RED LESIONS

RED LESIONS OF ORAL MUCOSA

1. RED LESIONS OF ORAL MUCOSA SOWMIYA L I MDS

2. Red lesions are a large, heterogeneous group of disorders of the oral mucosa. Traumatic lesions, infections, developmental anomalies, allergic reactions, immunologically mediated diseases, premalignant lesions, malignant neoplasm, and systemic diseases are included in this group.

3. The red color of the lesions may be due to thin epithelium, inflammation, dilatation of blood vessels or increased numbers of blood vessels, extravasation of blood into the oral soft tissues.

4. CLASSIFICATION

5. SOLITARY RED LESIONS TRAUMATIC ERYTHEMATOUS MACULES AND EROSIONS PURPURIC MACULES INFLAMMATORY HYPERPLASIA REDDISH ULCERS NON PYOGENIC SOFT TISSUE ODONTOGENIC INFECTION CHEMICAL OR THERMAL ERYTHEMATOUS MACULE NICOTINE STOMATITIS

6. ERYTHROPLAKIA, CARCINOMA IN SITU, SQUAMOUS CELL CARCINOMA CANDIDIASIS MACULAR HEMANGIOMA AND TELANGIECTASIA ALLERGIC MACULES HERALD LESION OF GENERALISED STOMATITIS OR VESICULOBULLOUS DISEASE METASTATIC TUMORS KAPOSI S SARCOMA

7. GENERALISED RED CONDITIONS & MULTIPLE ULCERS RECURRENT APHTHOUS STOMATITIS PRIMARY HERPETIC GINGIVOSTOMATITIS EROSIVE LICHEN PLANUS LICHENOID DRUG REACTION ERYTHEMA MULTIFORME ACUTE ATROPHIC CANDIDIASIS BENIGN MUCOUS MEMBRANE PEMPHIGOID PEMPHIGUS CHRONIC ULCERATIVE STOMATITIS

8. DESQUAMATIVE GINGIVITIS RADIATION AND CHEMOTHERAPY MUCOSITIDES XEROSTOMIA PLASMA CELL GINGIVITIS STOMATITIS AREATA MIGRANS ALLERGIES POLYCYTHEMIA LUPUS ERYTHEMATOSUS

9. RED CONDITIONS OF THE TONGUE MIGRATORY GLOSSITIS MEDIAN RHOMBOID GLOSSITIS DEFICIENCY STATES XEROSTOMIA

10. LOCALISED INFLAMMATORY LESIONS

11. ERYTHEMATOUS CANDIDIASIS Erythematous candidiasis is a relatively common form of candidiasis , with a high incidence in HIV-infected patients and rarely in patients receiving broad-spectrum antibiotics or steroids. It may be acute or chronic.

12. Etiology : Smoking , treatment with broad spectrum antibiotics , steroids Also known as antibiotic sore mouth, Atrophic oral candidiasis .

13. Clinical features : Clinically, it is characterized by erythematous patches or large areas, usually located on the dorsum of the tongue and palate. Not just reflect atrophy but increased vascularization Diffuse borders distinguish it from erythroplakia Palate and dorsum of tongue are the sites commonly affected. Burning sensation is a common symptom.

14. LAB DIAGNOSIS PAS staining – smear Swab culture Imprint culture technique Impression culture Salivary culture techniques Histopathologic examination

15. MANAGEMENT Identify the predisposing factor and eliminate it Proper denture hygiene Antifungals , topical and systemic Surgical excision of the lesion

16. ERYTHEMATOUS CANDIDIASIS

17. DEEP MYCOSIS Rare in the developed countries, except in HIV disease and other immunocompromised persons Histoplasmosis Cryptococcosis Blastomycosis Paracoccidiomycosis

18. HISTOPLASMOSIS

19. CRYPTOCOCCOSIS

20. BLASTOMYCOSIS

21. PARACOCCIDIOMYCOSIS

22. LICHEN PLANUS Etiology : The etiology of OLP is not known. Autoreactive T lymphocytes Stress Association of OLP with hepatitis C virus

23. LICHEN PLANUS Erythematous (atrophic) OLP is characterized by a homogeneous red area. Present in the buccal mucosa or in the palate, striae are frequently seen in the periphery. Some patients may display erythematous OLP exclusively affecting attached gingiva . This form of lesion may occur without any papules or striae and presents as desquamative gingivitis. Therefore, erythematous OLP requires a histopathologic examination in order to arrive at a correct diagnosis.

