Infections of the gingivae and oral mucosa

Infections of the gingivae and oral mucosa
Viral Infections
Bacteral Infections

1. Infections of the gingivae and oral mucosa Sana Rasheed Akhtar Saeed Medical and Dental College

2. A wide range of pathogenic organisms are present in the mouth but oral mucosa shows low susceptibility to primary infection? This is probably due to the activity of saliva. First line of defense: IgA is in the saliva and direct effect of this on the oral micro-organisms, a complex may be formed between the immunoglobulin and the oral epithelium itself resulting in a protective surface coating on the mucosa. Mechanical protective activi ty of saliva in that foreign material , including micro-organisms, is washed from the oral cavity to the stomach where bacteria are destroyed by gastric fluids.

3. BACTERIAL INFECTIONS

4. Acute necrotizing ulcerative gingivitis (ANUG) Definition Necrotizing ulcerative gingivitis is a relatively rare specific infectious gingival disease of young persons . Etiology The exact cause of ANUG is not known, but there is no doubt that during an attack there is a proliferation of spirochaetes and fusiform bacteria . There is also a proliferation of obligate anaerobic , non- sporulative rods . Fusobacterium nucleatum , Treponema vincentii , and probably other bacteria play an important role .

5. Acute necrotizing ulcerative gingivitis (ANUG) Predisposing Factors: Emotional stress Smoking P oor oral hygiene L ocal trauma HIV infection

6. Acute necrotizing ulcerative gingivitis (ANUG) Clinical Features: P ainful necrosis of the interdental papillae and the gingival margins Soreness and bleeding of gingiva F ormation of craters covered with a gray pseudomembrane . Halitosis I ntense salivation Fever malaise Lymphadenopathy

7. Acute necrotizing ulcerative gingivitis (ANUG) Diagnosis: D emonstration of a fusospirochaetal complex in a Gram-stained deep gingival smear. Bacteria cultured in ANUG include : Treponema vincentii , denticola , and macrodentium; Prevotella intermedia; Porphyromonas gingivalis ; Fusobacterium nucleatum .

8. Acute necrotizing ulcerative gingivitis (ANUG) Management S upragingival plaque control U se of a systemic antibiotic, such as metronidazole R efrain from smoking Gentle debridement of the gingival tissues Chlorhexidine mouthrinse and attempt gentle toothbrushing Metronidazole dose: A dose of 200 mg, three times daily, for 3 days is sufficient in most cases to reduce the symptoms dramatically in 24 hours.

9. Acute necrotizing ulcerative gingivitis (ANUG) Metronidazole is the antibiotic of choice for the initial management of ANUG. Patients should be warned not to take alcohol whilst taking metronidazole . Metronidazole is best avoided during pregnancy.

10. Syphilis Definition Syphilis is a sexually transmitted disease and the causative bacterial agent is Treponema pallidum . This gains entry to the body via mucous membranes and minute abrasions in the skin . Acquired syphilis is classified as primary , secondary and tertiary.

11. Syphilis Clinical Features Primary Syphlis (chancre ) Appears following a period of 2–3 weeks after infection T he chancre presents as a painless indurated swelling , dark red in colour with a glazed surface. Chancres are most likely to be found in the relatively soft and unrestricted tissues of the tongue, cheeks, or lips, gingiva and palate. N ontender enlargement of the cervical lymph nodes affecting the submental , submandibular, pre- and post-auricular, and occipital groups—the so-called ‘ syphilitic collar ’.

12. Syphilis After two weeks , Onset of the Second stage of disease occurs It may last for many years

13. Syphilis The oral symptoms most often described at Second stage of the disease are mucous patches (appearing as greywhite ulcers covered by a thick slough) and ‘snail track’ ulcers In this second stage lymph nodes may again be palpable as nontender, discrete structures .

