WHO 2017 Classification of tumours of Salivary Glands

General Pathology Multiple choice questions (MCQ)

1. Regarding cell injury and death

a)       Initially there is a reduction in cell size during cell necrosis

b)      Apoptosis is associated with an inflammatory response

c)       Necrosis results from caspases sequestered in mitochondrial membranes

d)      Cellular swelling and fatty change indicate reversible cell injury

2. In which of the following organs is steatosis NOT seen

a)       Heart

b)      Kidney

c)       Lung

d)      Liver

3. Dystrophic calcification can occur in

a)       Coagulative necrosis

b)      Caseous necrosis

c)       Enzyme necrosis of fat

d)      All the above

4. Cholesterol and its esters are

a)       Metabolised in a loosely regulated system within cells

b)      Are seen as xanthomas within monocytes in tendons

c)       Accumulate in macrophages in the gallbladder known as cholesterosis

d)      Are seen in the media propria of the aorta in atherosclerosis

5. Progressive atrophy of the brain in later adult life is thought to be part due to

a)       Decreased workload

b)      Loss of innervation

c)       Diminished blood supply

d)      Loss of endocrine stimulation

6. Inflammation is

a)       Fundamentally a destructive response acutely

b)      Is characterised by exudation of fluid and migration of neutrophils

c)       Results in scarring thru regeneration of native parenchymal cells

d)      Is activated by Toll like receptors on microbes

7. The most common mechanism for the formation of leaky endothelium in inflammation is

a)       Endothelial retraction

b)      Direct endothelial injury

c)       Leukocyte mediated endothelial injury

d)      Endothelial cell contraction

8,Regarding mediators of inflammation

a)       Histamine is a preformed vasoactive mediator causing arteriole vasoconstriction

b)      Histamine is considered to be the principle mediatory of the immediate transient phase of increased vascular permeability

c)       Nitric oxide has dual actions in inflammation, it relaxes vascular smooth muscle and also promotes the cellular response in the inflammatory response

d)      Platelet activating factor is found unique to platelets

9. In leukocyte migration thru blood vessels in inflammation

a)       Extravasation of the leukocyte occurs in the order of: adhesion to the wall, margination and then rolling of the leucocyte across the endothelial wall.

b)      Selectins are the primary molecule who play roles with neutrophil activation

c)       Integrins are  involved in firm adhesion of the leucocyte to the cell wall

d)      Endothelial cells will take 6-12hrs before they express their selctin ( E selectin ) in inflammation

10. Regarding some inflammatory patterns

a)       When mesothelial cells of the peritoneum, pleural and pericardial linings secrete fluid it is usually of a fibrinous nature

b)      A serous exudation consists primarily of neutrophils, liquefactive necrosis and oedematous fluid

c)       When there are large vascular leaks or an associated procoagulant stimulus you commonly see a suppurative exudate

d)      Ulcers can only occur when tissue necrosis and the resultant inflammation is on or near a surface

11.In chronic inflammation, all are true except

a)       It can be caused by prolonged exposure to toxic agents

b)      It involves mononuclear inflammatory cells

c)       It may contribute to the formation of atherosclerosis

d)      It primarily involves tissue destruction

12. The complement system

a)       Most critical step is the proteolysis of the 3^rd component C3 to C3a

b)      Is only involved in innate immunity reactions

c)       Causes decreased vascular permeability, chemotaxsis and opsonization of leukocytes

d)      Is a loosely controlled pathway

13, Regarding wound healing,

a)       The inflammatory response in primary healing is more intense than in secondary healing 

b)      At 1 week , the wound strength is 20% of that of unwounded skin

c)       Wound contraction is due in part to fibroblast contraction

d)      In primary union, collagen fibres appear with granulation tissue

14.The most important cause of delay of healing is

a)       Inadequate blood supply

b)      Infection

c)       Foreign body presence

d)      Poor nutritional state of the patient

15. Regarding the extracellular matrix, which is NOT CORRECT?

a)       Fibronectin in its plasma form is involved in blood clot stabilisation

b)      Laminin is the most abundant glycoprotein in the extracellular matrix

c)       Vit D is required for the hydroxylation of procollagen to collagen

d)      The cross linking of collagen is important in providing tensile strength to a wound

