Epiphysis: Supernumerary Epiphyseal Ossification Centers


Epiphysis: Supernumerary Epiphyseal Ossification Centers

Supernumerary epiphyseal ossification centers are often seen in diseases with greatly delayed bone growth.

Table 5.34 Epiphysis: supernumerary epiphyseal ossification centers




Normal epiphyseal maturation

Bipartite ossifications centers eventually fuse during development.

Bipartite often seen at the proximal femoral epiphysis.


Multiple epiphyseal dysplasia

Knees and hips.

Larsen syndrome

Multicentric epiphyseal ossification centers.

Bilateral dislocation of the knees (anterior dislocation of the tibia), pes cavus, cylindrically shaped fingers, and characteristic facies. Cervical kyphosis due to vertebral body hypoplasia (usually C4 and/or C5).

Table 5.35 Epiphysis: punctate and irregularly shaped epiphysis or apophysis




Normal variation in skeletal maturation

Fig. 5.52

Irregular ossification at the border between the epiphyseal ossification center and epiphyseal cartilage.

Classically described at the medial condyle of the distal femur, medial aspect of the proximal tibia, and distal fibula.


Fig. 5.53

Fig. 5.54a–c, p. 530

Fig. 5.55a–e, p. 531

Fig. 5.56a–d, p. 532

Focal lucency and sclerosis of the secondary ossification centers and apophyses.

Common sites are distal femoral condyle and olecranon of the elbow. Other sites are shown in Fig. 5.53 .

Steroid therapy

Generalized osteopenia with bone infarcts.

MRI usually shows much more extent of involvement than radiographs alone.

Physiologic epiphyseal defect (femoral notch)

Fig. 5.57a–d

Characteristic focus of lucency and sclerosis at the boundary of the secondary ossification center and epiphyseal cartilage. Heterogeneously increased T2-weighted signal intensity at characteristic location at distal femur.

Younger patients than with osteochondritis dissecans. Controversial whether it is a result of normal maturation or region of ischemia.

Sickle cell anemia

Bone infarct due to AVN.

Maternal ingestion of certain anticoagulants

Stippled epiphyses.

Dicoumarol or warfarin taken in early pregnancy.

Meyer dysplasia of the hip

Fig. 5.49, p. 528

Delayed or smaller multiple ossification centers of the femoral head. No collapse or metaphyseal abnormality.

Symptomless developmental disorder of the hip. Forty to sixty percent are bilateral. Heals completely. May be mistaken for Legg-Calvé-Perthes disease.

Chondrodysplasia punctata

Fig. 5.58a, b

Punctate calcifications in cartilage.

Multiple genetic forms. Type I: stippled foci of calcification in hyaline cartilage, coronal vertebral clefts, dwarfism, and joint contractures. X-linked: hypoplasia of the distal phalanges of the fingers.


Dysplasia epiphysealis hemimelica (Trevor disease)

Fig. 5.46, p. 526

Irregular ossification at sites of epiphyseal enchondromas. Cartilage may be seen capping the stalks of the enchondromas on MRI.

Osteochondromas of the epiphyses usually restricted to one side of the body.

Kniest dysplasia

Fig. 5.23, p. 514

Fig. 5.47, p. 527

Large epiphyses at the knees, large flattened proximal femoral epiphyses with broad metaphyses.

Spondyloepiphyseal dysplasia associated with deafness or myopia.

Fig. 5.52 Normal variation in ossification at the margin of the distal epiphysis of the femur (arrow) in a 2-year-old. Also note the normal cone-shaped appearance of the femur epiphysis.
Fig. 5.53 Osteochondrosis. Uncommon locations of pediatric osteochondritis.
Fig. 5.54a–c Osteochondritis dissecans at the medial femoral condyle (stable lesion). (a) Lucent lesion surrounded by sclerosis (arrows). Low signal intensity on T1 (b) and subchondral bone marrow edema with intact overlying cartilage on fluid-sensitive MRI (c).
Fig. 5.55a–e Osteochondritis dissecans at the olecranon. (a) Focus of lucency surrounded by sclerosis is present on the radiograph (arrow). (b–e) MRI further characterizes the size and stability of the lesion (arrows, c–e) on fluid-sensitive and T1 imaging in axial, coronal, and sagittal planes.
Fig. 5.56a–d Osteochondritis dissecans at the lateral femoral condyle (unstable lesion). (a) Bone marrow edema suppresses the fat around the lesion (arrow) on T1-weighted imaging. (b, c) Fluid undercuts the fragment on T2-weighted fat-saturated imaging. (d) The fragment is low in signal intensity on all pulse sequences, including proton-density imaging.
Fig. 5.57a–d Condylar notch. Radiograph shows a defect (arrow in a) in the epiphysis of the lateral condyle of the knee. The corresponding coronal T1 (b), coronal T2 fat-saturated (arrow in c), and sagittal proton-density (arrow in d) MRI suggests a diagnosis of normal variation of skeletal maturation rather than osteochondritis dissecans.
Fig. 5.58a, b Chondrodysplasia punctata. (a, b) Punc-tate calcifications involve the epiphyses of the proximal femurs and cartilage centers of the triradiate cartilage and transverse processes of the spine.

