Pehodontics

Gingival and periodontal alterations associated with infection withhuman immunodeficiency virus*Angelika Langford**

Various changes may occur in the gingiva and/or the periodontium as an expression ofexist-mg infection with human immunodeficiency virus. Thus, periodontal disease, characterizedby unusual course, progress, and resistance to treatment, may occur with increased frequency.Clinically, pseudomembranous or erythematous (atrophie) forms of candidiasis or so-calledpapillary hyperplasia may be caused by ubiquitous fungi. Although Candida albicans infec-tions arise frequently on the cheek, the palate, the dorsum of the tongue, and the corner of themouth (angular cheilitis), gingivo-periodontal manifestation is more unusual. Because of theexisting immune defect, infection with or reactivation of various viruses may occur. Recur-rent, progressive destructive ulcérations may be caused by herpes simplex virus 1 or 2, butapparently limited ulcérations may be an expression of a disseminated cytomegalovirus infec-tion. Oral Kaposi's sarcoma appears initially as bluish or reddish spots; these may transformduring the course of the disease into blue, occassionally lymphoma-like or lymphangioma-like, exophytic tumors. (Quintessence lnt I994;25:375-387-)

Introduction

Occurrence of unusual disease of the lungs from Pneu-mocystis carinii together with Kaposi's sarcoma inyoung homosexual men led, in 1981, to definition of theacquired immunodeficiency syndrome (AIDS), Ho-mosexual and bisexual men, intravenous-drug abusers,and hemophihacs requiring substitution therapy ap-peared to be affected most often. The obvious associa-tion of the disease with specific population groupsmade a viral cause probable early on. A previously un-known retrovirus was grown at the Institut Pasteur inParis from the lymph nodes of a diseased patient. Inquick succession, numerous similar isolates were de-

This article was previously published in German as "Gingivo-parodontale Veränderungen bei einer HIV-Infektion" (Par-odontologie 1990;2:l 19-132),University Clinic Rudolf Virchow, Department of MaxillofacialSurgery, Free University of Berlin, D-13353 Berlin, Germany,

scribed, particularly in the United States, In 1985, theseviruses were given the name human immunodeficiencyvirus type 1 (MTV 1) for the sake of standardization ofthe nomenclature. In the same year, HIV 2, a virus withlittle similarity to HIV 1, was isolated for the first timefrom West African patients. Today HIV 1 and HIV 2are recognized as the cause of AIDS.

The manifold clinical symptoms of this disease areexplained by the special affinity of HIV to a certain sur-face structure of the cell membrane {CD4 receptor).Such surface structures have been demonstrated oncell types as diverse as cells of the immune system (T-helper lymphocytes, monocytes. maerophages, Langer-hans cells, and ß-lymphocytes), endothelial cells, andnerve cells during the past several years. This special-ized surface facihtates adhesion and penetration of theHIV into the body cells. There, it can lead to viral inte-gration into the host-cell genome, viral replication, andrelease (Fig 1). The lifelong persistence of HIV in an in-fected cell complicates all therapeutic efforts.

Clinically, the disease manifests as the collapse ofcell-transmitted immunity and thus the ability of the

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AdsorptionVirus gp 120-I- Tj-receptor

Integration

A TranscriptionJ Reverse RNA-Copíes

Tronscripfion A" " M-RNA Genome-RNA

Maturation

Penetration Un coating

J Assembly^ + Building

Fig 1 interreiationship between HIV and a CD4 receptor-bearing ceii. The iifeiong integration of Ihe viral genome makeschemotherapy and immunologie therapy of HiV more difficuit in principie. Stimulation and activation of the [atent infected cellare prerequisites for the replication of HiV, (From Gelderbiom H, Zahnärzll Mitt 1988;78:604)

patient to combat opportunistic infections and the ap-pearance of malignant neoplasms.

With the increasing number of HI V-infected patientsand those suffering from AIDS, dentists are increas-ingly confronted with the problems of treating such in-dividuals. As in the case of other systemic diseases, thedentist has the opportunity to recognize initial signs orsymptoms important in the course of an HIV infectionthrough direct inspection of the mucosal surface, oftenon a regular recall basis,' A number of symptoms, someof them nonspecific, may appear in the gingival andperiodontal regions. Because of their atypical location,their resistance to treatment, or their development,they may be suggestive of HIV infection.^"'

Proper diagnosis requires appropriate understand-ing ofthe immunologie, systemic, and oral symptoms. It

is the purpose of this article to provide a review of theoral changes, particularly gingival and periodontal al-terations, that arise in the course of an HIV infection.

