilage, and
subchondral bone necrosis all have been proposed as the starting point
in the pathogenesis, recent literature strongly supports failure of blood
supply to growth cartilage as most likely.[1] Osteochondrosis can be
usually inherited.
OSTEOCHONDROSIS Osteochondrosis is a clinical term used to describe
the pathologic changes that occur in the intervertebral disc and in the
adjacent bone of the vertebral bodies as a result of disruption in the
region of the end plate of the disc. Following disruption of the
cartilaginous end plate, the other disc components exhibit rapidly
progressive degeneration, with focal necrosis, fissuring, radial or
circumferential tearing in the annulus fibrosus, and replacement of
normal disc tissue by fibrous tissue. Large horizontal clefts may develop
in the central part of the disc tissue and can be seen on clinical
radiographs, where they are often referred to, incorrectly, as the
vacuum phenomenon (Fig. 13-13). Disc calcification is common.
However, apatite crystal deposits can be easily overlooked in sections
prepared with hematoxylin and eosin staining (Fig. 13-14). Calcium
pyrophosphate dihydrate deposition disease (CPPD) is a frequent
finding in surgical specimens both of disc tissue and in the ligamentum
flavum (Fig. 13-15). As disc degeneration progresses, with subsequent
narrowing of the disc space, formation of new bone takes place around
the periphery of the disc, at the junction of the annulus and the
vertebral body resulting in marginal osteophytes. Ossification also
occurs within the disc as a result of endochondral ossification of the
cartilaginous end plate, contributing to narrowing of the disc space (Fig.
13-16). After vascular invasion, progressive breakdown of the disc
tissue contents will lead to their resorption. Frequently, the final stage
of the resorption process is a spontaneous bony fusion of adjacent
vertebral bodies.
Osteochondroses of the Elbow Osteochondrosis is defined as a group of
disorders affecting an ossification center in a child or adolescent
resulting in alteration of endochondral ossification. Histologic studies
have shown that the affected ossification center undergoes
degeneration or avascular necrosis followed by resorption and changes
of repair with recalcification. The osteochondroses of the elbow most
frequently occur in adolescent athletes, with involvement of the
capitellum and radial head resulting from compressive or shearing
forces whereas lesions of the olecranon and medial epicondyle result
from traction forces. Osteochondral lesions of the capitellum or radial
head most frequently occur in adolescent pitchers or gymnasts and
almost always involve the dominant arm. Repeated valgus stress across
the lateral compartment of the elbow in pitchers results in excessive
compressive or shearing forces leading to these osteochondral injuries.
In gymnasts, the lateral compartment of the elbow acts as a weightbearing joint and is subjected to excessive compressive forces. These
osteochondral injuries range from minimal subchondral marrow edema
and microtrabecular injury to a partially or completely detached
osteochondral fragment in situ or, in the most severe cases, to a
displaced osteochondral fragment. The stable injuries are usually
treated with conservative measures by placing the arm at rest and by
eliminating the aggravating activity. Unstable or displaced
osteochondral fragments require surgical reattachment or
debridement. In most cases, MRI can accurately differentiate between
the various stages of injury, and the most critical decision point is to
differentiate between a stable and an unstable fragment in situ
because the unstable lesions require surgical intervention. On occasion,
it may prove difficult using conventional MRI to differentiate between a
stable and an unstable in situ lesion (Fig. 8-20). Fluid, seen on a T2weighted image, extending completely beneath the osteochondral
fragment, indicates a loose but in situ lesion. However, loose
granulation tissue that holds a stable fragment in place may appear
very bright on T2-weighted MR images and mimic fluid surrounding an
unstable fragment. Direct MR arthrography can increase the specificity
in these cases. Gadolinium completely surrounding a fragment is
indicative of an unstable fragment. Occasionally, in adolescent pitchers
a purely chondral shearing injury results in a full-thickness chondral
defect and resultant loose body. This injury is occult on radiographs,
although a joint effusion may be present. MR imaging demonstrates a
full-thickness chondral defect and resultant loose body (Fig. 8-21).
The major pitfall with regard to the diagnosis of an osteochondral injury
of the capitellum is the presence of the pseudodefect of the capitellum.
This is a normal anatomic finding that can mimic an osteochondral
lesion of the capitellum on MR imaging. Along the posterolateral
margin of the articular surface of the capitellum, the articular cartilage
ends abruptly, and on sagittal and coronal images this gives the
appearance of an abrupt step-off of the chondral surface, which can
mimic an osteochondral lesion but actually represents the normal
appearance of the interface between the articular cartilage and the
nonarticular surface of the posterior capitellum. The key to
differentiating this from a true osteochondral lesion is to recognize that
the osteochondral lesions occur in the anterior aspect of the capitellum
as seen on sagittal images, whereas the pseudodefect of the capitellum
is located posteriorly and usually demonstrate little to no subchondral
signal abnormality (see Fig. 8-20). The medial epicondyle is another
location of common injury in adolescent pitchers, and osteochondrosis
of the medial epicondyle usually results from excessive traction forces
that are applied across the elbow during the motion of throwing. The
incidence of this injury has decreased significantly over the past decade
in the little league age group as a result of education of parents and
coaches. The lesion is now more commonly seen in the slightly older
age group and in athletes of early high school age (Fig. 8-22).
Osteochondrosis of the capitellum or Panner's disease is a self-limiting
abnormality of the osteochondral bone, which usually occurs in
children between the ages of 5 and 12 before the capitellum is fully
ossified. It is thought that the process is caused by avascular necrosis of
subchondral bone secondary to a lateral compression injury of the
elbow.50 Osteochondrosis is often visible in plain radiographs that will
show fragmentation of the ossification centre. MRI shows decreased T1
and increased T2 fluid signal with epiphyseal fragmentation. Loose
body formation is rare and the articular cartilage typically remains
intact. It is usual for the lesion to resolve over time with conservative
management, in contrast to osteochondritis dissecans. Osteochondritis
dissecans (OCD) or avascular necrosis of the elbow joint is typically
found in adolescents and young adults51 and most often occurs within
the capitellum, but may also be seen in the radial head or trochlea.
