Periosteal Reaction

10.1055/b-0034-87942

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**
Diagnosis	Findings	Comments
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**
Diagnosis	Findings	Comments
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
Osteoblastoma 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)**
Diagnosis	Findings/Comments
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.
Thalassemia 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).
Osteosarcoma 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.
Leukemia	Lamellar periosteal reaction in the long bones. Multiple sites.
Metastasis 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**
Diagnosis	Comments
Osteomyelitis	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.
Rickets
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**
Diagnosis	Comments
Metabolic	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**
Diagnosis	Comments
Trauma	Appearance will vary depending on the stage of healing.
Infection
Tumor	Langerhans cell histiocytosis, osteoid osteoma, osteosarcoma, Ewing sarcoma.
Vascular	Vascular malformation or venous status.

**Table 5.87 Periosteal reaction: diffuse**
Diagnosis	Comments
Physiologic Fig. 5.163, p. 607	Benign periosteal reaction of infancy
Infection	Sepsis, chronic granulomatous disease of childhood, syphilis, tuberculosis, fungal
Inflammation	Infantile cortical hyperostosis (Caffey disease)
Hematologic	Sickle cell anemia, thalassemia, hemophilia, leukemia
Metabolic	Rickets, scurvy
Congenital	Pachydermoperiostosis, Camurati-Engelmann disease
Medication/overdose	Prostaglandin therapy, hypervitaminosis
Tumor	Leukemia, metastases
Miscellaneous	Secondary hypertrophic osteoarthropathy