Cone-shaped epiphyses may be seen in the phalanges of the hand in many syndromes and bone dysplasias and after local epi-/metaphyseal trauma (osteomyelitis, hemorrhagic disruption in scurvy, bone infarction in sickle cell anemia, as well as after long-term ischemia of an extremity). A cone-shaped epiphysis in the foot is a normal variant ( Fig. 5.59 ).

Fig. 5.59 Cone-shaped epiphysis of the second to fourth proximal phalanges. A normal variant of the foot.

Table 5.36 Epiphysis: cone-shaped epiphyses




Physiologic cone shape of the distal epiphysis of the femur

Fig. 5.52, p. 529

Slightly cone-shaped without central fusion of the physis.

Common normal variant in young children.


Fig. 5.60a–c

Bone bar formation after trauma.

Causes of disruption include prior trauma, infection, and scurvy (Trümmerfeld zones; see Table 5.43 ).

Vitamin A toxicity

Usually greatest in the distal epiphyses. Often symmetric premature closure of the physes.

Seen after chronic overdose. Thickened cortex after the first year of life in the long bones (ulna and metatarsals).


Fig. 5.51, p. 528

Acrodysostosis, asphyxiating thoracic dystrophy, cleidocranial dysplasia, trichorhinophalangeal syndrome, etc.

Fig. 5.60a–c Acquired cone-shaped epiphysis. Bone bridge after meningococcemia produces cupping (a) at the metaphysis of the distal radius on radiography and coronal (b) and sagittal (c) CT.

Table 5.37 Epiphysis: focal defects




Physiologic epiphyseal defect

Fig. 5.57, p. 533

Characteristic focus of lucency and sclerosis at the boundary of the secondary ossification center and epiphyseal cartilage. Heterogeneously increased T2-weighted signal intensity at characteristic location at distal femur.

Younger patients than with osteochondritis dissecans. Controversial whether it is a result of normal maturation or region of ischemia.

Osteochondritis dissecans

Fig. 5.53, p. 529

Fig. 5.54, p. 530

Fig. 5.55, p. 531

Fig. 5.56, p. 532

Focal lucency in the subchondral bone with a rim of sclerosis.

Characteristic locations include the medial aspect of the lateral femoral condyle, capitellum, and tibiotalar joint. MRI can stage the lesion as stable or unstable.

AVN including Legg-CalvéPerthes disease

Fig. 5.61a, b

Fig. 5.36, p. 519

Segmental defects usually in the large epiphyses of the limbs. The appearance of the epiphyseal defect will depend on the stage of the disease.

Early disease will show bone marrow edema on MRI or increased activity on bone scan with normal radiographs. Focal lucencies and/or sclerosis; intact joint space progresses to collapse of the subchondral bone.

Dorsal defect of the patella

Round and lytic lesion with well-defined margins located in the superolateral aspect of the patella adjacent to the subchondral bone.

Controversy over whether this is an incidental finding or a cause of anterior knee pain.


(see Table 5.68 )


Cortical epiphyseal erosions and subchondral osteolysis.

Erosions in juvenile forms of inflammatory arthropathies are less common than in adults. New disease-modifying antirheumatic drug (e.g., tumor necrosis factor inhibitors) also have decreased the severity and number of erosions.

Osteoid osteoma

Well-defined lucency with a dense central calcification of the nidus.


(see Table 5.68 )

Langerhans cell histiocytosis

(see Table 5.68 )

Fig. 5.61a, b Legg-Calvé-Perthes disease. Focal epiphyseal lucency produced by AVN at the right hip (a) and corresponding subchondral signal abnormality on sagittal STIR MRI (arrows in b).

A ring epiphysis may develop when ossification is either decreased centrally or osteoblasts are active in the provisional zone of ossification. Increased bone formation in the provisional zone of ossification may be seen in the healing phase of diseases such as hyperparathyroidism and renal osteodystrophy.

Table 5.38 Ring epiphysis





Decreased bone demineralization that highlights the edge of the epiphysis.

Healing rickets

Fig. 5.62

Widened area of density in the epiphysis caused by calcium deposition in the provisional zone of ossification.

Visible approximately 3 wk after commencing therapy.


Well-delineated cortex of the epiphysis (Wimberger ring).

Metaphyseal changes (Trümmerfeld zones) are nearly always associated with the thickened zone of provisional calcification with osteopenia in the epiphysis (see Table 5.43 ).

Osteogenesis imperfecta

Osteopenia is due to insufficient synthesis of collagen matrix. Thin gracile long bones, wormian bones in the lambdoid sutures, fractures, and nonunion.

Fig. 5.62 Healing rickets. Vitamin D–resistant rickets with metaphyseal widening, irregularity, and sclerosis.

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Jul 12, 2020 | Posted by in PEDIATRIC IMAGING | Comments Off on Epiphysis: Supernumerary Epiphyseal Ossification Centers
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