24. Erythematous OLP of the gingiva exhibits a similar clinical presentation as mucous membrane pemphigoid . In pemphigoid lesions, the epithelium is easily detached from the connective tissue by a probe or a gentle searing force ( Nikolsky’s phenomenon). A biopsy for routine histology and direct immunofluorescence are required for an accurate differential diagnosis.

25. Ulcerating conditions such as erythema multiforme and adverse reactions to nonsteroidal antiinflammatory drugs (NSAIDs) may be difficult to distinguish from ulcerative OLP. The former lesions, however, do not typically appear with reticular or papular elements in the periphery of the ulcerations.

26. HISTOPATHOLOGIC FEATURES A saw-toothed appearance to the rete pegs, “liquefaction degeneration,” or necrosis of the basal cell layer; an eosinophilic band may be seen just beneath the basement membrane and represent fibrin covering the lamina propria . A dense subepithelial band–shaped infiltrate of lymphocytes and macrophages is also characteristic of the disease.

27. Basal cell degeneration Lymphotic infiltration

28. MANAGEMENT sub- and supragingival plaque and calculus removal steroid gels in prefabricated plastic trays may be used for 30 minutes at each application to increase the concentration of steroids in the gingival tissue.

29. REITER S DISEASE Reiter s syndrome - Arthritis , urethritis , mucocutaneous lesions and conjunctivitis Unknown etiology Clinical features Prevalent among adult men, between 20-30 yrs of age Urethritis may be the first sign of disease Arthritis is often bilateral and polyarticular Conjunctivitis is often mild

30. ORAL MANIFESTATIONS Painless, red, slightly elevated areas with a white circinate border on the buccal mucosa, lips and gingiva mistaken for aphthous ulcers Palatal lesions appear as small bright red purpuric spots while lesions on the palate resemble geographic tongue

31. HISTOLOGIC FEATURES Parakeratosis , acanthosis , neutrophil infiltration of the epithelium occur Sometimes microabscess formation similar to psoriasis occurs Treatment : disease undergoes spontaneous regression , antibiotics and corticosteroids are used.

32. REITER S DISEASE

33. GRAFT VERSUS HOST DISEASE The major cause of GVHD is allogeneic hematopoietic cell transplantation, also an autologous transplantation may entail GVHD. In GVHD, it is the transplanted immunocompetent tissue that attempts to reject the tissue of the host. Recognition of alloantigens by donor T lymphocytes Interaction between the recipient’s APCs and the donor’s T lymphocytes

34. Affects the entire GI system, including mouth and skin and the liver. Oral lichenoid reactions as part of GVHD may be seen both in acute and chronic GVHD. The clinical lichenoid reaction patterns are indistinguishable from what is seen in patients with OLP, that is, reticulum, erythema , and ulcerations, but lichenoid reactions associated with GVHD are typically associated with a more widespread involvement of the oral mucosa

35. The skin lesions often present with pruritic maculopapular and mobilliform rash, primarily affecting the palms and soles. Violaceous scaly papules and plaques may progress to a generalized erythroderma , bulla formation, and, in severe cases, a toxic epidermal necrolysis –like epidermal desquamation.

36. Diagnosis The presence of systemic GVHD facilitates the diagnosis of oral mucosal changes of chronic oral GVHD. In some instances, oral mucosa be the primary or even the only site of chronic GVHD involvement. It is not possible to distinguish between OLP and oral GVHD based on clinical and histopathologic features.

37. GVHD of tongue

38. BARTONELLA INFECTION Bacillary angiomatosis (BA) , also called epithelioid angiomatosis , is a disease characterized by unique vascular lesions caused by infection with small, gram-negative organisms of the genus  Bartonella . Virtually all patients with this disease are infected with HIV. BA occurs most frequently in the later stages of HIV infection.

39. Cutaneous BA is characterised by the presence of lesions on or under the skin. papules or nodules which are red, globular and non-blanching, with a vascular appearance a purplish lichenoid plaque a subcutaneous nodule which may have ulceration, similar to a bacterial abscess.

40. While cutaneous BA is the most common form of BA, BA can also affect several other parts of the body, such as the brain, bone, bone marrow, lymph nodes, gastrointestinal tract, respiratory tract, spleen and liver. Symptoms vary depending on which parts of the body is affected.

41. The best method for diagnosis of cutaneous BA remains biopsy with histopathologic study. Tissue specimens reveal a characteristic vascular proliferation on routine hematoxylin & eosin staining, in addition to numerous bacilli demonstrable by modified silver staining or electron microscopy.

42. These organisms are not visualized following staining for fungi or acid-fast mycobacteria ; staining with Brown- Brenn tissue Gram's stain is also negative, which distinguishes the  Bartonella  bacilli from most other small, gram-negative rods.

