Disease Mechanism.

Dystrophic calcification occurs in lymph nodes that have been chronically inflamed because of various diseases, frequently granulomatous disorders. The lymphoid tissue becomes replaced by hydroxyapatite-like calcium salts, nearly effacing all nodal architecture. The presence of calcifications in lymph nodes implies disease, either active or the result of previously treated pathosis. In the past, tuberculosis was the most common disease causing calcified lymph nodes (scrofula or cervical tuberculous adenitis). Other well-known causes of lymph node calcification include bacille Calmette-Guérin vaccination, sarcoidosis, cat-scratch disease, rheumatoid arthritis and systemic sclerosis, lymphoma previously treated with radiation therapy, fungal infections, and malignancy (treated Hodgkin’s lymphoma and metastases from distant calcifying neoplasms, most notably metastatic thyroid carcinoma).

Clinical Features.

Calcified lymph nodes are generally asymptomatic, and the nodes are first discovered as an incidental finding on a panoramic radiograph. The most commonly involved nodes are the submandibular and superficial and deep cervical nodes. Less commonly, the preauricular and submental nodes are involved. When these nodes can be palpated, they are hard, lumpy, round to oblong masses.

Imaging Features

Differential Diagnosis.

Management.

Calcified lymph nodes usually do not require treatment; however, the underlying cause should be established in case treatment is required, such as in the case of active disease.

Synonyms.

Synonyms for dystrophic calcification in the tonsils include tonsillar calculi, tonsil concretions, and tonsilloliths.

Disease Mechanism.

Tonsillar calculi are formed when repeated bouts of inflammation enlarge the tonsillar crypts. Incomplete resolution of organic debris (dead bacteria and pus, epithelial cells, and food) can serve as the nidus for dystrophic calcification.

Clinical Features.

Tonsilloliths usually manifest as hard, round, white or yellow objects projecting from the tonsillar crypts, usually of the palatine tonsil. Small calcifications usually produce no clinical signs or symptoms. However, pain, swelling, fetor oris, dysphagia, or a foreign body sensation on swallowing has been reported with larger calcifications. Giant tonsilloliths stretching lymphoid tissue and resulting in ulceration and extrusion are much less common. These calcifications have been reported to occur in individuals between 20 and 68 years old; they are found more often in older age groups.

Imaging Features

Differential Diagnosis.

The clinical differential diagnosis includes calcified granulomatous disease, syphilis, mycosis, or lymphoma, which may produce a firm tonsillar mass. The essential radiographic differential diagnosis is a radiopaque lesion within the mandibular ramus, such as a dense bone island. When in doubt, a right-angle view such as a posteroanterior skull view or an open Towne’s view may show that the calcification lies to the medial aspect of the ramus. Three-dimensional imaging such as MDCT or cone-beam computed tomographic (CBCT) imaging may be necessary for precise localization.

Management.

No treatment is required for most tonsillar calcifications. In symptomatic patients, tonsilloliths may be expressed manually, possibly with the patient under sedation to suppress the gag reflex. Large calcifications with associated symptoms are removed surgically. Treatment of asymptomatic tonsilloliths may be considered in elderly patients with mechanical deglutition disorders and immunocompromised patients because of the risk for aspiration pneumonia.

Disease Mechanism.

When humans ingest eggs or gravid proglottids from the parasite Taenia solium (pork tapeworm), the covering of the eggs is digested in the stomach, and the larval form (Cysticercus cellulosae) of the parasite is hatched. The larvae penetrate the mucosa, enter the blood vessels and lymphatics, and are distributed as cysticerci in the tissues all over the body, but they preferentially locate to brain, muscle, skin, liver, lungs, subcutaneous tissues, and heart. They are also found in oral and perioral tissues, especially the muscles of mastication. The glycoprotein-rich cyst wall is greater than 100 µm thick and rarely elicits any host response when intact. In tissues other than the intestinal mucosa, the larvae eventually die years after infection and are treated as foreign bodies, eliciting a strong inflammatory reaction causing granuloma formation, scarring, and calcification. There is currently an increased incidence of cysticercosis in the American Southwest and urban Northeast, especially among Koreans and Hispanics. The problem is endemic in developing countries of Central and South America, Asia, and Africa, where there is fecal contamination of agricultural soil and pork is a valued food.

Clinical Features.

Mild cases of cysticercosis are completely asymptomatic. More severe cases have symptoms that range from mild to severe gastrointestinal upset with epigastric pain and severe nausea and vomiting. Invasion of the brain may result in seizures, headache, visual disturbances, acute obstructive hydrocephalus, irritability, loss of consciousness, and death. Examination of the oral mucosa may disclose palpable, well-circumscribed soft fluctuant swellings, which resemble a mucocele or benign mesenchymal neoplasm. Multiple small nodules may be felt in the region of the masseter and suprahyoid muscles and in the tongue, buccal mucosa, or lip.

Imaging Features.

While alive, larvae are not visible radiographically. Death of the parasites and development of calcifications in subcutaneous and muscular sites occurs years after the initial infection.

Differential Diagnosis.

Cysticercus may appear similar to a sialolith. However, the small size of the calcified nodules of cysticerci and their widespread dissemination, particularly in brain and muscles, are highly suggestive of the diagnosis.

Management.

Although basic sanitation (proper preparation of pork and avoiding fecal contamination of water supplies and vegetables) is needed to extinguish this source of infection, the symptoms that accompany the initial infestation are best treated by a physician using an anthelmintic such as albendazole or praziquantel. Adjunctive corticosteroids help stem the inflammatory reaction, and anticonvulsants may prevent epileptic seizures. After the larvae have settled and calcified in the oral tissues, they are harmless. However, it is important to carry out a detailed investigation in each patient to rule out the presence of the parasite in other locations and to perform serologic testing on close contacts to identify a possible source of infection.

Disease Mechanism.

The hallmark of arteriosclerosis is the fragmentation, degeneration, and eventual loss of elastic fibers followed by the deposition of calcium within the medial coat of the vessel.

Clinical Features.

Most patients are asymptomatic initially, although late in the course of the disease clinical pathosis such as cutaneous gangrene, peripheral vascular disease, and myositis as a result of vascular insufficiency may occur. Patients with Sturge-Weber syndrome also develop intracranial arterial calcifications.

Imaging Features

Differential Diagnosis.

The radiographic appearance of arteriosclerosis is so distinctive as to be pathognomonic of the condition.

Management.

Evaluation of the patient for occlusive arterial disease and peripheral vascular disease may be appropriate. In addition, hyperparathyroidism may be considered because medial calcinosis frequently develops as a metastatic calcification in patients with this condition.

Disease Mechanism.

Stenotic atheromatous plaque in the extracranial carotid vasculature is the major contributing source of cerebrovascular embolic and occlusive disease. Dystrophic calcification can occur in the evolution of plaque within the intima of the involved vessel.

Imaging Findings

Differential Diagnosis.

Calcified triticeous cartilage may be mistaken for atherom/>