14. Syphilis Tertiary Stage Tertiary syphilis begins after a period of 4–7 years S yphilitic leukoplakia D evelopment of a ‘ gumma ’. This is essentially a chronic granuloma, often in the palatal tissues, that eventually breaks down with the consequent production of a tissue defect. Fibrosing glossitis . Osteomyelitis affecting the jaw M ental confusion

15. Syphilis Congenital Syphilis Treponema pallidum crosses the placental barrier and causes congenital syphilis in the fetus . The dental abnormalities mainly affect the permanent dentition. Mulberry Molars Hutchinson’s Incisors

16. Syphilis The diagnosis of syphilis S erological tests . Current serological tests include the Venereal Disease Reference Laboratory ( VDRL ) test, the Treponema pallidum haemagglutination assay ( TPHA ), the fluorescent Treponema antibody absorbed test ( F TA (abs) ), the Treponema pallidum immobilization ( TPI ) test

17. Syphilis The treatment of syphilis Penicillin is the treatment of choice and is given in high doses. In primary syphilis the course of antibiotics is up to 1 month but in L ate (or latent) syphilis this is for up to 12 weeks . Patients who are allergic to penicillin can be prescribed erythromycin or tetracycline .

18. Gonorrhoea Primary oral lesions are the result of transmission of the organism ( Neisseria gonorrhoea ) by direct mucosal contact .

19. Gonorrhoea Clinical Features Lesions appear in the pharynx They are a result of orogenital sexual contact . Diffuse erythematous and ulcerative oral lesions Tonsillitis P urulent gingivitis M ild to severe febrile symptoms , and the degree of oral discomfort. Difficulty swallowing . Submandibular lymphadenopathy On the skin: Ulcers , haemorrhagic lesions , and other manifestations of hypersensitivity to the disseminating microorganisms. Gonococcal infective arthritis of the temporomandibular joints --- pain, swelling , and trismus .

20. Gonorrhoea Diagnosis of gonorrhea Microbiological confirmation A Gram-stained smear of the oral lesions may show Gram-negative diplococci. Microbiological swabs should always be taken for culture and sensitivity.

21. Gonorrhoea Treatment of gonorrhea H igh doses of antibiotics . S ingle , high-dose intramuscular injection of procaine penicillin to oral amoxycillin (or ampicillin) to short courses of oral tetracycline or co- trimoxazole .

22. Non-specific urethritis Chlamydia species may be isolated from the urethra. Symptoms A burning sensation on micturition P urulent discharge in males. M ay be asymptomatic, particularly in females. Microbiological tests are essential to confirm the diagnosis and the majority of cases respond to tetracycline therapy in normal doses over a week or two. Reiter's syndrome predominantly affects young males and can present as a polyarthritis, urethritis, uveitis, and macular lesions on the palms and soles. Oral lesions have also been reported and include a ‘ circinate ’ stomatitis.

23. Tuberculosis Definition Tuberculosis is a chronic, granulomatous, infectious disease that primarily affects the lungs . Etiology Mycobacterium tuberculosis Clinical features The tuberculous ulcer is painless and irregular , with a thin undermined border and a vegetating surface , usually covered by a gray-yellowish exudate . The surrounding tissues are inflamed and indurated . The dorsum of the tongue is the most commonly affected site , followed by the lip, buccal mucosa, and palate . Osteomyelitis of the jaws , periapical granuloma , regional lymphadenopathy , and scrofula are less common oral manifestations. Tuberculous lympheadinitis .

24. Tuberculosis Diagnosis Sputum culture H istopathological examination C hest radiography Ziehl –Nielsen staining Immunofluorescent techniques Culture mycobacteria on Lowestein medium

25. Tuberculosis Management Investigations for pulmonary or other lesions. Chest radiograph

26. FUNGAL DISEASES

27. Oral Candidosis Definition Candidiasis is the most common oral fungal infection. Etiology It is usually caused by Candida albicans , and less frequently by other fungal species ( C . glabrata , C . krusei , C . tropicalis , C . parapsilosis ). Predisposing factors are local (poor oral hygiene, xerostomia, mucosal damage , dentures, antibiotic mouthwashes) and systemic ( broad-spectrum antibiotics , steroids, immunosuppressive drugs, radiation, HIV infection, hematological malignancies, neutropenia, iron-deficiency anemia, cellular immunodeficiency, endocrine disorders).

28. Oral Candidosis

29. Oral Candidosis

30. Oral Candidosis

31. Oral Candidosis

32. Oral Candidosis

33. Oral Candidosis

34. Pseudomembranous candidosis

35. Pseudomembranous candidosis The pseudomembrane consists of a network of candidal hyphae containing desquamated cells, microorganisms, fibrin , inflammatory cells, and debris. This pseudomembrane lies on the surface of the tissue and candidal hyphae penetrate superficially into the epithelium to provide anchorage .

