Imaging Review of Normal and Abnormal Skeletal Maturation

Bone Formation

Bone formation occurs by intramembranous and endochondral ossification. Intramembranous ossification takes place during the first few months of fetal development in the cranial vault, midclavicle, mandible, and maxilla. Endochondral ossification is the overall dominant process in the skeleton and occurs in the skull base, vertebral column, pelvis, and extremities (1). It utilizes an initial cartilage blueprint that is gradually replaced by bone (2). Both processes occur simultaneously in tubular bone. Longitudinal growth occurs by endochondral ossification, while increase in diameter occurs by intramembranous deposition from the surrounding periosteum (3,4).

The primary ossification center is located in the center of the bone and forms the future diaphysis. The primary physis is located in the ends of the primary ossification center and provides a cartilage precursor for new bone formation, with the newest bone forming the metaphyseal portion (5). The secondary ossification centers (SOCs) are located at the ends of the bone and form the epiphysis (when enclosed by articular cartilage) and apophysis (when it does not articulate with a joint)

Figure 2.

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Secondary Ossification Centers

The epiphysis begins as a mass of unossified hyaline cartilage between the joint and the primary physis, making it invisible at radiography (6–8). In infancy, epiphyseal cartilage has low signal intensity at T1-weighted imaging and intermediate-to-high signal intensity with fluid-sensitive sequences (6). As part of endochondral ossification, a preossification center may be visible in certain bones (eg, trochlea of the distal humerus), appearing at MRI as a well-delineated center of high signal intensity at fluid-sensitive imaging within the cartilaginous epiphysis (9). Ossification begins at the center of the cartilaginous epiphysis either as a single center or multiple centers. Newly formed ossification centers contain red marrow and therefore exhibit signal intensity similar to that of the adjacent metaphysis (6). On ossification, the signal intensity converts to that of yellow marrow, which occurs approximately 6 months after radiographic visibility (6,10,11). The remaining epiphyseal cartilage may become progressively heterogeneous with age, with lower signal intensity in the weight-bearing regions, a pattern that is especially observed in the distal femoral condyles (12).

During early development, epiphyseal and apophyseal ossification centers can be numerous, irregular, and fragmented, mimicking fractures, osteochondrosis, and osteochondritis dissecans (OCD) at radiographic examinations

Figure 3.

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Figure 4.

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Figure 5.

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Physis and Metaphysis

The primary physis is organized into three layers from the epiphysis to the metaphysis: the germinal, proliferative, and hypertrophic zones. The hypertrophic zone can be further subdivided into zones of maturation and degeneration and the zone of provisional calcification (ZPC). In the metaphyseal side abutting the ZPC is the primary spongiosa, a highly vascularized structure that contains the newly formed metaphysis (6,16,17). The cartilage layers of the physis, the ZPC, and the primary spongiosa produce a characteristic trilaminar appearance at T2-weighted fat-suppressed MRI (6) (Fig 6).

Figure 6.

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The physis starts as a flat disk before assuming a more undulating configuration during childhood. The thickness of the normal physis should be uniform throughout, and focal thickening is suggestive of a disturbance in endochondral ossification. Physiologic physeal closure depends on the evaluated bone, although it generally commences in the center before progressing to the periphery. The secondary physis surrounding the SOC has a signal intensity similar to that of the main physis but is thinner and less conspicuous. On physiologic closure, the physis leaves behind a physeal scar representing the residual ZPC (6).

Physiologic arrest of bone growth produces transverse sclerotic metaphyseal lines parallel to the physis, termed Park-Harris lines. When numerous, these lines are suggestive of prior infection, trauma, or the administration of bisphosphonates (8). These insults lead to slowing of cartilage conversion to bone but continued mineralization of the metaphyseal trabeculae, forming a visible growth recovery line (6). With focal insult to the physis, the recovery line deviates from its parallel orientation and remains focally tethered to the physis, forming a physeal bridge (18) (Fig 7). Systemic insults such as metabolic (eg, hypoparathyroidism) or nutritional (eg, vitamin D deficiency) derangements produce similar dense lines of calcification not during the stage of malnutrition but after refeeding (19). Growth arrest lines occur initially along the surface of the epiphysis or apophysis near which they are formed, resulting in a bone-within-bone appearance in vertebral endplates and patellae (8,19).

Figure 7.

