HIV Disease—Epidemiology

The world wide dissemination of the HIV disease continues to increase. At the end of 2002, over 41,000,000 persons were infected with the HI virus. There are grave differences between the industrialized nations on the one hand and the developing countries on the other: While in the USA, Western Europe, Japan, Australia and New Zealand the new infections of adults have generally stabilized, the rates for the African countries south of the Sahara Desert, and in Russia continue to increase. At the present time, two thirds of all the HIV-infected adults are found in sub-Saharan Africa and Russia, and 90% of all infected children!

Unprotected heterosexual intercourse, the dissemination of uncontrolled blood products and above all the lack of prevention (information), as well as the enormous costs of treatment may be responsible for the current situation. Even more perplexing is the fact that the HI virus appears in various types and subtypes (Reichart & Gelderblom 1998, Reichart & Philipsen 1999), which makes efforts toward treatment or even immunization infinitely more complex.

The battle against the AIDS pandemic must also be waged against the socioeconomic backdrop.

Ninety percent of all HIV-infected individuals world wide live in developing countries, but 90% of all monies spent for information, prevention and treatment are expended in the industrialized countries–ca. $10,000 per infected person per year.

Epidemiologic research has shown that we must differentiate not only between countries and their various stages of economic development. Even within the industrialized nations, there are clear differences between persons of different socioeconomic classes. For example, in the USA the infection rate for Blacks is almost five times higher than for white males. The difference between Afro-American and Caucasian females in the USA is even more dramatic (Fig. 304, right).

Because it is extremely unlikely that the differences between industrialized and developing nations, as well as between different socioeconomic standards will ever be reconciled, the highest priority must be given to the development of effective and inexpensive medicines, and above all an effective vaccine (Mann and Tarantola 1998).

Classification and Clinical Course of HIV Disease

With ever-increasing knowledge, the classification of the HIV disease has already been modified many times, and additional variations will surely be implemented in the future. The classification derives from data from the USA Centers for Disease Control and Prevention (CDCP). This classification is based on the number of CD4 cells (stages 1–3) in relation to clinical symptoms (stages A–C) (Fig. 305).

Besides this classification, today the most significant parameter of the clinical course of disease is the number of free virus copies per milliliter of blood plasma, the so-called “viral load.” This is determined using the polymerase chain reaction (PCR).

HIV disease develops very rapidly following the initial infection. Billions of HIV particles destroy millions of CD4 lymphocytes. This bitter “war of attrition” between HI viruses and host cells goes on continually for years. During the further (average) course of the disease–about 6 months after infection–the number of freely circulating viruses decreases dramatically and the number of immune cells again increases. A balance between attack and defense can remain constant for ca. 10 years, until the number of viruses again increases dramatically and the host defense breaks down (Fig. 306).

Even from patient to patient, the disease can assume extra-ordinarily different clinical courses. “Long survivors” are those individuals who live longer than 10 years after infection, while others with the disease have only a short postinfection life span. A prognosis concerning the course of the disease is possible by measuring the viral load. Mellors (1998) measured the viral load in 1,600 untreated HIV-infected males, and reported that 70% of his study population who exhibited more than 30,000 virus copies per milliliter of blood plasma died within six years (mean lifespan: 4.4 years). In contrast, less than 1% of the untreated patients died within six years if their viral load was below 500 copies/ml. In the latter group, the mean life expectancy was more than 10 years.

It is now clear that the determination of viral load provides important information concerning prognosis and therapy. Using today’s anti-retroviral medicinal polytherapy (p. 149), the number of virus particles can be held below the level of detection.

Oral Manifestations of HIV Disease

In addition to numerous somatic symptoms, the HIV disease can also be characterized by pronounced oral manifestations. The progress in systemic medical therapy has fortunately reduced many oral symptoms, e.g., bacterial and fungal infections, viral infections, neoplasms and other pathology of unknown etiology (Fig. 307).

The oral lesions are often painful and can compromise the patient’s quality of life. The time of appearance of oral manifestations will be determined by the CD4 cell count and the viral load (Fig. 308). Occasionally, however, oral alterations—especially linear gingival erythema (LGE) and necrotizing periodontitis (NUP)—occur at unpredictable times during the course of the HIV disease.

The dentist must be fully aware of the oral manifestations of HIV disease; in numerous cases, a dentist has diagnosed oral alterations that lead to suspicion of HIV infection, only to have those suspicions subsequently corroborated after medical examination by the physician.

Bacterial Infections in HIV

• Linear gingival erythema (LGE)

• Necrotizing gingivitis/periodontitis (NUG/NUP)

The disease states marked with a solid bullet (•) on this page and the pages that follow are depicted and described.

LGE is clearly differentiable from simple plaque-elicited gingivitis. It is characterized by a clearly demarcated band of reddening in the marginal gingiva. Classic periodontitis—both “chronic” and “aggressive” forms—do not occur in HIV-disease patients any more frequently than in other individuals; on the other hand, NUP occurs much more frequently, often exhibiting an extremely rapid clinical course of attachment loss.

Th significance of certain microorganisms in the etiology of LGE and NUP remains unclear. One finds periodontopathic microorganisms as seen in aggressive forms of periodontitis (p. 96), but often also significant increases in Candida albicans (Ca). The spotty erythema on the attached gingiva, and the frequent observation of this fungus in niches and pockets can be attributed to Ca. In those not responding to mechanical therapy, the cytomegalovirus is often detected.

Fungal Infections

• Candidiasis

  • Atrophic/Erythematous

  • Angular cheilitis

  • Pseudomembranous

  • Hyperplastic

    • Histoplasmosis

The most common and earliest appearing fungal infection in HIV disease is candidiasis in its many and varied forms. Approximately 95% of all fungal diseases are caused by Candida albicans; other fungi have only minor medical significance. Candida albicans is also found in a high percentage of healthy individuals, without causing any clinical symptoms. If host defense mechanisms are reduced, as is the case in HIV disease, proliferation of the fungi can occur by growth of hyphae and the formation of mycelia. The latter can invade the mucosa and lead to clinical manifestations of the types listed above. Oral Candida infections have a tendency to recur. Spread into the respiratory tract or the gastrointestinal tract is an indication of progression of the HIV disease, and is a complication to be taken very seriously by the patient and the physician.