36. Pseudomembranous candidosis

37. Pseudomembranous candidosis CLINICAL FEATURES Appears as a thick, white coating or series of patches on the affected tissue The pseudomembrane can be wiped away and, since the more superficial layers of the epithelium may be included, a red and bleeding base is left behind . Any of the mucosal surfaces of the mouth may be affected by thrush , as may the posterior pharyngeal wall . Extension into the oesophagus and trachea is possible and may prove fatal . This is likely to occur only in the severely debilitated patient.

38. Pseudomembranous candidosis Diagnosis Clinical test to distinguish thrush from other white lesions of the mucosa and confirmation may also be obtained by taking a direct smear from the lesion. This may be fixed by gentle heat and immediately stained, using the periodic acid–Schiff (PAS) reagent . The hyphae are readily identified under the microscope . A swab should be taken and sent to the microbiological laboratory for culture and sensitivity.

39. Pseudomembranous candidosis Management Treatment same as in the table above.

40. Erythematous candidosis Definition This can be ‘ acute’ or ‘chronic’ depending on the duration of the oral lesions . Acute erythematous candidosis was formerly known as ‘acute atrophic candidosis ’ or ‘antibiotic sore mouth ’ and usually occurred as a result of medical treatment involving antibiotics or steroid preparations. A significant number of patients (adults and children ) are now using steroid inhalers for pulmonary disease and these can predipose to the development of either erythematous or pseudomembranous candidosis .

41. Erythematous candidosis CLINICAL FEATURES Acute erythematous candidosis resembles ‘thrush’ without the overlying pseudomembrane . Clinically, the mucosa involved is red and painful . This is, in fact, the only variant of oral candidosis in which pain and discomfort is marked . T he epithelium is thin and atrophic with candida hyphae embedded superficially in the epithelium . This form of candidosis is common in patients with the suppressed immune function of AIDS as well as patients undergoing prolonged antibiotic or steroid therapy.

42. Erythematous candidosis MANAGEMENT Topical antifungal therapy is usually effective. Patients who regularly require a steroid inhaler should be instructed to rinse their mouth with water after use . Use of a spacer device for the inhaler may be necessary

43. Hyperplastic candidosis Chronic hyperplastic candidosis is also known as ‘ candida leukoplakia ’ and is associated with chronic infection of the oral Mucosa with candidal species, usually C. albicans . This chronic form of candidosis is considered to be a premalignant lesion and is more likely to occur in patients who smoke .

44. Hyperplastic candidosis CLINICAL FEATURES Chronic hyperplastic candidosis classically presents as a fixed white patch at the commissures of the mouth . Other areas of the mouth, particularly the palate, may be affected but the tongue is less commonly involved . Clinically, the lesion(s) appear as raised,irregular white plaques, which may be ‘speckled’ or nodular in appearance . There is frequently evidence of oral candidosis elsewhere , particularly on the palate of patients with full dentures and/or angular cheilitis.

45. Hyperplastic candidosis MANAGEMENT Management involves the eradication of predisposing factors , such as smoking and institution of appropriate antifungal therapy—either topical or systemic. An initial course of fluconazole for 2–3 weeks can be combined with topical therapy as in the table. Denture hygiene and other factors predisposing to oral candidosis , either local or systemic . Haematological investigations should be undertaken to check for haematinic deficiencies such as iron deficiency , and a blood glucose test is advisable to exclude diabetes . Excision of persistent lesions or those with a significant degree of dysplasia is preferably carried out with a laser. Long-term follow-up is essential.

46. Candida-associated, denture-induced stomatitis This is by far the most common form of oral candidosis and is also referred to as chronic erythematous candidosis (or, more colloquially in the past, as ‘denture sore mouth ’—a misnomer because the condition is nearly always painless). This form of denture stomatitis represents the end-result of secondary candida infection of tissues, traumatized by a dental appliance.

47. Candida-associated, denture-induced stomatitis CLINICAL FEATURES marked redness of the palatal mucosa covered by the appliance there may be a corresponding area of spongy ‘ granular looking ’ tissue, but otherwise the affected mucosa is smooth .