43. BACILLARY ANGIOMATOSIS

44. REACTIVE LESIONS

45. PYOGENIC GRANULOMA RESPONSE OF THE TISSUE TO NONSPECIFIC INFECTION It is a tumor like growth that is considered an exaggerated conditioned response to minor trauma Also called pregnancy tumor Etiology : calculus, food materials, and overhanging dental restoration margins

46. The prevalence of pregnancy epulides increases toward the end of pregnancy (when levels of circulating estrogens are highest), and they tend to shrink after delivery (when there is a precipitous drop in circulating estrogens). This suggests that hormones play a role in the etiology of the lesion, secondary to an increase in angiogenic factor expression and a reduction in the apoptosis of granulation tissue.

47. Both pyogenic granulomas and pregnancy epulides may mature and become less vascular and more collagenous , gradually converting to fibrous epulides .

48. They are composed of proliferating endothelial tissue, much of which is canalized into a rich vascular network with minimal collagenous support. Neutrophils , as well as chronic inflammatory cells, are consistently present throughout the edematous stroma , with microabscess formation. Histologically , differentiation from a hemangioma is important.

49. MANAGEMENT The existence of these lesions indicates the need for a periodontal consultation, and treatment should include the elimination of subgingival irritants and gingival pockets throughout the mouth, as well as excision of the gingival growth.

50. PYOGENIC GRANULOMA

51. PERIPHERAL GIANT CELL GRANULOMA Peripheral giant cell granuloma or the so-called “giant cell epulis ” is the most common oral giant cell lesion. It normally presents as a soft tissue purplish-red nodule consisting of multinucleated giant cells in a background of mononuclear stromal cells and extravasated red blood cells. This lesion probably does not represent a true neoplasm, but rather may be reactive in nature, believed to be stimulated by local irritation or trauma, but the cause is not certainly known.

52. ETIOLOGY : local irritation due to plaque or calculus, poor dental restorations, ill fitting dentures, dental extractions CLINICAL FEATURES : common in females Asymptomatic, rapid growth rate , occurs on gingiva or alveolar process frequently anterior to molars. It can be sessile or pedunculated Dark red, vascular in appearance commonly exhibits surface ulceration.

53. HISTOLOGIC FEATURES Non encapsulated mass of tissue composed of a delicate reticular and fibrillar connective tissue stroma containing ovoid or spindle shaped young connective tissue cella and multi nucleated giant cells. Capillaries are numerous around the periphery of the lesion Foci of hemorrhage with liberation of hemosiderin pigment Spicules of newly formed osteoid or bone are often found scattered through out the vascular and cellular fibrous lesion.

54. Peripheral cuffing of bone

55. MANAGEMENT Conservative excision Recurrence rate is 10-15%

56. ATROPHIC

57. GEOGRAPHIC TONGUE Geographic tongue, also known as erythema migrans ,ectopic geographic tongue or erythema circinata migrans , benign migratory glossitis , is a common benign hereditary disorder of unknown etiology that primarily affects the dorsal surface of the tongue. clinical features : Rarely, other areas of the mucosa are also affected.

58. Clinically it is often asymptomatic , patients may complain of smarting sensation, tenderness or a burning sensation, particularly upon eating sour food. It manifests as circumferentially migrating and leaves an erythematous area behind, scattered, flat, irregular red lesions that are often surrounded by a grey-yellowish ( keratotic ) ring. Sometimes, it occurs in individuals with psoriasis.

59. Red areas extend, heal and are then replaced by new lesions in other areas. Geographic tongue sometimes affects patients with fissured tongue (lingua plicata ).  Diagnosis/ Histopathological features : In the peripheral region of erythema migrans , characteristic histopathological features are: hyperkeratosis, acanthosis and elongation of the epithelial rete ridges.

60. In the red portion of the lesion, localised loss of filiform papillae is seen with epithelial atrophy and mild subepithelial T lymphocyte infiltration. In addition, the epithelial surface is frequently necrotic, and collections of neutrophils with formation of microabscesses are observed within the epithelium. Because these features are reminiscent of psoriasis, this is called a  psoriasiform mucositis .

61. Differential diagnosis : The histopathological appearance of mucosal lesions in psoriasis pustulosa generalisata  and Reiter's syndrome cannot be distinguished from erythema migrans . It may also be mistaken for lichen planus .