16. The causes of liver steatosis do not include:

a)       Alcohol abuse

b)      Protein malnutrition

c)       XI-antitrypsin deficiency

d)      CCl4

17.Regarding metastatic calcification, which of the following is not a cause?

a)       Renal failure

b)      Paget’s disease

c)       Sarcoidosis

d)      Hypoparathyroidism

18. Depletion of AtP cause all EXCEPT

^a)                 efflux of Ca²⁺

b)      efflux of K

c)       influx of Na⁺

d)      decrease pH cells

19.The most common causes of fatty liver in the developed world  are

a)       Hypercholesterolaemia and lipid storage diseases

b)      Alcohol abuse and hypercholesterolaemia

c)       NAFLD and alcohol abuse

d)      NAFLD and hypercholesterolaemia

20   .Examples of intracellular accumulations of lipid do NOT include

a)       Niemann-Pick disease type C

b)      Atherosclerosis

c)       Xanthomas

d)      Amyloidosis

21. .Regardig white cell extravasation in acute inflammation which of the following pairs are incorrect

a)       P selectin: neutrophil rolling

b)      ICAM: neutrophil rolling

c)       E selectin neutrophil rolling

d)      CD34: neutrophil rolling

22.Which of the following disorders are examples of chronic leukocyte induced injury

a)       Arthritis

b)      Asthma

c)       Atherosclerosis

d)      Septic  shock

23.Leukotrienes does not mediate the following actions

a)       Vasoconstriction

b)      Chemotaxis

c)       Increased vascular permiability

d)      Vasodilatation

24.Which is NOT true regarding blood clot formation?

a)       The clot contains red cells, fibrin, fibronectin and complement

b)      Within 24 hours of injury, macrophages migrate in along the fibrin scaffold

c)       Neutrophils release proteolytic enzymes that clean out debris and bacteria

d)      Platelet adhesion and aggregation, and formation of the clot leads to inflammation

25.          Which of the following is true about formation of granulation tissue:

a)       Granulation tissue forms around day 6 from proliferation of fibroblasts and vascular endothelial cells

b)      Characteristic histological feature is presence of new small blood vessels (angiogenesis) and proliferation of fibroblasts

c)       The new vessels in angiogenesis are tight and restrict passage of plasma proteins.

d)      There is a similar amount of granulation tissue in wounds healing by both primary and secondary intention

26.          The following complications of healing are true, except:

a)       Hypertrophic scars result from accumulation of granulation tissue

b)      Keloid scars grow beyond the boundaries of the original wound and don't regress

c)       Dehiscence, common after abdominal surgery, is due to increased abdominal pressure

d)      Wounds can ulcerate because of inadequate vascularisation

27.          Which is NOT true regarding wound healing?

a)       A scar is composed of fibroblasts, collagen, elastic tissue and other ECM components.    

b)      Wound contraction is important in healing by secondary intention.

c)       The initial matrix of fibrin, fibronectin and type I collagen is ultimately replaced by type III collagen.

d)      The tensile strength after one week in an incisional surgical wound is about 10% of unwounded skin.

28. Which of the following is not an example of peripheral immunologic tolerance?

a)       Anergy

b)      Thymic deletion

c)       Suppression by regulatory T-cells

d)      Antigen sequestration

29. Regarding mitochondrial alterations, which is true?

a)       In cell hypertrophy, there is corresponding increase in mitochondrial size.

b)      Mitochondrial myopathies are associated with increased numbers of morphologically abnormal mitochondria

c)       Oncocytomas are malignant tumours consisting of cells with abundant enlarged mitochondria

d)      Hepatocytes in alcoholic liver disease assume megamitochondria -> extremely large, normally shaped mitochondria (abnormal shapes)