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The chondro-osseous junction in flat bones and the outermost part of the SOC are referred to as metaphyseal equivalents and include the triradiate cartilage, ischiopubic synchondrosis, sacroiliac joint, and periphery of round bones (eg, talus). These sites are highly vascularized with sluggish blood flow and are therefore vulnerable to osteomyelitis and other hematogenous processes, similar to the typical metaphyses of long bones (20).

Periosteum and Perichondrium

The periosteum is subdivided into an outer fibrous layer and an inner osteogenic cambium layer. It lines almost the entire length of long bones, extending along the primary ossification center and the extra-articular portions of the SOC. Sesamoid bones like the carpus and intra-articular portions of SOCs are largely devoid of periosteum (3). At MRI, it is possible to identify the layers of the periosteum. The outer fibrocartilaginous layer exhibits low signal intensity at T2-weighted MRI, is continuous with the perichondrium, and terminates inferiorly with the junction of the epiphyseal articular cartilage. The inner vascular layer (cambium layer) surrounds the cortex and forms a long strip of high signal intensity at T2-weighted imaging that avidly enhances after intravenous administration of a contrast agent (21).

The perichondrium lies at the junction of the physis and the periosteum, surrounding the main physeal cartilage. Its main role is increasing the cross-sectional area of the physis, enabling growth of both length and diameter (20). The groove of Ranvier, a triangular area of intermediate-to-low signal intensity at T2-weighted imaging, lies in the deep portion of the perichondrium and consists of loosely packed cells that induce chondrogenesis and osteogenesis. Transverse fibers extend from the perichondrium to the periphery of the germinal zone of the physis. These transverse fibers tightly secure the perichondrium to the underlying physis, preventing separation of the epiphysis or metaphysis from the physis during trauma and acting as a barrier to the spread of subperiosteal abscesses and tumors (21). Contrary to this tight perichondral-physeal attachment, the attachment of the periosteum to the cortex is very loose. Hemorrhage, pus, or neoplastic cells can easily elevate the periosteum and form subperiosteal collections (6). The chondro-osseous junction of the perichondrium forms the ring of LaCroix, which is composed of a thin bone spur at the periphery of the physis and a straight contour on the metaphysis (3,21) (Fig 8).

Figure 8.

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The perichondrium becomes progressively weaker and less prominent with maturation until it is completely replaced by periosteum after physeal closure. In young children, fractures at the physeal-metaphyseal junction spare the perichondrium, which is contrary to injuries in older children

Bone Marrow

Bone is composed of red (hematopoietic) and yellow (fatty) marrow, the proportions of which evolve with skeletal maturation. Hematopoietic or red marrow is 40% fat and 40% water, while yellow or fatty marrow is 80% fat and 15% water (22). Neonatal marrow is predominantly hematopoietic because of an increased demand for oxygen. Conversion from red to yellow marrow occurs during the first few months of life, following a well-established pattern (10,23). In a single long bone, conversion begins in the epiphysis followed by the diaphysis and distal metaphysis before finally reaching the proximal metaphysis. Within the body, this transformation proceeds from the periphery (phalanges) to the center (humeri and femora) of the appendicular skeleton (22,24).

Bone marrow conversion is generally complete by the time an individual reaches 25 years of age. Adult marrow is predominantly yellow, with areas of residual red marrow in the axial skeleton and proximal metaphyses of the appendicular skeleton (ie, proximal femora and humeri) (Fig 9). In situations requiring increased hematopoietic demand (eg, chronic anemia, smoking, at high altitude, and during athletic activities), reconversion from yellow to red marrow occurs in the reverse order from axial to the appendicular skeleton and within the long bones proceeding from the proximal metaphysis, distal metaphysis, diaphysis, and finally, epiphysis (24).

Figure 9.

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Changes in the proportions of red and yellow marrow during conversion and reconversion determine their signal intensity (6). Red marrow is depicted with low-to-intermediate signal intensity at T1-weighted imaging, generally lower than that of yellow marrow but higher than that of muscle or intervertebral disks. At fat-suppressed and short τ inversion-recovery (STIR) imaging, the signal intensity is intermediate to high and higher than in yellow marrow. Mild enhancement with administration of intravenous gadolinium-based contrast agent (GBCA) is observed owing to its vascularity (25). Yellow marrow signal intensity is high at T1-weighted imaging and low at fat-suppressed and STIR imaging, similar to that in subcutaneous fat. In the fetus and neonate, the signal intensity of red marrow is typically lower than in muscle or intervertebral disks (10). This appearance should not be mistaken for a hematopoietic or infiltrative marrow disorder (Fig 10).