62. GEOGRAPHIC TONGUE

63. LUPUS ERYTHEMATOSUS Definition :  Lupus erythematosus is a chronic immunologically mediated disease. Etiology  : Autoimmune. the main feature is the formation of antibodies to DNA, which may initiate immune complex reactions, in particular a vasculitis . Clinical features  : Two main forms of the disease are recognized: discoid (DLE) and systemic (SLE). Oral lesions develop in 15–25% of cases in DLE and in 30–45% of cases in SLE, usually in association with skin lesions.

64. Three subtypes of lupus-specific skin lesions have been described: acute, subacute , and chronic. Acute cutaneous lupus occurs in 30 to 50% of patients and is classically represented by the butterfly rash–mask-shaped erythematous eruption involving the malar areas and bridge of the nose but typically (as opposed to dermatomyositis [DM]) sparing nasolabial folds. Bullous lupus and localized erythematous papules also belong to the acute lupus category.

65. Subacute lupus – cutaneous , non indurated psoriasiform annulay polycyclic lesions that resolve without scaring , although occasionally with post inflammatory dyspigmentation Chronic cutaneous lupus – classic discoid rash localised or generalised , hypertrophic lupus in verrucous form, mucosal lupus, lichen planus overlap

66. The oral lesions are characterized by a well-defined central   atrophic red area surrounded by a sharp elevated border of irradiating   whitish striae , brush border appearance. Telangiectasia , petechiae , edema, erosions, ulcerations,   and white hyperkeratotic plaques may be seen. Buccal mucosa, gingiva , and labial mucosa are the most commonly affected intraoral sites. Isolated erythematous areas are also common, especially on the palate.

67. Differential diagnosis  : Lichen planus , geographic glossitis , speckled leukoplakia , erythroplakia , cicatricial pemphigoid , syphilis. Treatment  : Steroids, Nonsteroidal anti-inflammatory drugs ( nsaids ) are frequently used in SLE for symptomatic relief of arthritis but are of little benefit in more severe disease. Cyclosporine, tacrolimus , sirolimus , methotrexate , and intravenous immunoglobulins have also been used in SLE. Antimalarials , such as hydroxychloroquine , are effective in cutaneous lupus with fewer adverse effects.

68. ERYTHROPLAKIA Definition :  Erythroplakia , or Queyrat erythroplasia , is a premalignant lesion that rarely occurs on the oral mucosa. It is defined as a red patch or plaque that cannot be classified clinically or pathologically under any other condition. Etiology : Unknown ( smoking and alcohol abuse are important risk factors )

69. Clinical features  : It appears as a usually asymptomatic, fiery red, well demarcated plaque, with a smooth and velvety surface. The red lesions may be associated with white spots or small plaques. The floor of the mouth, retromolar area, soft palate, and tongue are the most common sites of involvement.

70. Homogeneous erythroplakia Erythroplakia interspersed with patches of leukoplakia Granular or speckled erythroplakia Erythroplakia occurs more frequently between the ages of 50 and 70 years. Over 91% of erythroplakia s histologically demonstrate severe dysplasia, carcinoma in situ, or early invasive squamous -cell carcinoma at the time of diagnosis.

71. Laboratory tests :   Histopathological examination. Differential diagnosis :   Erythematous candidiasis , lichen planus , early squamous -cell carcinoma, local irritation. Treatment  : cold knife Surgical excision laser surgery.

72. ERYTHROPLAKIA – SPECKLED

73. THERMAL BURN Definition and etiology  : Thermal burns to the oral mucosa are fairly common, usually due to contact with very hot foods, liquids, or hot metal objects. Clinical features :  Clinically, the condition appears as a red, painful erythema that may undergo desquamation, leaving erosions.

74. The lesions heal spontaneously in about a week. The diagnosis is made exclusively on clinical grounds. Differential diagnosis   : Chemical burn, traumatic lesions, herpes simplex, aphthous ulcers, drug reactions. Treatment :  No treatment is required.

75. DRUGS AND CHEMICAL BURN Aspirin tablets/powder Tooth ache drops containing creosote, guaiacol , phenol derivatives Dental medicaments such as chromic acid, trichloroacetic acid, silver nitrate, beechwood creosote, eugenol , paraformaldehyde , ticture of iodine

76. DRUGS Erythema multiforme – antibiotics like sulfonamides, tetracyclines , amoxicillin, ampicillin . Anticonvulsants – phenytoin , barbiturates Stevenson johnson syndrome – acetaminophen and NSAID s

77. THERMAL BURN

78. AVITAMINOSIS B12 Avitaminosis  is any disease caused by chronic or long-term vitamin deficiency or caused by a defect in metabolic conversion, such as tryptophan to niacin. They are designated by the same letter as the vitamin Avitaminosis B12 causes pernicious anemia