30.Regarding lysosomes which is incorrect?

a)       Primary lysosomes are membrane bound

b)      Contain hydrolytic enzymes

c)       Are synthesised in the smooth endoplasmic reticulum

d)      May persist in the cell as residual bodies

Wait for the answers

Pigmentation and Discoloration of Oral and Facial Tissues

Pigmentation and Discoloration of Oral and Facial Tissues

Pigmentation is a discoloration of the oral mucosa or gingiva due to the wide variety of lesions and conditions. Oral pigmentation has been associated with a variety of endogenous and exogenous etiologic factors. Also it can be explained as Oral mucosal discolouration, which ranges from brown to black may be due to superficial (extrinsic) or deep (intrinsic in or beneath mucosa) causes.

Types of Oro-maxillofacial Pigmentation

Extrinsic discoloration

Extrinsic discoloration is usually caused by extrinsic pigments. It is rarely of consequence and is usually caused by colored foods, drinks or drugs. Extrinsic discoloration usually affects both mucosae and teeth are discolored. Causes include the following:

• Foods and beverages, such as beetroot, red wine, coffee and tea.

• Confectionery, such as liquorice.

• Drugs, such as chlorhexidine, iron salts, griseofulvin, crack cocaine, minocycline, bismuth subsalicylate, lansoprazole and HRT.

• Tobacco: this may cause extrinsic discolouration, but can also cause intrinsic pigmentary incontinence, with pigment cells increasing and appearing in the lamina propria. This is especially likely in persons who smoke with the lighted end of the cigarette within the mouth (reverse smoking), as practiced mainly in some Asian communities. Tobacco is a risk factor for cancer.

• Betel: this may cause a brownish-red discolouration, mainly on the teeth and in the buccal mucosa, with an irregular epithelial surface that has a tendency to desquamate. It is seen mainly in women from South and Southeast Asia. Betel chewer’s mucosa epithelium is often hyperplastic, and brownish amorphous material from the betel quid may be seen on the epithelial surface and intra- and intercellularly, with ballooning of epithelial cells. Betel chewer’s mucosa is not known to be precancerous, but betel use predisposes to submucous fibrosis and to cancer.

Intrinsic staining

Causes for intrinsic hyperpigmentation are Increased melanin or number of melanocytes, or other materials. Intrinsic discolouration may have more significance than the extrinsic type. Normal intrinsic pigmentation is due to melanin, produced by melanocytes dendritic cells prominent in the basal epithelium.

Localized areas of pigmentation are usually caused by benign conditions:

• Embedded amalgam (amalgam tattoo)

• Embedded graphite (graphite tattoo)

• Other foreign bodies

• Local irritation/inflammation

• Melanotic macule

• Naevi

• Melanoacanthoma.

However, neoplasms, such as Kaposi sarcoma or malignant melanoma, are occasionally responsible. The anterior pituitary gland releases melanocyte stimulating hormone (MSH), which increases melanin production. Melanin pigmentation thus increases under hormonal stimulation, either by MSH, or in pregnancy, or rarely due to the action of adrenocorticotrophic hormone (ACTH), the molecule of which is similar to MSH, or under the influence of other factors (e.g. smoking). Thus in all patients systemic causes should be excluded, such as:

• Drugs; including smoking and the contraceptive pill

• Hypoadrenalism; there is increased ACTH production

• Peutz–Jeghers syndrome

• HIV infection

• Von Recklinghausen’s disease

• Albright syndrome

• Rarely, palatal pigmentation from bronchogenic carcinoma.