Bade rial infections

It is widely known that facultative or obhgatory peri-odontitis occurs as a side effect of various severe gener-alized diseases, such as panmyelopathy, erythroblasticanemia, and leukemia. An increased frequency of gin-givoperiodontal disease characterized by unusualcourse, progress, and resistance to therapy has been re-ported in the framework of HIV-associated reducedfunction of the immune system.^

Human immunodeficiency, virus-associated gingiv-iiis, the so-called "gingival erythema," is found on one

376 Quintessence Internalional Volume 25, Number

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Bacterial infections:

- Necrotizinggingivoperiodontitis

- Gingival erythema

- Progressiveperiodontitis

- Actinomycoses

- Oat-scratchdisease

Fig 2 Bacterial infections: gingival erythema characterized by band-shaped, reddened gingivae that have a tendency tobleed spontaneously, although the associated teeth show littie plaque formation.

or more teeth of either arch, usually in asymptomaticHIV-infected patients. The free gingiva often is charac-terized by red banding and tends to hemorrhage spon-taneously, while the associated teeth usually have onlylight calculus deposits (Fig 2). Frequently there are pe-techialike or diffuse erythemas, associated with clearlydefined vessels, on the oral vestibule (Fig 3), The strongresistance of this gingivitis to the usual local treatmentmeasures is striking.''

Human immunodeficiency virus-associated necro-tizing ulcerative gingivitis (HIV-NUG), which usuallytakes a chronic or subacute course, may appear initiallyin the form of fibrin-coated ulcérations (Fig 4), but of-ten proceeds to destruction of the interdental papillaand the interdental bone septum and thus to the forma-tion of clinically and radiographically recognizable cra-ters (Fig 5), Characteristic of HIV-NUG is its rapidprogression and conversion to necrotizing periodon-titis.

Microscopically, fusiform bacteria, spirochetes,Borelia, and Candida albicans predominate. The causalrelationship between these microbes and the develop-ment of HIV-NUG is not established, but it appearsthat reduced local resistance facilitates invasion by spi-rochetes and other anaerobic organisms. In general.

great significance is accorded today to the various pro-cesses of immune response in the development of gin-gival and periodontal lesions.

Left untreated, or in the course of an increasingly al-tered immune resistance, such gingivitis can resolveinto progressive periodontitis. which is characterized byits extremely rapid progression and destruction of theperiodontal and bony substance, usually accompaniedby severe pain (Fig 6), Like HlV-associated gingivitis,HIV-associated periodontitis has no preferred sitesand affects all groups of teeth with equal frequency. Inmost patients, only individual sites are affected; in rareinstances, such periodontal destruction is generalized.In chronic inflammatory periodontal disease, attach-ment loss progresses more rapidly than the destructionof the gingiva and bone, thus leading to pocket forma-tion ;̂ in progressive periodontitis, however, destruc-tion of the periodontal hard and soft tissues is usuallysimultaneous {Fig 7). These changes can occur in a mat-ter of a few weeks and may lead to complete loss of at-tachment, resulting in spontaneous loss of the tooth. '̂̂In the active phase of tissue destruction, soft tissue cra-ters and interproximal necroses are characteristic ofsuch regions of rapidly progressing bone loss. When theacute inflammatory phase has healed, crater-shaped

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Gingival erythema:

- Little plaque formation

- Petechia-like or diffuse erythema

- Expansion, frequently into the oralvestibule

- Obviously therapy resistant

Fig 3 Bacterial infections: petechia-like or diffuse erythemas in the oral vestibule, with a clear depiction of vessels, in HiV-as-sociated gingivitis, the so-cafled "gingivai erythema."

Fig 4 Bacterial infections: HIV-assooiated hecrotizing ul-cerative gingivitis with fibrin-covered uiceration in the regionof the mandibuiar anterior teeth in a 28-year-oid infectedpatient who showed no H i V-associated gênerai symptoms.

Fig 5 Bacteriai infections: necrotizing ulcerative periodon-titis with destruction of the interdentai papillae, the Inter-aiveoiar bone septum, and palatal mucosa.

interproximal defects remain, ofien reaching to theregion of the alveolar mucosa (Fig 8).

In some instances, especially in patients who do notreceive treatment or who have reduced defense mech-anisms, inflammation of the surrounding soft tissuemay occur, leading to the chnical appearance of anoma-like change (Fig 9). Such necrotic regions of tis-sue, together with the underlying defect, form favor-able conditions for the tinimpeded multiplication ofunusual oppcrtnnistic agents, such as mucomycoses.This progressive mycotic infection is characteristic: The

organisms enter the vessels, cause thromboses, andlead to rapidly progressing destruction of the surroutid-ing hard and soft tissues in a tnatter of weeks (Fig 10).The course of the disease, in part because of the exist-ing reduced defense mechanisms of the patient, is ful-minant and is associated with a high mortahty.

