A tumor of putative vascular origin, Kaposi’s sarcoma (KS)
was rarely encountered in the oral cavity prior to 1983. The classic form generally appeared in two distinct clinical settings: (1) elderly men (in the oral mucosa and on the skin of the lower extremities) and (2) children in equatorial Africa (in lymph nodes). The former is the classic form as originally described by Moritz Kaposi and is an indolent tumor with slowly progressive growth. Although classified as a malignancy, classic Kaposi’s sarcoma does not show a great tendency for metastasis and probably has never caused the death
of a patient. The oral and cutaneous tumors are considered to be of multifocal origin rather than metastases from a distant primary tumor. The oral tumors are red, blue, and purple, and the hard palate is the favored site; the skin tumors tend to localize in the dorsal aspect of the feet and great toe. The African form is characterized by lymph node enlargement and can progressively involve many node groups, being an aggressive and potentially lethal disease. Since it does not present with oral lesions, this form of KS is not discussed further.was rarely encountered in the oral cavity prior to 1983. The classic form generally appeared in two distinct clinical settings: (1) elderly men (in the oral mucosa and on the skin of the lower extremities) and (2) children in equatorial Africa (in lymph nodes). The former is the classic form as originally described by Moritz Kaposi and is an indolent tumor with slowly progressive growth. Although classified as a malignancy, classic Kaposi’s sarcoma does not show a great tendency for metastasis and probably has never caused the death
After 1983, oral KS became much more prevalent, being the most common neoplastic process to accompany HIV infection. Indeed, the mere presence of KS lesions in HIVseropositive subjects constitutes a diagnostic sign for acquired immunodeficiency syndrome (AIDS). The cutaneous lesions begin as red macules and enlarge to become blue, purple, and ultimately brown nodular tumefactions. The lower extremity shows no predilection over other cutaneous sites, and lesions may appear on the arms, face, scalp, or trunk. The oral lesions continue to show a predilection for the posterior hard palate, and they also begin as flat red macules of variable size and irregular configuration (Figure 6-2). Although they may appear as a focal lesion, typical oral KS lesions are multifocal, with numerous isolated and coalescing plaques. Eventually, these lesions increase in size to become nodular growths, and some will involve the entire palate, protruding below the plane of occlusion. The facial gingiva is the second most-favored oral site; in the early stages, the differential diagnosis includes pyogenic granuloma and giant cell granuloma. It is uncommon for AIDSassociated KS to arise in the buccal mucosa, tongue, and lips.
Laboratory studies have disclosed that the cell population is not transplantable into athymic nude mice as with most malignant tumors; rather, the human neoplastic cells secrete a variety of cytokines that induce KS lesions of mouse origin in
the transplant recipient animals. Thus, even in the context of HIV infection, KS should be considered a low-grade sarcoma.
Microscopically, KS lesions show proliferating spindle cells with mild pleomorphism associated with plump endothelial cells oriented about small lumina. Typically, extravasation of erythrocytes is a prominent feature, and hemosiderin granules are commonly encountered. The more hemosiderin present, the browner the tumor will appear clinically. Overall, the pattern of growth in larger lesions is multinodular.
The early plaque or macular stage lesions are painless and do not require treatment. Nodular lesions may become unsightly and interfere with mastication; in this situation, therapy may be desirable. Surgical excision is not usually attended by severe hemorrhage, but electrocautery is recommended, either as a primary form of surgery or as a coagulative hemostatic adjunct to conventional excision. Intralesional injection of 1% sodium tetradecyl sulfate will result in necrosis of the tumefactions; however it is painful, and the patient should be prescribed a moderate-strength analgesic. Intralesional 1% vinblastine sulfate is also beneficial; because it is not a sclerosing agent, it is not associated with significant postinjection pain. Multiple biweekly injections of vinblastine can be given to eradicate the tumors.
Microscopically, KS lesions show proliferating spindle cells with mild pleomorphism associated with plump endothelial cells oriented about small lumina. Typically, extravasation of erythrocytes is a prominent feature, and hemosiderin granules are commonly encountered. The more hemosiderin present, the browner the tumor will appear clinically. Overall, the pattern of growth in larger lesions is multinodular.
The early plaque or macular stage lesions are painless and do not require treatment. Nodular lesions may become unsightly and interfere with mastication; in this situation, therapy may be desirable. Surgical excision is not usually attended by severe hemorrhage, but electrocautery is recommended, either as a primary form of surgery or as a coagulative hemostatic adjunct to conventional excision. Intralesional injection of 1% sodium tetradecyl sulfate will result in necrosis of the tumefactions; however it is painful, and the patient should be prescribed a moderate-strength analgesic. Intralesional 1% vinblastine sulfate is also beneficial; because it is not a sclerosing agent, it is not associated with significant postinjection pain. Multiple biweekly injections of vinblastine can be given to eradicate the tumors.