Figure 10.

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A common finding in the pediatric population is heterogeneous residual red marrow. These areas have a typical appearance and location, allowing differentiation from pathologic conditions (22). Normal residual metaphyseal hematopoietic marrow is characterized by a flame-shaped configuration with a base at or adjacent to the physis and straight vertical margins (6,24). Patchy or hemispheric T1-weighted hypointense foci similar to that of the red marrow of the metaphysis can also be seen in the epiphysis, especially in the subarticular regions of the proximal humerus and proximal femur. With T1-weighted sequences, normal red marrow should exhibit higher signal intensity compared with that of adjacent muscle (7). Scattered foci of patchy marrow hyperintensity at T2-weighted imaging throughout the hind and midfoot are also common in children. They are nonspecific and are typically caused by immobilization, residual red marrow, or physiologic stress (6).

Vascular Supply

The metaphysis and epiphysis are supplied by two separate vascular beds. During the first 18 months of life, transphyseal vessels connect the metaphysis and epiphysis through the physis, enabling direct and easy spread of infections and metastatic cells (7,26–28). Epiphyseal extension leads to destruction of the articular cartilage, with a predisposition to a higher incidence of septic arthritis in this age group (27). These vessels completely involute at approximately 18 months of age after which terminal vessels of nutrient arteries stop or loop just short of the physis, creating microarcades of sluggish vascular flow, causing a predisposition to easy spread of hematogenous processes to the metaphysis while sparing the epiphysis (29,30).

Disorders of Bone Development: Osteochondrosis

Osteochondrosis refers to a group of disorders characterized by abnormal endochondral ossification of the epiphyses or epiphyseal-equivalent bones. The pathogenesis is not fully understood, but genetic causes, repetitive trauma, vascular abnormalities, mechanical factors, and hormonal imbalances have been implicated (31). Some cases appear to be primarily traumatic, whereas others are mainly ischemic, in which the role of trauma is hypothetical (Figs 11–13). Each osteochondrosis has a designated eponymous clinical diagnosis based on location (32) (Table).

Figure 11.

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Figures 12, 13.

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Common Osteochondroses

Imaging appearance depends on disease stage and severity. Radiography is useful in the initial assessment, showing sclerosis, fragmentation, and collapse of the SOC.

Fragmentation of certain areas such as the tibial tubercle, calcaneal apophysitis, and tarsal navicular (Osgood-Schlatter disease, Sever disease, and Köhler disease, respectively) can be seen in healthy asymptomatic individuals, making marrow and soft-tissue evaluation with MRI crucial

Disorders of the Physis

Salter-Harris Fractures.—The Salter-Harris classification system subdivides physeal fractures on the basis of anatomy and fracture pattern (17) (Fig 14). These fractures occur at the ZPC, a transition point that is weaker than the surrounding structures and is therefore more prone to trauma (34). Horizontally oriented fractures (Salter-Harris types I and II) that follow the plane of the physis result in less bone bridge formation than vertically oriented fractures traversing the physis and breaching the reserve and proliferative layers (Salter-Harris types III and IV) (16).

Figure 14.

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Radiographic findings include a frank physeal fracture, growth arrest line, or a physeal bony bridge (7). Subtle nondisplaced fractures may necessitate imaging of the contralateral side for comparison. Physeal fracture causing growth arrest is the most common cause of bone bridging across the physis (35) (Fig 15). Most bridges occur in areas of physeal undulation such as the distal femoral physis and medial aspect of the distal tibial physis (the Kump bump). Isolated areas of normal physeal undulation should not be mistaken for a bridge (26). Radiographic follow-up to evaluate for growth disturbances is recommended in high-risk physeal injuries. In a high-energy displaced distal femur fracture, radiography should be performed every 3 months until normal growth has resumed and has been documented (36). In many cases, the recommended period of observation can amount to anywhere from 2 years up to skeletal maturity (36,37). Close radiologic monitoring could help identify an angular growth deformity before it is clinically apparent, increasing the chances of successful surgical correction (37). CT enables accurate measurement of the bone bar when surgical excision is contemplated. MRI helps evaluate more complex injuries, directly depicting cartilage and soft-tissue involvement and potential complications (34). Physeal fracture shows low signal intensity with T1-weighted sequences and high signal intensity with fluid-sensitive sequences with disruption of the normal trilaminar appearance of the physis (7,38) (Figs 16–17).

