Periosteal Reaction


Periosteal Reaction

The periosteum is a membrane that covers the majority of bone except at locations at and near cartilage. How periosteum responds to stimuli (e.g., trauma, infection, metabolic process, and neoplasm) can often give clues to the etiology of the underlying stimulus. An aggressive or destructive process will often greatly alter the periosteum, whereas a nonaggressive process usually gives the periosteum the opportunity to remodel with a more orderly architecture. The distribution of periosteal reaction (focal or diffuse) may give clues to the underlying process. Periosteal reaction may also be grouped into several patterns: smooth, solid or thick, and aggressive (laminar, sunburst, Codman triangle, and cloaking).

Smooth periosteal reaction consists of one or multiple unbroken layers of ossified periosteum along the cortical surface. Smooth periosteal reaction indicates orderly new bone formation; the bone has had time to heal or remodel toward its original architecture. As a rule, the unbroken lamellar reaction suggests a process that is not very aggressive.

Table 5.81 Periosteal reaction: smooth




Benign periosteal reaction of the newborn

Fig. 5.163

Smooth symmetric periosteal reaction of rapidly growing bones.

Typically involves rapidly growing bones: femur, tibia, and humerus. Symmetric distribution and age (newborn) also support this diagnosis.

Healing fracture or infection

Smooth periosteal reaction at and adjacent to the injury.

Often seen in plastic/bowing fractures.

Margins of an aggressive process

The periosteum at margins of an aggressive process may be less affected than at the site of maximal destruction. The lesion should be classified based on the more aggressive features.

Vascular insufficiency

Periostitis of affected limb (s).

Especially venous stasis.

Hypertrophic osteoarthropathy

Symmetric periostitis of the radius and ulna > femur, humerus, metacarpals, and metatarsals.

Associated with underlying cardiopulmonary diseases (e.g., cystic fibrosis), infection, and malignancy. Adults > children. Digital clubbing. May affect a single extremity in arterial infections.

Idiopathic hypertrophic osteoarthropathy (pachydermoperiostosis)

Early stage: symmetric subperiosteal new bone formation along the diaphyses of the extremities, hands, and feet. Advanced stage: diffuse subperiosteal bone formation, ossification of ligaments and tendons, ankylosis, acroosteolysis.

Rare hereditary disorder: Digital clubbing, thickened skin, and periostosis. Increased uptake along cortical margins on bone scan.

Fig. 5.163 Benign periosteal reaction of the newborn (arrows).

Table 5.82 Periosteal reaction: solid or thick new bone formation




Mature fracture healing

Thick bridging callus formation.

Chronic osteomyelitis

Fig. 5.164a–c

Thick periosteal reaction with adjacent mixed lucency and sclerosis.

When thick periosteal reaction is seen on radio-graphs, CT is useful to distinguish among chronic osteomyelitis, stress fracture, and osteoid osteoma.

Stress fracture

Thick periosteal reaction surrounding a thin fracture line.

Fracture line may only be detectable by CT.

Osteoid osteoma

Fig. 5.141, p. 593

Thick periosteal reaction superficial to the nidus.

Periosteal reaction may be related in part to prostaglandin synthesis by the nidus.54


Fig. 5.142, p. 594

Fig. 5.143, p. 595

Similar appearance as osteoid osteoma but larger nidus.

Chronic sclerosing osteomyelitis (Garré)

Regional periosteal and endosteal new bone formation.

Primarily affects mandible and proximal tibia.

Idiopathic hypertrophic osteoarthropathy (pachydermoperiostosis)

(see Table 5.81 )

Fig. 5.164a–c Chronic osteomyelitis with thick irregular periosteal reaction enveloping a sequestrum (arrows) on radiography (a, b) and CT (c).

Aggressive periosteal reaction is likely the result of disorganized new bone in response to a destructive process. New bone formation cannot keep pace with the accelerated rate of bone destruction. In response to a rapidly destructive process, new bone formation along the periosteum produces several characteristic patterns. Lamellar (onion peel) periosteal reaction appears as successive layers of new bone arising from the periosteal surface. Spiculation is caused by calcification of the periosteal Sharpey fibers, which are oriented perpendicular to the cortical surface. The radial sunburst pattern is a classic sign of osteosarcoma and affects mainly mineralized osteoid. However, the sunburst pattern may also be seen in hemolytic anemias, thalassemia, and sickle cell anemia. The Codman triangle is another sign indicating an aggressive process. The Codman triangle is an acutely-angled triangle of periosteal reaction along the cortex surface and indicates the transition between the periosteum of the aggressive disease process and the uninvolved bone. No tumor cells are found in the Codman triangle. Just as the physis will act as a temporary barrier to the spread of tumor or infection, the periosteal collar will remain intact.