Amalgam Tattoo

Betel Stains

Peutz Jeghers Syndrome

List Causes of hyperpigmentation

Localized

• Amalgam, graphite, carbon, dyes, inks or other tattoos

• Ephelis (freckle)

• Epithelioid angiomatosis

• Kaposi’s sarcoma

• Malignant melanoma

• Melanoacanthoma

• Melanotic macule

• Naevus

• Pigmented neuroectodermal tumour

• Verruciform xanthoma

Multiple or generalized

Genetic:

• Racial

• Carney syndrome

• Complex of myxomas, spotty pigmentation and endocrine overactivity

• Laugier–Hunziker syndrome

• Lentiginosis profusa

• Leopard syndrome

• Peutz–Jeghers syndrome

Drugs:

• ACTH

• amiodarone

• antimalarials

• betel

• busulphan

• chlorpromazine

• clofazamine

• contraceptive pill

• ketoconazole

• menthol

• metals (bismuth, mercury, silver, gold, arsenic, copper, chromium, cobalt, manganese)

• methyldopa

• minocycline

• phenothiazines

• smoking

• zidovudine

Endocrine:

• Addison’s disease

• Albright’s syndrome

• Nelson’s syndrome

• pregnancy

Post-inflammatory

Others:

• Gaucher’s disease

• generalized neurofibromatosis

• haemochromatosis

• HIV disease

• incontinentia pigmenti

• thalassaemia

• Whipple’s disease

 

List the Causes of Pigmentation 

Melanin

Melanin, a nonhemoglobin derived brown pigment, is the most common of the endogenous pigments and is produced by melanocytes present in the basal layer of the epithelium. Melancocytes have a round nucleus with a double nucleus membrane and clear cytoplasm lacking desmosomes or attachment plates. Melanin accumulates in the cytoplasm, and the melanosome is transformed into a structureless particle no longer capable of melanogenesis. The number of melanocytes in the mucosa corresponds numerically to that of skin; however,in the mucosa their activity is reduced. Various stimuli can result in an increased production of melanin at the level of mucosa including trauma, hormones, radiation, and medications.Thyrosinase activity is present in premelanosome and melanosomes but absent in melanin granules.

Melanoid

Granules of melanoid pigment are scattered in the stratum lucidum and stratum corneum of the skin. Initially it was assumed melanoid was a degradation product of melanin, but more recently it has been shown that such a relationship is highly improbable. Melanoid imparts a clear yellow shade to the skin.3

Oxyhemoglobin and Reduced Hemoglobin

Oxyhemoglobin and reduced hemoglobin are pigments resulting from hemosiderin deposits.

The skin color is affected by the capillary and venom plexuses shining through the skin.

Carotene

Carotene is distributed in the lipids of the stratum corneum and stratum lucidum and gives a deep yellow color to the skin. It is found in higher concentrations in more women than in men. Pigmented lesions of the oral cavity are of multiple origin. Different classifications are used at this time. Some researchers divide the lesions into two main groups as either endogenous or exogenous lesions. Brocheriou et al.

subdivides pigmented lesions as follows:

• Non tumoral pigmentations

• Non melanin pigmented tumors or tumor like lesions

• Benign melanin pigmented tumors

• Malignant melanomas

In several articles on oral pigmentation, Dummett and others implicate many systemic and local factors as causes of changes in oral pigmentation.

Epidemiology

Oral pigmentation occurs in all races of man.There were no significant differences in oral pigmentation between males and females. The intensity and distribution of racial pigmentation of the oral mucosa is variable, not only between races, but also between different individuals of the same race and within different areas of the same mouth. Physiologic pigmentation is probably genetically determined, but as Dummett suggested , the degree of pigmentation is partially related to mechanical, chemical, and physical stimulation. In darker skinned people oral pigmentation increases, but there is no difference in the number of melanocytes between fair-skinned and dark-skinned individuals. The variation is related to differences in the activity of melanocytes.There is some controversy about the relationship between age and oral pigmentation. Steigmann and Amir et al. stated all kinds of oral pigmentation appear in young children. Prinz, on the other hand, claimed physiologic pigmentation did not appear in children and was clinically visible only after puberty.