Figure 15.

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Figures 16, 17.

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Chronic Stress Injuries.—The pediatric skeleton is prone to stress injuries because of increased physical activity, decreased muscle mass and bone mineral content, and a weak chondro-osseous junction.

The physeal cartilage of the epiphysis and apophysis is the weakest structure, and injuries to this location disrupt endochondral ossification, ultimately leading to growth disturbances if the stressor is not removed

Radiographs show physeal widening, irregularity, and fragmentation (39). MRI demonstrates effacement of the ZPC, adjacent marrow edema, and T2-weighted and STIR-hyperintense unmineralized cartilage extending into the metaphysis (7,39,40). Physeal widening owing to chronic stress must be distinguished from an acute Salter-Harris type I injury (40) (Fig 18).

Figure 18.

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Focal Periphyseal Edema.—Focal periphyseal edema (FOPE) is a distinct MRI finding in the distal femur, proximal tibia, and proximal fibula of adolescents with knee pain (41). It manifests with focal bone marrow edema centered at an open but narrow physis that extends into the metaphysis and epiphysis (41,42). It is most conspicuous at fat-suppressed or fluid-sensitive imaging, which optimally depict the starburst pattern of edema surrounding the closing physis (41,43). A few authors suggest that it represents a normal step of physeal fusion given the remarkably consistent age and degree of skeletal maturation of patients and location within the affected bone (41). Adjacent marrow edema may be confused for chronic overuse injury, and distinction can be made on the basis of the appearance of the physis (Fig 19).

Figure 19.

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Disorders of the Epiphysis

Developmental Dysplasia of the Hip.—Developmental dysplasia of the hip is a common developmental disorder caused by an abnormal relationship between the femoral head and acetabulum (44). Imaging findings vary with age and range from an immature and shallow acetabulum to hip subluxation and frank dislocation (45). The exact cause is unclear, with multiple risk factors, including mechanical causes (oligohydramnios, breech positioning, neuromuscular disorders, postnatal swaddling in adduction with the hips extended), family history, and female predisposition.

The use of imaging techniques is dictated by the age of the infant. US is the initial imaging modality of choice and should be performed during the first 6–8 weeks (44). It evaluates acetabular morphology, femoral head coverage by the bony and cartilaginous acetabular rim and labrum, joint congruency, and stability through stress dynamic maneuvers (46). Radiography is recommended at 4–6 months of age and allows evaluation of ossification development and symmetry, acetabular morphology, and the relationship between the femoral head and acetabulum (44,47). The use of advanced imaging techniques such as CT and MRI is reserved for complex cases and pre- or postoperative evaluation (Fig 20). MRI helps assess acetabular retroversion and femoral head coverage, shows structures that may hamper reduction, and depicts potential postoperative complications (eg, avascular necrosis) (7,45).

Figure 20.

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Blount Disease.—Blount disease is a developmental abnormality due to delayed endochondral development of the medial aspect of the proximal tibial epiphysis, producing varus and procurvatum deformity of the tibia (7,48). It has a bimodal distribution, typically occurring during early childhood (infant variety) or in adolescence (32). Early-onset or infantile Blount disease (<4 years) is hypothesized to be a form of osteochondrosis, while late-onset disease (≥4 years) is due to premature closure of the medial tibial physis (7,32). Bilateral involvement is common and typically affects children with obesity who are of African American or Scandinavian descent (7).

Standing anteroposterior weight-bearing radiography of both knees is the initial imaging method of choice but is limited in demonstrating the extent of physeal aberration and bone bridge formation. MRI findings include widening, depression, and irregularity of the posteromedial physis; small chondral intrusions into the metaphysis; focal osteochondral defects; and varus deformity of the lower leg (48) (Fig 21). Bone bridge formation between the tibial epiphysis and metaphysis leads to gait deviations, limb-length discrepancy, and premature arthritis (7,48).

Figure 21.