79. The clinical symptoms are weakness, fatigue, shortness of breath and neurologic abnormalities. The presence of oral signs and symptoms, include glossitis , angular cheilitis , recurrent oral ulcer, oral candidiasis , diffuse erythematous mucositis and pale oral mucosa. Management is through vitamin supplements

80. VITAMIN B COMPLEX Vitamin B 1  (thiamine) Vitamin B 2  (riboflavin) Vitamin B 3  (niacin or nicotinic acid) Vitamin B 5  ( Pantothenic acid) Vitamin B 6  (pyridoxine,  pyridoxal ,  pyridoxamine ) Vitamin B 7  (biotin) Vitamin B 9  (folic acid) Vitamin B 12  (various  cobalamins ; commonly  cyanocobalamin  or  methylcobalamin  in vitamin supplements)

81. VITAMIN B12 DEFICIENCY

82. Session 2

83. PURPURA Purpura  is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin usually secondary to  vasculitis .  They measure 0.3–1 cm (3–10 mm), whereas  petechiae  measure less than 3 mm, and  ecchymoses  greater than 1 cm

84. Purpura are a common and nonspecific medical sign. Platelet disorders (thrombocytopenic purpura ) Primary thrombocytopenic purpura Secondary thrombocytopenic purpura Post-transfusion purpura Vascular disorders ( nonthrombocytopenic purpura ) Microvascular injury, as seen in senile (old age) purpura , when blood vessels are more easily damaged

85. Hypertensive states Deficient vascular support Vasculitis , as in the case of  Henoch-Schönlein purpura Coagulation disorders - Disseminated intravascular coagulation (DIC) Scurvy (vitamin C deficiency) - defect in collagen synthesis which results in weakened capillary walls and cells

86. PURPURA

87. IDIOPATHIC THROMBOCYTOPENIC PURPURA Definition  Thrombocytopenic purpura is a hematological disorder characterized by a decrease in platelets in the peripheral blood. Etiology  Presumably a nonspecific viral infection, myelotoxic agents.

88. Clinical features  The oral manifestations consist of red lesions in the form of petechiae , ecchymoses , or even hematomas, usually located on the palate and buccal mucosa. Spontaneous gingival bleeding is a constant early finding. Purpuric skin rash, epistaxis , and bleeding from the gastrointestinal and urinary tract are common.

89. Laboratory tests  Peripheral platelet count, bone-marrow aspiration, bleeding and clotting times. Differential diagnosis   Aplastic anemia, leukemias , polycythemia vera , agranulocytosis , drug reactions. Treatment  Steroids, platelet transfusions, cessation of drug treatment if it is drug-related.

90. VASCULAR

91. TELANGECTASIA Persistent dilatation of small, superficial blood vessels; rarely inherited They are red seldom over 5mm in diameter and blanch readily on digital pressure, which easily differentiates them from red petechiae . They may occur as red solitary lesions or multiple lesions.

92. The uncommon Osler-Weber- Rendu syndrome (hereditary haemorrhagic teleangiectasia ; HHT) is inherited via an autosomal dominant trait, however, family history can be negative. Clinically, oral and peri -oral telangiectasias are observed, as well as telangiectasias in the nose, the gastro-intestinal tract and on the palms of the hands. They may bleed which may cause chronic iron-deficiency anaemia .

93. OSLER WEBER RENDU SYNDROME

94. SCLERODERMA Scleroderma is a rare autoimmune disorder of blood vessels and connective tissue, which is divided into a progressive systemic and a localised form (circumscribed scleroderma). The disease most commonly affects adult middle-aged females. In later stages, development of a mask-like face with restricted mouth opening ( microstomia ), telangiectasias , smooth tongue surface and shortened lingual frenum .

95. SCLERODERMA

96. CREST SYNDROME A relatively mild variant is characterised by subcutaneous calcification (CREST syndrome: calcinosis cutis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly and telangiectasia ); frequent association with Sjögren's syndrome.

97. CREST SYNDROME

98. Differential diagnosis Oral lesions in Osler-Weber- Rendu syndrome: scleroderma, chronic liver diseases, post-irradiation state Oral lesions in scleroderma: Osler-Weber- Rendu syndrome, oral submucous fibrosis, secondary Sjögren's syndrome

99. Treatment and prognosis Osler-Weber- Rendu syndrome: local haemostasis ( cryo -surgery or laser), treatment of anaemia .  Scleroderma: management is difficult; enhancement of micro-circulation , corticosteroids, in some cases immunosuppressants . Prognosis is dependent on type of disease; from favourable to poor and lethal.