Clinical Characteristics

The gingivae are the most frequently pigmented intraoral tissues. Microscopically, melanoblasts are normally present in the basal layers of the lamina propria.The most common location was the attached gingiva (27.5%) followed in decreasing order by the papillary gingiva, the marginal gingiva, and the alveolar mucosa.The total number of melanophores in the attached gingival was approximately 16 times greater than in the free gingival. The prevalence of gingival pigmentation was higher on the labial part of the gingiva than on the buccal and palatal/lingual parts of the arches.The shade of pigment was

classified as very dark brown to black, brown, light brown-yellow.3 Melanin pigmentation of the

oral tissues usually does not present a medical problem, but patients complain of black gums.

Classification and Differential Diagnosis

Oral pigmentation has been associated with a variety of lesions and conditions. Differential diagnosis of oral mucous membrane pigmentations are made according to the following situations:

A. Localized Pigmentations: Amalgam tatoo, graphite or other tattoos, nevus, melanotic macules, melanoacanthoma, malignant melanoma, Kaposi’s sarcoma, epithelioid oligomatosis, verruciform xanthoma

B. Multiple or Generalized Pigmentations

1. Genetics: Idiopathic melanin pigmentation (racial or physiologic pigmentation), Peutz-Jegher’s syndrome, Laugier-Hunziker syndrome, complex of myxozomas, spotty pigmentation, endocrine overactivity, Carney syndrome, Leopard syndrome, and lentiginosis profuse

2. Drugs: Smoking, betel, anti-malarials, antimicrobials, minocycline, amiodarone, clorpromazine, ACTH, zidovudine, ketoconazole, methyldopa, busulphan, menthol, contraceptive pills, and heavy metals exposure (gold, bismuth, mercury, silver, lead, copper)

3. Endocrine: Addison’s disease, Albright’s syndrome, Acanthosis nigricans, pregnancy, hyperthyroidism

4. Postinflammatory: Periodontal disease, postsurgical gingival repigmentation

5. Others: Haemochromatosis, generalized neurofibromatosis, incontinenti pigmenti, Whipple’s disease, Wilson’s disease, Gaucher’s disease, HIV disease, thalassemia, pigmented gingival cyst, and nutritional deficiencies

Systemic and Local Causes of Pigmentation

Many systemic and local factors are caused by changes in oral pigmentation. Some of the important factors are discussed below.

Amalgam Tattoo

The pigmentation of the oral mucous membrane by tooth restoration material (amalgam) is a

common finding in dental practice. Amalgam pigmentation is generally called amalgam tattoo.The lesion represents embedded amalgam particles and usually manifests itself as an isolated bluish or black macule in various areas of the mucosa. The color is usually described as black, blue, grey, or a combination of these. Almost half were located on the gingiva and alveolar mucosa, the mandibular region being affected more than the maxillary region. Almost half of the lesions were asymtomatic and were discovered during routine dental examination. The amalgam granules and fragments were found mainly in the lamina propria but were sometimes seen in the submucosa.

Pigmented Nevi

Pigmented nevi of the oral cavity are uncommon. The pigmented nevi are classified as intramucosal, junctional, compound, or blue according to their histological features. Nevi are seen particularly on the vermillion border of the lips and the gingivae. They are usually grey, brown, or bluish macules and are typically asymptomatic. Melanocytes are pigment producing cells characterized by the ability to syntesize via the enzyme dihydroxyphenylalanine (DOPA). A group of melanocytes (generally four or more) are in contact with the basal layer of the epithelium.

Oral Melanotic Macules

Oral melanotic macules are relatively rare oral mucosal lesions, analogous to skin freckles, due to the focal increase of melanin production.These melanotic macules have been variously termed ephelis, melonosis, lentigo, solitary labial lentigo, labial melanotic macule, and oral melanotic macule.The vermillion border of the lower lip is most commonly involved.The buccal mucosa, palate, and gingiva are less commonly affected. The color is usually described as grey, brown, blue, black, or a combination of these.Histologically, ephelis shows increased melanin pigmentation in the basal cell layer without an increase in the number of melanocytes; otherwise, the epidermis is normal.