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Osteochondritis Dissecans.—OCD is a distinct clinical-pathologic entity resulting from localized disturbance and cessation of normal ossification of a segment of the secondary physis. The segment remains cartilaginous, lagging behind the rest of the epiphysis, which continues to ossify from the center to the periphery, producing a defect that is radiolucent relative to the rest of the secondary physis. This “inside-out” mechanism is contrary to the “outside-in” pathomechanism of acute traumatic osteochondral injury, which affects articular cartilage first and subchondral bone last. With incessant forces applied to the joint surface, the segment can partially ossify or detach from the parent bone (49). An often-implicated mechanism is repetitive epiphyseal trauma that interrupts endochondral ossification at the secondary physis, similar to that of stress injuries in the primary physis (40,50).

The condition can manifest either in childhood (juvenile OCD [JOCD]) or middle age (adult OCD), most commonly between the ages of 10 and 15 years (7,49). Males, especially high-level athletes, are affected more often than females (49). The most commonly affected joint is the knee, followed by the ankle, elbow, shoulder, and hip (51). It is most common in the lateral intercondylar aspect of the medial femoral condyle, with or without extension to the central weight-bearing aspect. Other sites include the inferocentral (weight bearing) aspect, lateral condyle, and patella (49,50).

MRI is primarily performed for detection of the osteochondral defect and bone fragment in situ and to evaluate stability (7). Criteria for instability in JOCD slightly differ from that of adult OCD and include a fluidlike high T2-weighted signal intensity rim around the fragment, a second outer rim of low T2-weighted signal intensity, a high-signal-intensity line extending through the articular cartilage overlying the lesion, osteochondral defect filled with joint fluid, and multiple breaks in the subchondral bone plate (52). In JOCD lesions, multiple cysts and a single cyst greater than 5 mm in diameter have low sensitivity but high specificity for the differentiation between stable and unstable lesions (52). In the knee, a normal developmental ossification may be mistaken for JOCD. The two entities can be differentiated on the basis of location in the femoral condyle, status of the overlying cartilage, and marrow signal intensity (Fig 22). In contrast to JOCD, normal developmental ossification is located in the non–weight-bearing portion of the lateral femoral condyle, with normal overlying cartilage and marrow signal intensity. Untreated JOCD may progress to articular surface incongruity, loose bodies, and early joint degeneration (7,49,50).

Figure 22.

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Growth Abnormalities of the Epiphysis.—Dysplasia epiphysealis hemimelica (DEH) or Trevor disease is a rare benign developmental disorder characterized by asymmetric osteochondral overgrowth in the medial or lateral aspect of the developing epiphysis (7,53). It manifests with a lobulated protruding mass containing a cartilaginous cap similar to that of an osteochondroma (7). Whereas DEH is comprised of clusters of disorganized chondrocytes and unabsorbed cartilage fragments, osteochondromas follow a more orderly contiguous ossification process that closely simulates normal physeal development. It typically affects the lower limb rather than the upper limb and the medial rather than the lateral side. Symptoms depend on the size and location of the lesion and include pain, swelling, and limited movements (53).

Radiography shows multiple ossific masses, asymmetric epiphyseal enlargement, an irregular ossification center, or a combination of these findings. Long-standing disease is characterized by increasingly prominent and numerous ossification centers that are greater than expected for age farther from the central epiphyseal ossification center and asymmetric to the unaffected limb (53). MRI is an invaluable tool for complete assessment of the nonossified components of the lesion, effect on surrounding tissues, and status of the physis and articular cartilage (54,55) (Fig 23).

Figure 23.

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Acquired growth abnormalities of the epiphysis can manifest with a configuration similar to that of the developmental disorders of the epiphysis. Fishtail deformity of the elbow is a delayed complication of a remote supracondylar, condylar, or Salter-Harris type I epiphyseal fracture of the humerus in early childhood (56). Precarious blood supply in the lateral trochlea causes a predisposition to osteonecrosis and failure of development or resorption of the lateral trochlear ossification centers, resulting in bony concavity of the central portion of the humerus and the characteristic fishtail configuration (56). The differential diagnosis includes normal preossification center, idiopathic osteonecrosis, OCD, and epiphyseal dysplasia, which are considered in the absence of prior distal humeral fracture (56).