48. Candida-associated, denture-induced stomatitis

49. Candida-associated, denture-induced stomatitis

50. Candida-associated, denture-induced stomatitis Diagnosis By taking swabs or carrying out direct inoculation from the fitting surface of the denture involved it is practically always possible to isolate a heavy growth of Candida . Biopsy may be done in persistent or atypical cases to confirm the diagnosis. Histopathology

51. Candida-associated, denture-induced stomatitis Treatment Denture hygiene E limination of trauma by the adoption of suitable prosthetic techniques. U se of tissue conditioners. The use of an antifungal cream or miconazole gel on the fitting surface of the appliance. Careful and regular cleaning of all surfaces of the denture is also of great importance . A lacquer containing miconazole is now available and painted on to the fitting surface of the upper denture.

52. Candida-associated angular cheilitis Angular cheilitis presents as erythema and cracking at the angles of the mouth and is commonly a Candida -associated lesion.

53. Median rhomboid glossitis Median rhomboid glossitis is classified as a ‘ Candida -associated’ lesion and characteristically presents as an area of depapillation on the midline of the dorsum of the tongue , immediately in front of the circumvallate papillae . ‘rhomboid-shaped ’ lesion. Its surface may be red, white, or yellow in appearance .

54. Secondary oral candidoses: chronic mucocutaneous candidiasis syndromes A spectrum of conditions in which candidosis of the oral cavity, the skin , and other structures such as the fingernails may occur. The skin lesions may include widespread and disfiguring lesions of the face and scalp. Granulomatous lesions of the lips may also occur, similar to those that affect the skin. A variant ( familial chronic mucocutaneous candidosis ) is genetically determined and is transmitted as an autosomal recessive condition. In the candidosis – endocrinopathy syndrome white candidal plaques in the mouth and candidal infections of the nails are associated with disorders of the parathyroids or adrenals.

55. Secondary oral candidoses: chronic mucocutaneous candidiasis syndromes MANAGEMENT Reduction of Candida species. Predisposing factors for oral candidosis should be eliminated. Treatment is with long-term systemic antifungal therapy such as fluconazole. Regular monitoring of liver function is essential.

56. VIRAL INFECTIONS

57. Herpes simplex virus infections Primary herpetic gingivostomatitis

58. The herpes simplex virus (HSV) is a DNA virus. Herpes simplex, type 1 , affects the oral mucosa , pharynx, and skin. Herpes simplex, type 2 , predominantly involves the genitalia .

59. Primary herpetic gingivostomatitis

60. Primary herpetic gingivostomatitis Primary herpetic gingivostomatitis is the most common viral infection affecting the mouth . It affects patients in two main age groups— young children and young adults . The incubation period is about 5 days .

61. Primary herpetic gingivostomatitis CLINICAL PRESENTATION There is history of recent exposure to a patient with a herpetic lesion . Initial Prodromal stage (lasts a day or two) symptoms: Malaise with tiredness. Generalized muscle aches. Sore throat. S ubmandibular lymph nodes are often enlarged and tender.

62. Primary herpetic gingivostomatitis Followed by: A ppearance of oral and, sometimes, circumoral lesions . Groups of vesicles form on the oral mucosa and rapidly break down to produce shallow ulcers . T he breakdown of confluent groups may result in the formation of large areas of ulceration . Apart from the ulcerated areas, the whole of the oral mucosa may be bright-red and sore . M arked gingivitis in young children.

63. Primary herpetic gingivostomatitis Complications Encephalitis Meningitis Dissemination throughout body

64. Primary herpetic gingivostomatitis Diagnosis HSV can be grown in tissue culture systems Serology

65. Primary herpetic gingivostomatitis MANAGEMENT S ymptomatic with general supportive measures: Rest Fluids Antipyretics Analgesics Antiseptic or tetracycline mouthwash Analgesic mouthwash In most immunocompetent patients, HSV infections are self-limiting and last 10–14 days.

66. Primary herpetic gingivostomatitis Acyclovir is used for the systemic and topical treatment of herpes simplex infections affecting the skin and mucous membranes . Systemic antiviral therapy is essential if the patient is immunocompromised. If the signs and symptoms of primary herpetic gingivostomatitis fail to improve after 2 weeks, then the patient should be referred for a specialist opinion to exclude blood dyscrasias and other underlying systemic conditions.

67. Secondary (recurrent) herpes simplex infections

68. Secondary (recurrent) herpes simplex infections The usual site of the recurrent lesion: on or near the lips and the lesion is known as ‘herpes labialis ’ or a ‘cold sore’. Less commonly, the skin and mucosa of the nose and nasal passages are involved occasionally , almost any site on the face .