Melanoma

Melanoma is a cancerous condition of the melanocyte. Special corpusles in this cell, known as melanosomes, contain the necessary enzyme (tyrosine) to transform amino acids into melanin. Melanocytes are found among the basal cells of the epidermis. Histopathogically, the mucosal epithelium is abnormal with large atypical melanocytes and excessive melanin. Malignant melanoma of the oral mucosa affects both sexes equally usually after 40 years of age. The great majority of the lesions (about 70-80%) occur on the palate, upper gingival, and alveolar mucosa.Initially there usually is a solitary small asymtomatic brown or black macule.

Physiologic Pigmentation

Physiologic pigmentation of the oral mucosa is clinically manifested as multifocal or diffuse melanin pigmentation with variable prevalence in different ethnic groups.2 Melanin is normally found in the skin of all people. In dark skinned persons the gingiva may contain melanin pigment to a greater extent than the adjacent alveolar mucosa. The melanin pigment is synthesized in specialized cells, the melanocytes, located in the basal layer of the epithelium. The melanin is produced as granules. The melanosomes are stored within the cytoplasm of the melanocytes, as well as in the cytoplasm of adjacent keratinocytes. Melanocytes are embryologically derived from neural crest cells that eventually migrate into the epithelium. If pigmented gingiva is surgically resected, it will often heal with little or no pigmentation; therefore, surgical procedures should be designed so as to preserve the pigmented tissues.

Peutz-Jeghers Syndrome

Peutz-Jeghers syndrome (intestinal polyposis) is a genetic disorder characterized by mucocutaneous pigmentation and hamartomas of the intestine.It manifests itself as frecklelike macules about the hands, perioral skin, and intraorally to include the gingiva, buccal, and labial mucosa. Pigmented spots are 1 to l0 mm in diameter. Pigmented spots are particularly found on the lower lip and buccal mucosa but rarely on the upper lip, tongue, palate, and gingiva.

Smoker’s Melanosis

Smoker’s melanosis is a benign focal pigmentation of the oral mucosa. It tends to increase significantly with tobacco consumption. Tobacco smokers have significantly more oral surfaces pigmented than non-tobacco users.Clinically, the lesion usually presents as multiple brown pigmented macules less than 1 cm in diameter, localized mainly at the attached labial anterior gingival and the interdental papillae of the mandible. Smoker’s melonosis is more common in females usually after the third decade of life.

Antimalaria Drug Use

Several antimalarial drugs are known to be capable of inducing intraoral melanin pigmentation. These drugs include: quinacrine, chloroquine, and hydroxychloroquine Longterm use may cause pigmentation of the oral mucosa. The pigmentation of the oral mucosa is described as slate-grey in color, bearing some resemblance to pigmentation caused by silver arsplenamine.

Minocycline Use

Minocycline is a synthetic tetracycline that is commonly used in the treatment of acne vulgaris.Although tetracycline causes pigmentation of bones and teeth, minocycline alone is also responsible for soft tissue pigmentation.It is usually seen as brown melanin deposits on the hard palate, gingiva, mucous membranes, and the tongue.

Heavy Metals

Heavy metals absorbed systemically from therapeutic use or occupational environments may discolor the gingiva and other areas of the oral mucosa. Bismuth, arsenic, and mercury produce a black line in the gingiva which follows the contour of the margin. Lead results in a bluish red or deep blue linear pigmentation of the gingival margin (Burtonian line). Exposure to silver causes a violet marginal line, often accompanied by a diffuse bluish-grey discoloration throughout the oral mucosa.

Addison’s Disease

Addison’s disease or primary adrenocortical hypofunction is due to adrenocortical damage

and hypofunction.Bronzing of the skin and increased pigmentation of the lips, gingivae, buccal mucosa, and tongue may be seen. Oral pigmentation may be the first sign of the disease.A biopsy of the oral lesions shows acanthosis with silver-positive granules in the cells of the stratum germinativum. Melanin is seen in the basal layer.