100. ANGIOMA Developmental vascular malformation ( hamartoma ) or benign vascular tumour . Two types - cavernous and capillary types. In the oral cavity, the most common mesenchymal tumour of infancy. Commonest localisation : tongue, lips, buccal mucosa.

101. Capillary hemangiomas are further classified into juvenile , senile , nevus flammeus Juvenile hemangioma Most common type of capillary hemangioma Majority occur in head and neck region shortly after birth Period of rapid growth then begin to regress after about a year Fully developed hemangioma is elevated, lobulated , sharply circumscribed, and bright red They require no treatment.

102. STRAWBERRY HEMANGIOMA

103. Senile hemangioma Start appearing in early adulthood, and the number of lesion increases with age. The lesions are bright red and vary in dia from 1mm to several mm s. The larger lesions are soft and dome shaped.

104. CHERRY HEMANGIOMA

105. Nevus flammeus Also known as port wine stains, are present at birth are unilateral and located on face and neck Sharply circumscribed and range from small red macules to large red flat patches that are blanched by pressure. Haemangiomatous vascular malformation of the face related to maxillary division of the trigeminal nerve (port wine stain) and involvement of the leptomeninges occur in  Sturge -Weber syndrome

106. Complications: epilepsy, contralateral hemiplegia (rare), mental retardation (common). 

107. ANGIOMAS Angiomatous syndromes Osler- Weber- Rendu syndrome (hereditary hemorrhagic telangiectasia ) blue rubber bleb nevus syndrome Bannayan - Zonana Sturge -Weber Klippel-Trénaunay syndrome Servelle-Martorell syndrome von Hippel-Lindau syndrome Maffucci’s syndrome

108. HEMANGIOMA

109. CAVERNOUS HEMANGIOMA

110. ANGIOKERATOMA FABRY S DIASEASE Angiokeratoma  is a benign  cutaneous  lesion of capillaries, resulting in small marks of red to blue color and characterized by hyperkeratosis. Angiokeratoma corporis diffusum  refers to  Fabry's disease is a rare genetic  lysosomal storage disease, inherited in an X-linked manner. Fabry disease can cause a wide range of systemic symptoms. It is a form of  sphingolipidosis , as it involves dysfunctional metabolism of sphingolipids .

111. Clinical features – dermatological manifeatations – Angiokeratomas occur commonly on the thighs, lower abdomen, and groin) Anhidrosis  (lack of sweating) is a common symptom, and less commonly  hyperhidrosis  (excessive sweating). Ocular involvement may be present showing cornea verticillata  (also known as vortex keratopathy ), i.e. clouding of the corneas. This clouding does not affect vision.

112. HISTOPATHOLOGY Angiokeratomas characteristically have large dilated blood vessels in the superficial dermis and hyperkeratosis (overlying the dilated vessels).

113. NEOPLASMS

114. SQUAMOUS CARCINOMA The early stage of squamous -cell carcinoma may present as an asymptomatic, atypical red patch. The clinical features are identical to erythroplakia , erythematous candidiasis , or contact reactions to dental materials. In these cases, a biopsy should be taken to allow a conclusive diagnosis.

115. KAPOSIS SARCOMA Malignant neoplasm composed of spindle cells and vascular elements Occurs in homosexual men affected with AIDS commonly Classic , Endemic and epidemic types Classic or sporadic type – commonly occurs in older persons of jewish origin, involves the skin of lower extremities Oral mucosal involvement is rare in this

116. Endemic form – occurs in native black population Epidemic form affects those with HIV and other immunological disorder Lesions widely distributed over the skin Mucosa and lymph nodes are involved and response to treatment is poor

117. KS can involve any oral site but most frequently involves the attached mucosa of the palate, gingiva , and dorsum of the tongue. Lesions begin as blue purple or red purple flat discolorations that can progress to tissue masses that may ulcerate. The lesions do not blanch with pressure. Initial lesions are asymptomatic but can cause discomfort and interfere with speech, denture use, and eating when lesions progress.

118. The differential diagnosis includes ecchymosis , vascular lesions, and salivary gland tumors. Definitive diagnosis requires biopsy. Because KS is a multicentric neoplastic disease, multiple sites of involvement can occur, including skin, lymph nodes, gastrointestinal tract, and other organ systems.

119. TREATMENT Surgical excision, electrocautery and radiation therapy. Patients with disseminated disease may be treated with immunomodulators and single agent or combination chemotherapy.