While the process may be idiopathic, there is often a history of trauma
involving a valgus or axial compression injury, repetitive valgus stress or
a risk factor for avascular necrosis such as high levels of endogenous or
therapeutic steroids, marrow pathology (e.g. leukaemia, sickle cell
disease and Gaucher's disease) or alcohol abuse. Radiographs are the
first-line investigation of OCD, although it should be stressed that the
sensitivity of plain radiographs in detecting early OCD is low and
radiographs may appear normal at initial presentation.51 By the time
that OCD is visible with radiographic examination, the pathology will
already be well advanced. Plain radiographs will show subchondral
lucency, often with cortical irregularity, and a defect may be present
within the capitellum once fragmentation has occurred. Early detection
of suspected OCD should therefore be made using MRI when the initial
radiograph is normal,40 or with scintigraphy when MRI is
contraindicated.
MRI will show a focus of low to intermediate T1 signal within the
subchondral bone, with a low T1 signal margin. The lesion may have
variable signal on fluid-sensitive sequences, with high T2 fluid signal
progressing to low T2 signal when sclerosis is present. Fragment
instability is indicated by well-defined high T2 fluid signal separating the
osteochondral fragment from the underlying bone marrow, a cleft in
the articular cartilage at the lesion margin and a high T2 cystic structure
deep to the lesion.52,53 Instability is more often associated with
lesions with a largest dimension greater than 1 cm in size52 or greater
than 0.8 cm2 in area.54 Direct MR arthrography can be used to clearly
demonstrate the more sharply defined margin seen in unstable lesions,
with contrast outlining the loose fragment.55 Indirect MR arthrography
will show enhancement of granulation tissue around an unstable lesion,
as well as demonstrating contrast-enhanced synovial fluid extending
between the unstable fragment and the adjacent marrow. One
significant pitfall of MR imaging of the capitellum is the pseudodefect, a
normal anatomical depression found at the junction of the posterior
margin of the capitellar articular cartilage and the posterior aspect of
the lateral epicondyle. The pseudodefect is found posteriorly, in
contrast to OCD, which is typically found within the anterior aspect of
the capitellum. When MRI is contraindicated and the initial radiograph
appears normal or does not clearly show whether the fragment is
stable or not, other modalities may be used to make the diagnosis. CT
arthrography will show mixed sclerosis and lucent change that confirms
the diagnosis of OCD, and contrast will outline an unstable fragment.56
CT arthrography may also be used to look for intra-articular loose
bodies and to assess bony congruence. Alternatively, the rarely utilized
investigation of technetium 99 MDP bone scanning with dynamic triplephase imaging (immediate blood flow, 10-minute blood pooling and
delayed bone uptake) can also be used to detect occult unstable
lesions. Unstable OCD lesions show increased uptake during blood
pooling and delayed phases of scintigraphy.54 Conversely, with stable
OCD increased uptake during the blood pool phase is rarely seen and
there is less marked uptake of the technetium tracer during the
delayed phase, which allows differentiation between stable and
unsOsteochondrosis of the metatarsal head, or Freiberg's disease,
involves an evolutionary process of deterioration and collapse of the
articular surface and underlying subchondral bone. It occurs more
commonly in adolescents when the epiphysis is still present, and 75% of
the cases are female.40 The second metatarsal is the most common
site (68%) followed by the third and forth metatarsal heads being
affected.41 The second metatarsal head is involved more commonly
when it is longer than the first. It has been proposed that this results in
increased pressure over the head and possibly disruption of the
vascular supply with repeated microtrauma (i.e., running or dancing en
pointe). The athlete typically presents with forefoot pain that is
worsened with impact activities. Activities that cause extremes of
motion at the metatarsal heads during weight-bearing activities such as
sprinting and repetitive jumping particularly seem to exasperate
symptoms. Athletes usually will complain that the pain symptoms are
continuing to worsen by the time they seek medical help. The physical
examination may show some mild swelling over the metatarsal head.
Palpation of the midfoot and forefoot typically isolates pain to the
affected metatarsal head and its metatarsophalangeal (MTP) joint.
Motion at the affected MTP joint will be decreased and painful.
Radiographs of the foot should be obtained when a young athlete
presents with these symptoms and physical examination findings to
evaluate for Freiberg's disease and to rule out other causes, such as
infection or stress fractures. Initial plain film findings, such as widening
of the affected MTP joint space, may be subtle. Osteosclerosis of the
metatarsal head may be seen within several weeks on plain films (Fig.
23-3). As the disease progresses, there is increased resorption of
necrotic bone with resulting fragmentation and collapse of the
metatarsal head.42 Bone scan may be helpful when the clinical
examination and history are suspicious but radiographs are negative.
The bone scan will show increased uptake in the proximal metatarsal
head and decreased uptake over the necrotic area. Treatment consists
of taking anti-inflammatories and decreasing the load to the area for a
period of time. Initial immobilization in a walking boot will help to calm
symptoms. The athlete then may be transitioned into an orthotic and
started back to nonimpact activities initially. It is not always possible to
stabilize the joint and prevent pain and progressive deformity. In severe
cases with persistent pain, surgery may be required to alleviate
symptoms and remove impingement. In later stages, it is believed that
the discomfort is associated with loose bodies. There are several
procedures, depending on the extent of the disease and whether loose
bodies are present. All have reported very good results.