Chondroblastomas.—Chondroblastomas are rare benign cartilaginous tumors with a good prognosis and low morbidity (57). An epiphyseal or apophyseal location is an important diagnostic feature, although the tumor may occasionally extend to the physis and rarely to the metaphysis (57,58). Radiographs show lucent lesions with circumscribed margins and a thin sclerotic rim (57,58). MRI demonstrates prominent marrow edema and periosteal reaction adjacent to the otherwise well-defined tumor (58) (Fig 24). The characteristic heterogeneous, lobular, or cobblestone pattern of a chondroid lesion is visualized with T1-weighted sequences, while low, intermediate, and high signal intensity at T2-weighted imaging represent calcifications, cellular chondroid matrix, and fluid. Enhancement of the surrounding reactive zones relative to the tumor is disproportionately intense, a feature that is also seen in osteomyelitis, osteoblastoma, eosinophilic granuloma, and osteoid osteoma (57,58).

Figure 24.

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Disorders of the Metaphysis

Metaphyseal Fractures.—The classic metaphyseal corner fracture or bucket handle fracture is highly specific for child abuse before walking age. It results from tractional and torsional forces applied to the extremity of infants younger than 1 year of age (59). It is characterized by separation of the epiphysis and adjacent physis from the metaphyseal bone at the level of the tight perichondrium attachment (21). Tangential views demonstrate the small corner of metaphysis separated from the metaphyseal edge by a thin linear radiolucency, and this may assume a bucket handle configuration with slight cranial or caudal angulation (59) (Fig 25). This fracture should be differentiated from the normal perichondral bone spur that is thin, linear, and attached to the adjacent bone with no intervening lucency (21).

Figure 25.

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Metaphyseal Tumors.—Cortical desmoids are benign self-limiting cortical irregularities that are typically seen in the medial supracondylar femur. They are common among boys aged 10–15 years old and are believed to be tug lesions secondary to traction at the insertion of the adductor magnus aponeurosis or at the origin of the medial head of the gastrocnemius tendon (60). At radiography, they manifest with bone erosion with chronic periosteal reaction. At MRI, they exhibit a low-signal-intensity rim with all sequences, with normal appearance of adjacent bone (8).

Nonossifying fibroma (NOF) is a nonneoplastic tumor of the long bones in individuals younger than 20 years old (61). Radiography demonstrates a well-defined lucent eccentric lesion close to the physis, typically in the posterior or medial cortex. It is called a fibrous cortical defect when the diameter is less than 2 cm (61). Because of its rapid growth and metaphyseal remodeling, it appears to migrate into the diaphysis, distinguishing it from the relatively fixed location of cortical desmoids. NOFs can increase or decrease in size or even disappear. Tumor size greater than 33 mm in the longitudinal plane or greater than 50% in the transverse plane causes a predisposition to a pathologic fracture, although cortical thinning, tumor location, and patient-related factors (eg, age, weight, and activity) contribute to overall fracture risk (62,63) (Fig 26).

Figure 26.

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A simple or unicameral bone cyst is a true cyst of intraosseous origin with the vast majority occurring in the 2nd decade of life (64,65). Radiography shows a moderately expansile lucent tumor with sharp and well-defined margins, characterized by a fallen fragment of bone within the medullary cavity when fractured. This fragment is considered pathognomonic of a simple bone cyst, although it is present in only 5% of cases (64).

An aneurysmal bone cyst is much rarer than a simple bone cyst but occurs in the same age group. Over 50% are seen in long bones, whereas 20% are seen in the spine (64). It is neither a cyst nor a neoplasm and is considered to be a reactive vascular process owing to previous trauma or a precursor tumor such as a giant cell tumor, chondroblastoma, osteoblastoma, chondromyxoid fibroma, or NOF. Radiography demonstrates an eccentric location, rapid bone destruction, and marked expansile remodeling leading to a blown-out appearance. Uneven remodeling localized to the outer cortical margin leads to imperceivable borders that simulate a more aggressive lesion (64). MRI shows fluid-fluid levels representing areas of blood of variable age (65).

Osteochondroma is a surface lesion composed of lamellar bone covered by a cartilage cap. It can arise from any bone undergoing endochondral maturation but is most common in long bones, particularly around the knee. Clinical symptoms are related to neurovascular impingement, osseous deformity, fracture, overlying bursa, pseudoaneurysm development, and rarely, malignant transformation. At imaging, it demonstrates cortical and medullary continuity, with location at the metaphysis, growing away from the joint (55).