69. Secondary (recurrent) herpes simplex infections The recurrences may be provoked by a wide range of stimulae , including sunlight , mechanical trauma mild febrile conditions such as the common cold . Emotional factors also play a part in precipitating recurrences in many patients.

70. Secondary (recurrent) herpes simplex infections CLINICAL PRESENTATION Mild degree of tiredness and malaise . Followed by, A period of irritation and itching over the area of the lip involved in recurrence. W ithin a few hours, vesicles appear surrounded by a mildly erythematous area . In a short time the vesicles burst and a scab is formed.

71. Secondary (recurrent) herpes simplex infections MANAGEMENT N o therapeutic measure available that provides reasonably consistent results and that entirely prevents further recurrences. Topical therapy for ‘cold sores’ (herpes labialis ) should be applied in the prodromal phase of the lesion. Aciclovir and penciclovir creams are available for topical application.

72. Varicella zoster virus infections Varicella zoster virus is a DNA virus that causes chickenpox and herpes zoster. Chickenpox Primary infection. And common disease of the childhood. I ncubation period of 14–21 days. The infection is spread by direct contact or droplet infection and is established first in the upper respiratory tract . CLINICAL PRESENTATION Just before the rash, oral lesions may appear on the hard palate, pillar of fauces , and uvula and appear as small ulcers, with a red halo . The rash initially manifests as pink, maculopapular lesions that develop into itchy vesicles on the back, chest, face, and scalp . Other presentations: Malaise Fever Lymphadenopathy

73. Varicella zoster virus infections Complications : Pneuomonia Encephalitis Treatment: Symptomatic

74. Shingles Occurs in middle aged or older persons. Sometimes in younger patients. Predisposing factors: Debilitating diseases Immunosuppression

75. Shingles CLINICAL PRESENTATION A vesicular eruption in an area of distribution of a sensory nerve . A band like distribution of the shingles on the trunk. When the eruption affects the trigeminal nerve, the facial skin and oral mucosa in the sensory area may be affected . Of the three divisions of the trigeminal nerve the ophthalmic is the most frequently involved. Cervical nerves may also be affected .

76. Shingles Initial Symptoms: P ain and tenderness in the affected area. The prodromal phase may last for 2 or 3 days and is succeeded by the appearance of vesicles in a rash. T here may be corneal ulceration, which can lead to scar formation. Ulcers within the mouth . The skin vesicles may form firm crusts and, particularly if these are disturbed, marked scarring may occur . Following the fading of the rash the major complication of the condition— postherpetic neuralgia —may appear.

77. Shingles Postherpetic neuralgia A naesthesia , paraesthesia , and trigeminal neuralgia-like pains may affect the area and may persist for a period of years, occasionally reappearing after a prolonged absence. This is a highly refractory condition that may fail to respond to any form of medical treatment.

78. Shingles Due to facial nerve involvement: Facial weakness, loss of taste sensation, and symptoms such as dizziness resulting from labyrinthine disturbance may occur. This is the Ramsay Hunt syndrome .

79. Shingles

80. Shingles MANAGEMENT H igh doses of systemic aciclovir or famciclovir for ophthalmic division of trigeminal nerve involvement. Early use of antiviral therapy . Topical treatment for oral lesions ( tetracycline mouthwashes ).

81. Epstein–Barr virus infection

82. Epstein–Barr virus infection The EBV is considered to be an oncogenic virus and associated with the formation of malignant lymphomas ( Burkitt's lymphoma ) and nasopharyngeal carcinoma and oral hairy leaukoplakia in immunocompromised patients. It causes infectious mononucleosis.

83. Infectious mononucleosis Early adulthood disease Patient with glandular fever feels ill and has a fever and enlargement of the lymph nodes that may extend over the whole of the body. May be minor or require hospitalization. Sore throat Oral ulceration Petechiae may be visible at the junction of the hard and soft palate . Management: Antibiotic mouthwashes Symptomatic treatment

84. Infectious mononucleosis Diagnosis: Lab tests : Blood Film Differential white cell count Lymphocytosis is acute phases and Dauncy cells produced. S lide agglutination test called the ‘ monospot ’.