Overwhelming or uncontrolled local immune reac-tions and specific microorganisms can be responsiblefor this aggressively advancing periodontal disease.The appearance of progressive destructive periodontaldisease is associated with the appearance of manifest

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Periodontics

Progressive periodontitis:

- Pain and spontaneous bleeding

- Formation of interproximal craters

- Edema, with intensive erythema

- Progressive bone andattachment loss

Progressive periodontitis:

- Pain and spontaneous bleeding

- Interproximal crater formationand necroses

- Edema, with intensive erythema

- Extremely progressive bone ioss

Fig 6 Bacterial infections: destruction ot periodontai andbone substance in HIV-associated periodontitis at inter-proximai space between teetii 25 and 26, Like i-IIV-asso-ciated gingivitis, HIV-associated periodontitis has no pre-ferred sites and appears with equal frequency at all toothsites.

HIV-associatedprogressive periodontitis:

/ \Immunosuppression •< • virulence of the infecting agenl

Fig 7 Bacterial infections; progressive periodontitis may affect only a lew sites or, rareiy, it may be generalized. Thesechanges may lead inonlyafew weeks to complete ioss of attachment and thus to spontaneous ioss of teeth.

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Fig 8 Bacteriai infections: after the acute infiammation ofiHIV-associated periodontitis heais, crater-iike interproximaidefects remain, frequently extending into the aiveoiar mu-cosa.

Fig 9 Progression of periodontal infections: extension ofthe inflammation to the surrounding soft tissue, the result ofabsence of treatment and/or especially reduced immune re-sponse.

Fig 10 Progression of periodontal infections: fulminant le-thal fungai infection (mucomycosis], prabably arising fromuntreated periodontal disease.

AIDS symptoms such as Kaposi's sarcoma or opportu-nistic infections,^"

Present knowledge limits treatment of HlV-associ-ated gingivitis and HIV-NUG to local therapy in theform of professional oral hygiene measures and rinsingwith disinfectants (hydrogen peroxide or chlorhexi-dine), together with a regular prevention program,^'Treatment of acute HIV-associated periodontitis con-sists of conventional, usually conservative, local thera-py combined with a strict recall program, accompanied

by such systemic antibiotic therapy (amoxillin and/ormetronidazole) as required by the general symptoms.Because of potential pharmacologie interactions, closecooperation with the patient's internist is desirable,

Mycotic infections

Reduction of immunologie defense mechanisms canlead to development of various chnical symptoms fromubiquitous fungi,'" Oral candidiasis is included in theCenters for Disease Control's'^ classification of HIV-associated diseases. Frequently the development oforal candidiasis has been followed by the manifestationof symptoms of AIDS.'^ Candida albicans infection isusually found in the region of the cheeck, the dorsum ofthe tongue, and the comer of the mouth {angular che-ilitis) (Fig \i). Thepseudomembranoui iorm oí Calbi-cans infection is characterized by white patches (sooror oral thrush) (Fig 11), while the erythematous(atrophie) form may appear clinically as a deeply red-dened area (Fig 12).

Changes on the palate of prosthesis wearers, inducedby poorly fitting dentures, microtrauma, or candidal in-fection, are ealled papillary hyperplasia. In completelydentulous HIV patients, this change on the palate canoccur as an expression of chronic candidiasis; less fre-quently, it may appear on the gingiva (Fig 13),

Candida are recognized in culture or microscopicallythrough the demonstration of hyphae or spores. De-pending on the extent of the spread of oral candidiasis,treatment may be local (miconazole or nyslatin) or

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Peri odontic;

Mycotic infections:

- Candidiasis:PseudomembranousEryttiematous

- Histoplasmosis

- Geotrichosis

- Cryptococcosis

Causes of candidiasis:

- Prolonged antibiotic ttierapy- Cort¡costeroid or cytostatic ttierapy- Diabetes mellitus- Cachexia

- HiV infection

Fig 11 Fungai infection: pseudo-membranous form of infection withC atbicans. manifested as a whitecoating, in the region of the gingivaofthe mandibular anterior teeth.

¡¿JFig 12 Fungai infection; erythem-atous form of C aibicans infection,appearing as a deeply reddenedmucosal area in the region of thehard palate and the gingiva.