At MRI, the cartilage cap can be measured from the osseous interface of the exostosis stalk to the edge of the cartilage cap at its thickest portion (66,67) (Fig 27). There is variability in the reported size criteria for the cartilage cap, although measurements greater than 1–3 cm after skeletal maturation should raise concern for malignant transformation to chondrosarcoma (67). A few authors recommend imaging surveillance of osteochondromas with cartilage caps approaching 2 cm as a reasonable and less morbid alternative to resection (67).

Figure 27.

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Osteosarcoma is the most common primary malignant bone tumor in adolescents and young adults. The vast majority is the conventional type and is readily identified at radiography as an intramedullary mass with immature cloudlike bone formation in the metaphysis of long bones (68). Metaphyseal involvement often extends into the epiphysis, and initial or isolated manifestation within the epiphysis is rare. Radiologic features are aggressive and include periosteal reaction (Codman triangle, laminated, hair-on-end, or sunburst patterns), soft-tissue mass, and destruction of the bone cortex without osseous expansion (69).

Osteomyelitis.—Osteomyelitis primarily affects young children, with nearly 50% of cases occurring in preschool-aged children. It is twice as common as septic arthritis and has an incidence rate of 2–13 per 100 000 individuals in high-income countries and up to 80 per 100 000 individuals in low-income countries (22,27). Staphylococcus aureus is the most common pathogen. Methicillin-resistant Staphylococcus aureus (MRSA) infection is on the rise and leads to increased debilitation with higher serum inflammatory markers, prolonged fever, and a longer hospital stay. Kingella kingae is increasingly recognized and is currently the leading gram-negative pathogen among children with osteomyelitis younger than 4 years of age (27).

Acute osteomyelitis primarily affects the highly vascular metaphysis of long bones, especially the femur, pelvis, tibia, and humerus. Epiphyseal involvement is more common in infants younger than 18 months of age when transphyseal vessels are still present. However, more recent studies suggest that epiphyseal involvement of pyogenic osteomyelitis is more common than classically taught. Factors associated with physeal disruption include aggressive organisms, the pressure of abscess formation, and contiguous avascular spread (30) (Fig 28).

Figure 28.

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Radiography, while an important early diagnostic step, is more useful in excluding fracture or malignancy rather than in helping diagnose osteomyelitis itself. MRI remains the most accurate tool, with higher sensitivity and specificity than radiography and bone scintigraphy. Acute osteomyelitis is characterized with low signal intensity at T1-weighted imaging (compared with that of adjacent muscle) and high signal intensity at fluid-sensitive imaging, reflecting the combination of infiltrated cells and reactive inflammatory response (22).

Chronic osteomyelitis is defined as symptoms of infection that last longer than 3 months, with imaging findings such as necrotic bone (sequestrum) surrounded by pus and reactive bone sclerosis (involucrum) (27,70). A linear defect in bone that allows drainage of purulent material to the soft tissues and skin is termed a cloaca. As with any pediatric disease, extension to the physis causes a predisposition to bone bridge formation, growth arrest, and limb angulation and shortening (27).

Chronic Nonbacterial Osteomyelitis or Chronic Recurrent Multifocal Osteomyelitis

Chronic nonbacterial osteomyelitis or chronic recurrent multifocal osteomyelitis (CRMO) is a skeletal disorder of unknown cause, primarily occurring in children and adolescents with an average age of 10 years (22,71). It is a diagnosis of exclusion based on criteria including unknown causative organism, lack of abscess formation, prolonged course with recurrent episodes, nonspecific histopathologic results, laboratory findings that are consistent with subacute or chronic osteomyelitis, and association with pustulosis palmoplantar or acne (72,73). A lack of response to antibiotic therapy, symptomatic relief with nonsteroidal anti-inflammatory drugs (NSAIDs), and bilateral involvement also favor the diagnosis (74,75).

It is most common in the lower extremity metaphysis, although the pelvis, spine, and medial clavicle can also be affected. The radiographic findings range from normal to lytic, lytic with sclerotic rim, purely sclerotic, or mixed pattern (75). MRI is highly sensitive in the assessment of active disease and extent by depicting marrow edema and contrast enhancement (73). Biopsy results aids in excluding entities that are usually considered first, such as tumors and pyogenic infections (71) (Fig 29).

Figure 29.

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