120. WEGENER S GRANULOMATOSIS Granulomatosis with polyangiitis  (GPA), formerly referred to as Wegener's granulomatosis  (WG), is a systemic disorder that involves both granulomatosis  and  polyangiitis . It is a form of  vasculitis  (inflammation of blood vessels) that affects small- and medium-size vessels in many organs Oral cavity: strawberry gingivitis, underlying bone destruction with loosening of teeth, non-specific ulcerations throughout oral mucosa

121. MIDLINE LETHAL GRANULOMA Lethal midline granuloma  is a condition affecting the nose and palate. Macroscopically the lesions usually look like necrotic granulomas and are characterized by ulceration and destruction of the nose and paranasal sinuses with erosion of soft tissues, bone and cartilage of the region.

122. The patients show an aggressive and lethal course with rapid destruction of the nose and face (midline), therefore the term “lethal midline granuloma ”. This disease occurs around the fourth decade and occurs commonly in males.

123. The major symptoms are nasal stuffiness with or without nasal discharge. Oral or nasal ulcer with conjunctivitis may also occur. Perforation of the nasal septum with mutilation of the surrounding tissues eventually occurs. Morphologically it is characterized by extensive ulceration of mucosal sites with a lymphomatous infiltrate that is diffuse, but has an angiocentric and angiodestructive growth pattern.

124. GENERALISED

125. DENTURE STOMATITIS Definition   : Denture stomatitis , or denture sore mouth, is a frequent condition in patients who wear dentures continuously for extended times. Etiology :  Mechanical irritation from dentures, Candida albicans , or a tissue response to microorganisms living beneath the dentures. Also caused by bacteria such as streptococcus, veillonella , lactobacillus, prevotella and actinomyces .

126. Clinical features  : The condition is characterized by diffuse erythema , edema, and sometimes petechiae and white spots that represent accumulations of candidal hyphae , almost always located in the denture bearing area of the maxilla. The condition is usually asymptomatic. The diagnosis is based on clinical criteria. Type I – localised to minor erythematous areas caused by trauma from denture

127. Type II – affects major part of denture covered mucosa Type III – granular mucosa in the central part of the palate Differential diagnosis  : Allergic contact stomatitis due to acrylic. Treatment :  Improvement of denture fit, proper oral hygiene, and topical antimycotics .

128. DENTURE STOMATITIS

129. MEDIAN RHOMBOID GLOSSITIS Definition  : Median rhomboid glossitis is a rare condition that occurs exclusively on the dorsum of the tongue. Etiology : Presumably developmental, Candida albicans , bacteria may also be involved. Clinical features  : It presents as a well-demarcated erythematous rhomboid area,

130. along the midline of the dorsum of the tongue, immediately anterior to the circumvallate papillae.   The surface of the lesion may be smooth or lobulated . Atrophy of filiform papillae. Differential diagnosis :   Candidiasis , lymphangioma , geographic tongue, syphilis, hemangioma . Treatment :  No treatment is required.

131. KISSING LESIONS A concurrent erythematous lesion may be observed in the palatal mucosa and it is called kissing lesion. Management is restricted to a reduction in predisposing factors.

132. KISSING LESION ON THE PALATE

133. MEDIAN RHOMBOID GLOSSITIS

134. RADIATION MUCOSITIS Definition and etiology  : Oral radiation mucositis is a side effect of radiation treatment of head and neck tumors. Clinical features :  The oral lesions are classified as early and late. Early reactions may begin at the end of the first week of radiotherapy, and consist of erythema and edema of the oral mucosa.

135. Soon after, erosions or ulcers may develop, covered by a whitish-yellow exudate . Xerostomia , loss of taste, and burning and pain during mastication, swallowing, and speech are common. The diagnosis is made clinically.

136. Differential diagnosis :   Mucositis due to chemotherapy, graft- versushost disease, erythema multiforme , herpetic stomatitis , lichen planus . Treatment  : Supportive treatment. Cessation of the radiation treatment, B-complex vitamins, and sometimes low doses of steroids are indicated.

137. RADIATION MUCOSITIS

138. POLYCYTHEMIA Also called erythremia is chronic and sustained elevation in the number of erythrocytes and level of hemoglobin. Primary secondary

139. Primary – polycythemia vera is a neoplastic condition of erythropoietic sysyem Secondary – is a sustained elevation of erythrocytes and hemoglobin usually resulting from bone marrow stimulation caused by living at high altitude or chronic pulmonary disease such as emphysema

140. The entire oral mucosa of patients with polycythemia has a deep red or purple color. Soft palate and gingiva are prone to easy bleeding and petechial hemorrhages may be seen on the palate and labial mucosa Infarcts may occur in the smaller blood vessel leading to ulcers

141. DIAGNOSIS Increase in erythrocytes Hemoglobin concentration hematocrit

142. PLASMA CELL GINGIVITIS Definition : Plasma-cell gingivitis is a rare and unique gingival disorder, characterized histopathologically by a dense chronic inflammatory infiltration of the lamina propria , mainly of plasma cells. Etiology :  Unknown. Reactions to local allergens, chronic infections, and plasma-cell dyscrasias have been considered as possible causes.