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Local therapy:

- Nystatin (rinse or

lozenge)- Clotrimazole

(iozenge)- Miconazoie (gel)- Chlorhexidine

Systemic therapy:

- Ketoconazole- Amphotericin B- Flucytosine

Fig 13 Fungal infection: papillary hyperplasia as an expression of a chronic Candida infection in the gingival region.

systemic (ketoconazole or flucytosine). Because of theexisting immune defect, the clinical manifestationsrecur regularly when drug therapy is discontinued.

Viral infections

Infections caused by a variety of viruses, or their reacti-vation, may occur because of the immunologie defect.These infections also may have oral manifestations.'^

Recurrent intraoral and genital herpes lesions with aprolonged course may arise frequently in HIV pa-tients,''' Two principal types may be differentiated: theprimary infection, which may be asymptomatic or ap-pear as herpetic gingivostomatitis, and the recurringherpes simplex infection. As a rule, the diagnosis ismade on the basis of the clinical appearance (painfulvesicles or ulcérations) together with the demonstra-tion of HSV 1 or2onbiopsy or smear specimens. Ther-apy is directed at prevention of a superinfection (eg,through rinsing with chlorhexidine) and local orsystemic application of virostatic agents (eg, acyclovir)if required.^^ In addition, manifestations of the varicel-la zoster virus are found in the form of oral varicella.Furthermore, changes through human papillomavirusmay occur as verruca vulgaris condyiomata accumina-tum, or focal epithelial hyperplasia (Fig 14),

Progressively destructive oral ulcérations appearinglike punched-out lesions can indicate disseminated in-fection with cytomegalovirus'*'^ (Fig 15), The diagnosiscan be established histologically on the basis of the typ-ical shape of cytomegalovirus-infected cells ("owl eyecells"} and the immunohistochemical demonstration ofthe virus antigen, usually within endothelial cells.

Neoplasms

In addition to infection from opportunistic organisms,Kaposi's sarcoma (KS) and/or non-Hodgkin's lympho-ma are considered to be symptoms of manifest AIDSdisease. Approximately 30% of patients with AIDShave KS; among 80% of these patients, KS appearsorally,'^''' Kaposi's sarcoma associated with AIDS ischaracterized clinically by sometimes single, but tisti-ally multiple, patches or nodules that usually appear in-itially on the skin along the superficial veins and intra-orally along the palatal artery (Fig 16), In addition tothe region of the hard palate, the uvula, and the tongue,the gingival region frequently exhibits KS (Fig 17).Kaposis's sarcoma appears initially as bluish or reddishspots that develop during the course of the disease toblue, occasionally lymphomalike or lymphangioma-like, exophytic tumors^" (Fig 18),

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Viral infections:

- Herpeticgingivostomatitis

- Hairy leukoplakia

- Herpes zoster

- Verruca vulgaris

- Condylomataaccuminata

- Focal epithelial hyperplasia

Fig 14 Viral infections: peduncuiated alteration in the region of the gingivai margin caused by human papillomavirus (verrLvulgans). '̂ *

Fig 15 Viral infections: punched-out appearance of a progressively destructive orai ulcération in the region cf the gingiva, thefirst symptom of an existing disseminated cytomegalovirus infection.

Assuringthe diagnosis of cytomegaiovirus:

Vesicular state: Uicerous state:- Oytoiogic smear - Biopsy

Serclogy, virus culture, immunohisto-chemistry, electron microscopy,in situ hydridization

Changes associatedwith cytomegalovirus:

- Gastrointestinal ulcérations

- Cerebral infections

- Oral ulcérations

- Punched-out appearing ulcéra-tions, usually with only slightlyinflamed margins, in variouslocations

Virus

- Cytomegalovirus

- Herpessimplex virus

- Varicellazoster virus

- Humanpapillomavirus

Therapy

- GancyclovirAcyclovirFcscarnet

- AcyclovirVidarabine

- AcyclovirVidarabine

- CryotherapySurgeryCaustic agents

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Fig 16 Neopiasms: livid blue spotted changes in the re-gion of ttie palatai mucosa, histologicaily characterized asKaposi's sarcoma.

Fig 17 Neoplasms: exophytic Kaposi's sarcoma in thegingival region.