85. Coxsackievirus infections

86. Coxsackievirus infections Group A viruses are principally responsible for two i nfections that affect the oropharyngeal region: ‘ hand, foot, and mouth disease’ herpangina

87. Herpangina Predominantly seen in children. The patient complains of a moderate degree of malaise and of a sore throat , while occasionally T here is also a minor degree of muscle weakness and pain . Small vesicular lesions appear in the posterior part of the mouth, in particular , on the soft palate . This is a self-limiting condition. The lesions fade after some 3–5 days and complications are extremely rare.

88. Paramyxovirus infections

89. Paramyxovirus infections Paramyxoviruses include the mumps virus and the morbillivirus that causes measles.

90. Mumps B ilateral swelling of the parotid glands The salivary gland ducts usually appear red and inflamed and patients occasionally report a dry mouth . Trismus may be present and the glands are extremely painful and tender to touch . Complications: Pancreatitis Encephalitis Orchitis Oophoritis Deafness Management: Symptomatic

91. Measles Measles usually presents as a systemic, febrile illness with an initial nasal discharge , (catarrhal stage). Koplik's spots are bluish-white, pinpoint spots, with dark-red aveolae , that appear on the buccal mucosae and disappear after 3–4 days. A maculopapular skin rash then appears but resolves after a few days—disappearance of the rash heralds recovery.

92. Measles Complications: Encephalitis Pneumonia Secondary Otitis Management: Symptomatic with general supportive measures.

93. Human papillomavirus infections cause warty lesions on the skin and mucous membranes

94. Human papillomavirus infections The common wart ( verruca vulgaris ) is commonly seen on the skin and oral mucosa, where it is indistinguishable from a squamous cell papilloma. The clinical presentation is of a ‘ cauliflowerlike ’ lesion. Intraoral lesions or those affecting the lips are often the result of autoinoculation by chewing warts on the hands. Heck'sdisease is a rare oral manifestation of HPV infection in the mouth

95. Human immunodeficiency virus and AIDS

96. Human immunodeficiency virus and AIDS The human immunodeficiency virus (HIV) is a retrovirus responsible for the acquired immune deficiency syndrome (AIDS ). Transmission Transmission of the virus is currently thought to be predominantly via blood and blood products and semen. Perinatal and postnatal transmission occur in about 20 per cent of infants born to infected mothers.

97. Human immunodeficiency virus and AIDS The most significant effect of the virus is in the infection and consequent inactivation of CD4-expressing cells, that is, the helper and delayed-type hypersensitivity T cells. Infection with the virus is a slow process, but eventually the host's immune system is functionally disabled.

98. Human immunodeficiency virus and AIDS Management: A ntiretroviral therapy and the treatment of opportunistic Infections and malignancies associated with AIDS. Azidothymidine (AZT ).

99. Human immunodeficiency virus and AIDS ORAL CANDIDOSIS IN HIV INFECTION Erythematous candidosis commonly occurs in HIV infected individuals and affects the hard and soft palate, tongue, and buccal mucosae. Pseudomembranous candidosis is frequently chronic and angular cheilitis may also be present.

100. Human immunodeficiency virus and AIDS HAIRY LEUKOPLAKIA AND HIV INFECTION It occurs on the lateral margins of the tongue and has a folded, corrugated, or ‘hairy’ appearance and generally is asymptomatic. PERIODONTAL DISEASE IN HIV INFECTION Three periodontal manifestations of HIV have been described: A linear gingival erythema that appears as a red band on the marginal gingiva and is not particularly associated with poor oral hygiene; A necrotizing ulcerative gingivitis , associated with pain and spontaneous bleeding; and A necrotizing ulcerative periodontitis that is destructive and rapidly progressive.

101. Human immunodeficiency virus and AIDS KAPOSI'S SARCOMA The mouth and, in particular, the mucosa of the hard palate is a common site for this lesion. The lesion is described as a pigmented, nonpainful , slightly nodular lesion of the mucosa with a characteristic histological appearance . Homosexual men are considered to be more at risk from Kaposi's sarcoma than other groups with HIV infection. The herpes virus 8 (HHV-8 ) is now considered to have a role in the aetiology of this sarcoma. LYMPHOMA S welling or ulcerative lesion in the mouth Swelling of the salivary glands, xerostomia and melanotic pigmentation has also been associated with HIV infection.

102. References Tyldesley’s Oral Medicine https:// www.crossstreetmedical.com.sg https:// www.drelist.com https://www.healthexpress.co.uk / https://www.dovemed.com / https://www.news-medical.net/