143. Clinical features :  Clinically, both free and attached gingiva are bright red and edematous, with a loss of normal stippling. The gingivitis may be localized or widespread, and is frequently accompanied by a burning sensation. Rarely, similar lesions may be seen on the tongue and lips. Ulcers , epithelial sloughing and desquamation may be present. Patient may complain of pain, sensitivity and bleeding of gingiva during brushing.

144. Laboratory tests  : patch testing to identify the allergen, Histopathological and histochemical examination, immunofluorescence . Histopathology : parakeratosis , epithelial hyperplasia , dense infiltrate of plasma cells in the lamina propria , dilated blood capillaries. Differential diagnosis  : Desquamative gingivitis, erosive lichen planus , vesiculobullous disorders.

145. Pubertal or pregnancy induced gingivitis, plaque associated gingivitis. Rapid onset - PCS. Treatment  : Remove the allergen if possible. Pain control, Topical or systemic steroids. Gingivectomies to recontour lesions that are long standing and fibrotic.

146. PLASMA CELL GINGIVITIS

147. PEMPHIGUS

148. PEMPHIGOID

149. ERYTHEMA MULTIFORME EM is an acute, self-limited, inflammatory mucocutaneous disease that manifests on the skin and often oral mucosa, although other mucosal surfaces, such as the genitalia, may also be involved.

150. EM is classified as E M minor if there is less than 10% of skin involvement and there is minimal to no mucous membrane involvement, whereas EM major has more extensive but still characteristic skin involvement, with the oral mucosa and other mucous membranes affected. Historically, fulminant forms of EM were labeled Stevens- Johnson syndrome (SJS) and toxic epidermal necrolysis [TEN (Lyell disease)].

151. ETIOLOGY EM is a hypersensitivity reaction, and the most common inciting factors are infection, particularly with HSV, or drug reactions to NSAIDS or anticonvulsants. Other viral, bacterial, fungal, and protozoal infections and medications may also play a role.

152. CLINICAL FEATURES EM generally affects those between ages 20 and 40 years, with 20% occurring in children. There is often a prodrome of fever, malaise, headache, sore throat, rhinorrhea , and cough. Skin lesions begin as red macules that become papular , starting primarily in the hands and moving centripetally toward the trunk in a symmetric distribution. The most common sites of involvement are the upper extremities, face, and neck.

153. The skin lesions may take several forms—hence the term multiforme - irregular bullae , erosions, or ulcers surrounded by extensive areas of inflammation, Severe crusting and bleeding of the lips are common. The classic skin lesion consists of a central blister or necrosis with concentric rings of variable color around it called typical “target” or “iris” lesion that is pathognomonic of EM; variants are called “atypical target” lesions .

154. ORAL MANIFESTATIONS mild erythema and erosion to painful ulcerations. When severe, ulcers may be large and confluent, causing difficulty in eating, drinking, and swallowing, and patients with severe EM may drool blood-tinged saliva.

155. Differential diagnosis : Primary HSV gingivostomatitis , Autoimmune vesiculobullous disease such as pemphigus and pemphigoid , recurrent aphthous ulcers. Management : systemic or topical analgesics, corticosteroids, antiviral medication, azathioprine and dapsone , antimalarials prevents recurrence.

156. REFERENCES Peripheral giant cell granuloma Padam Narayan Tandon , S. K. Gupta, 1   Durga Shanker Gupta,  Sunit Kumar Jurel, 2  and  Abhishek Saraswat Oral Manifestations of Vitamin B12 Deficiency: A Case Report Hélder Antônio Rebelo Pontes, DDS, MSc , PhD; Nicolau Conte Neto , DDS; Karen Bechara Ferreira, DDS; Felipe Paiva Fonseca; Gizelle Monteiro Vallinoto ; Flávia Sirotheau Corrêa Pontes, DDS, MSc , PhD; Décio dos Santos Pinto Jr , DDS, MSc , PhD

157. Text book of Burket s oral medicine Text book of Differential Diagnosis of oral and maxillofacial lesions by Norman K Wood and Paul W Goaz Shafer s text book of oral pathology