Because this angiosarcoma arises initially in the snb-epithelial or snbmncosal connective tissue, pathologicchanges of the bone or the periodontal tissue can beseen only after some growth of the tumor. Radiographsof early KS lesions reveal no pathologie conditions inthe gingival region. Diffuse osteolysis in the region ofthe alveolar bone and expansion of periodontal spacesare fotind only during late, exophytically growing KS(Fig 19), These may occur simuhaneonsly with clinicalsymptoms of sensitivity to percussion and loosening ordislocation of the teeth,-'

Amalgam tattoos, hemangioma, lymphangioma.giant-cell granuloma, oral nevi, and hypcrpigmenta-tion are among the conditions that must be consideredin the differential diagnosis.

Any clinical suspicion that KS is present must be con-firmed histologicaily. The histologie picture is charac-terized by vessel-like empty spaces, spindle cells,and/or atypical endothelial cells which are believed tobe the probable source of these neoplasms.'^ Sympto-matic, palliative therapy for oral KS lesions maybecome necessary if they hinder nutrition, breathing,appearance, or mastication. Radiation, medicationwith interferon, and/or antiviral agents such as azido-thymine or snifated polyanions have had favorable,confirmed results, Beeause the effectiveness ofcytostatic therapy is limited by the existing immuno-deficiency, small tumors, particularly those of the peri-odontium, may be treated by local injection of cytostat-ic agents.

Regression of KS has been confirmed in HlV-sero-negative organ transplant recipients after reduction orinterruption of immunosuppressive therapy and—rarely—spontaneously in HIV-infected patients."^These clinical findings, together with the histologie pe-culiarities, pose new questions about the etiology ofthis neoplasm, which has never been firmly established,

Lymphomas of the B-cell type are a well-knowneomplication of long-term immunosuppressive thera-py. Together with the suppression of cell-mediated im-munity, there is increased B-cell activity in the frame-work of an HIV infection. Lymphomas associated withAIDS appear as especially aggressive, poorly differen-tiated tumors frequently accompanied by unusual clin-ical symptoms, no primary lymphatic locahzation. anda poor prognosis,'' -"' Intraorally, malignant lymphomascan lead to suddenly loosened teeth, to tissue growth(Fig 20), and occasionally to nnusua! tisstie defects(Fig 21),

Alterations of unknown etiology

In HIV-infected patients various symptoms have beenobserved for which the etiology and the pathogenesisare not yet firmly established. These include recurringaphthous ulcérations that appear as widespread necro-ses or erosions persisting frequently for weeks, Auto-immunologic phenomena may play a role in the eti-ology, Idiopathic thrombocytopenia, a disease elictedby circulating immune complexes, can lead to oral

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Fig 18 Neopiasms: iymphoma-iike or lymphangioma-like Kaposi's sarcoma that hasexpanded in the gingival region and the orai vestibule.

Fig 19 Neopiasms: Diffuse oste-oiysis in the region of the alveolarbone and expanded periodontaispaces as a result of a long-stand-ing, exophytically growing Kapcsi'ssarcoma that is accompanied bysensitivity to percussion and loos-ening or dislocation of teeth.

Fig 20 Neoplasms: maiignant B-cell iymphoma that hasled to sudden tissue growth and loosening of the teeth.

Fig 21 Neopiasms: Pooriy differentiated malignant Iym-phoma in the region of the oral vestibuie. it appeared ciini-cally as an unusual tissue defect.

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Fig 22 Aiterations of unknown elioiogy; petechia-iikechanges or spontaneous bleeding of the gingiva as an indi-cation of an existing idiopathic thrombocytopenia.

Fig 23 Alterations of unknown eliolog/: spontaneouslyappearing spotty hyperpigmentation ofthe gingiva. Hyper-pigmentation also may appear on the palate, cheeks, ortongue in HIV-infected patients.

petechia-like changes, often in the region of the hardpalate, or to cleft formation in the gingiva (Fig 22). Inaddition to drug-induced hyperpigmentation (fromclofazimine, for example), spontaneously appearingspot-sized or surface-covering pigmentation of thegingiva has been found on the palate and the tongue ofHIV-infected patients'^ (Fig 23).

Conciusions

While, on the one hand, true causal therapy of HIV-as-sociated diseases is not yet possible, a variety of symp-toms such as Pneumocystis carinii pneumonia, a dis-ease with a high mortality rate, can be prevented in partby appropriate prophylactic therapy. Early diagnosis ofan existing HIV infection and recognition uf a worsen-ing immunologie condition, observations to which theappearance of progressive periodontal disease can con-tribute, therefore are important for the patient. Lack oftreatment or insufficient treatment of acute oral infec-tions can lead to complications that are no longer lo-cally controllable. Careful examination of the oral mu-cosa and the periodontium by the dentist can providemany clues as to the condition of the patient with HIV,

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