Table 5.83 Periosteal reaction: aggressive (laminar, sunburst, and Codman triangle)



Acute osteomyelitis

Fig. 5.165a–c

Bone destruction with varying types of periosteal reaction: Codman triangle, cortical and periosteal destruction, and disorganized periosteal new bone formation.


Fig. 5.166, p. 610

Perpendicular speculation of the long bones and hair-on-end periosteal reaction. Hyperplastic hematopoiesis may extend into the subperiosteal space.

Sickle cell disease

Fig. 5.167, p. 610

Hair-on-end appearance of the skull. Hand-foot syndrome in infancy with dactylitis (periosteal elevation and subperiosteal new bone formation).


Fig. 5.124, p. 579

Fig. 5.146, p. 596

Codman triangle, sunburst pattern, and disorganized periosteal new bone formation.

Ewing sarcoma

Codman triangle and disorganized periosteal new bone formation.


Lamellar periosteal reaction in the long bones. Multiple sites.


Fig. 5.168, p. 610

Cortical destruction. Aggressive periosteal reaction.

Fig. 5.165a–c Acute osteomyelitis and subperiosteal abscess formation. Fluid has developed deep to the periosteum (arrows in b and c) around the radius on T2-weighted (a) and enhanced T1-weighted (b, c) MRI.
Fig. 5.166 Thalassemia. Hair-on-end appearance of the skull (arrows).
Fig. 5.167 Sickle cell disease with aseptic dactylitis. Periostitis layers along the diaphysis (arrow).
Fig. 5.168 Metastatic neuroblastoma with moth-eaten pattern of lytic bone destruction in the femoral diaphysis and distal metaphysis.

Periosteal cloaking occurs when a long segment of periosteal membrane is altered by disease and results in a long segment of exuberant thickening. Rapidly growing bones appear to be predisposed to producing cloaking in response to injury. Trauma and infection are the most common causes of cloaking.

Table 5.84 Periosteal reaction: cloaking




Including syphilis.

Subperiosteal hemorrhage

Fig. 5.68, p. 541

Usually after trauma. May be seen in neurofibromatosis type 1 or hemophilia after minor trauma, which leads to chronic dysplastic changes in the bone.

Prostaglandin therapy

Periosteal elevation early in treatment (9–11 d) followed by cloaking.55 Periosteal elevation is relatively common in infants treated with prostaglandins. After cessation of therapy, the periostitis resolves and the bones normalize.


Metaphyseal fractures in infants

(see Table 5.98 )

Fractures in neuropathic diseases

Mucopolysaccharidosis II (Hunter syndrome)

Fig. 5.169

Severe osteopenia, widened ribs, and periosteal reaction including cloaking.

Minor trauma in scurvy

Subperiosteal hemorrhage (see Table 5.43 ).

Infantile cortical hyperostosis (Caffey disease)

Subperiosteal cortical hyperostosis. Epiphyses spared. Fever and soft-tissue swelling adjacent to involved bones. Rarely appears after 5 mo and usually resolves spontaneously by 2 y. Imaging appearance will depend on phase of disease.

Table 5.85 Periosteal reaction: fluffy or indistinct




Appearance of periosteum will depend on the stage of treatment.

Infantile cortical hyperostosis (Caffey disease)

(see Table 5.84 )

Fig. 5.169 Mucopolysaccharidosis II (Hunter syndrome). Severe osteopenia, widened ribs, and periosteal reaction including cloaking that involves the ribs and humeri.

Table 5.86 Periosteal reaction: focal




Appearance will vary depending on the stage of healing.



Langerhans cell histiocytosis, osteoid osteoma, osteosarcoma, Ewing sarcoma.


Vascular malformation or venous status.

Table 5.87 Periosteal reaction: diffuse




Fig. 5.163, p. 607

Benign periosteal reaction of infancy


Sepsis, chronic granulomatous disease of childhood, syphilis, tuberculosis, fungal


Infantile cortical hyperostosis (Caffey disease)


Sickle cell anemia, thalassemia, hemophilia, leukemia


Rickets, scurvy


Pachydermoperiostosis, Camurati-Engelmann disease


Prostaglandin therapy, hypervitaminosis


Leukemia, metastases


Secondary hypertrophic osteoarthropathy

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jul 12, 2020 | Posted by in PEDIATRIC IMAGING | Comments Off on Periosteal Reaction

Full access? Get Clinical Tree

Get Clinical Tree app for offline access