Periodontal Diseases

Periodontal diseases often produce discolorations of the oral mucosa. The pigmentation is worsened by gingivitis, which increases vascular permeability and allows the heavy metals access to the soft tissues.51 Melanin re-pigmentation is related to after surgical inury.

Hemachromatosis

Hemachromatosis (bronze diabetes) is a chronic disease characterized by the deposition of excess iron (ferritin and hemosiderin) in the body tissues, resulting in fibrosis and functional insufficiency of the involved organs. Hyperpig mentation may appear both in skin and mucous membranes (oral and conjunctiva). Gingival or mucosal pigmentation is reported to occur in 15 to 25% of patients with hemachromatosis. The oral mucosa shows diffuse homogeneous pigmentation of gray-brown or deep brown in about 20% of the cases. The buccal mucosa and the attached gingiva are the most frequently involved sites.

HIV Infection

In patients infected with human immunodeficiency virus (HIV), progessive hyperpigmentation of the skin, oral mucosa, fingernails, and toenails have been reported being related to primary adrenocortical deficiency and to zidovudine (azidothymidine) therapy in some cases.Clinically, oral pigmentation appears as irregular macules with brown or dark brown color. The tongue, buccal mucosa, and palate are the most commonly affected sites.

Classification of oral diseases of HIV- associated immune suppression (ODHIS)

         Present classification systems for HIV – associated oral lesions developed in the early 1990’s which was named as HAART. Patterns of oral conditions keep on changing very frequently. This highlights the need of new system.

Classification of oral diseases of HIV – associated immune suppression (ODHIS)

System should consider:

·         Changes in epidemiology of oral lesions

·         Therapeutics

·         Development of lesions and immune systems

·         Oral lesions to oral disease

Definition of Oral disease:  abnormality characterized by a defined set of signs and symptoms in the oral cavity, extending from the vermilion border of the lip to the oropharynx, with the exception of salivary gland disease

New Classification- Classification of oral diseases of HIV – associated immune suppression (ODHIS)

Group 1 – ODHIS associated with severe immune suppression (CD4<200 cells/mm³)

Group 2 – ODHIS associated with immune suppression (CD4<500 cells/mm³)

Group 3 – ODHIS assumed associated with immune suppression

A) More commonly observed

B) Rarely reported

Group 4 – Therapeutically-induced oral diseases

Group 5 – Emerging oral diseases

Oral diseases do not belong exclusively to one classification Group

Overlap may exist

Use of the New Classification

·         Identifying undiagnosed individuals

·         Provides additional rationale for HIV testing

·         Affects access and type of HIV-related healthcare

·         Provides clinical markers for therapeutic interventions and efficacy

Group 1. ODHIS associated with severe immune suppression (CD4<200 cells/mm³)

1.      Major recurrent aphthous ulcer

2.      Neutropenia-induced ulcers

3.      Necrotizing ulcerative periodontitis

4.      Necrotizing stomatitis

5.      Cytomegalovirus (CMV)

6.      Chronic HSV

7.      Histoplasmosis

8.      Esophageal, pseudomembranous, and hypertrophic candidiasis

9.      Oral hairy leukoplakia

10.   Kaposi’s sarcoma

11.   Idiopathic Necrotizing Stomatitis    

Hyperplastic candidosis

Oesophageal candidosis

Pseudomembranous Candidosis

Kaposi's Sarcoma

Histoplasmosis

Periodontitis

Neccotizing Sialometaplasia

Chronic HSV

Group 2. ODHIS associated with immune suppression (CD4,500 cells/mm3)

1.       Major recurrent aphthous ulcer

2.       Increased frequency, harder to treat, atypical location

3.       Erythematous candidiasis

4.       Salivary gland disease

5.       Drug induced low salivation

6.       Facial palsy

7.       Neuropathies

8.       Hyposalivation

9.       Human papilloma virus (HPV)

10.   Linear gingival erythema

11.   Non-Hodgkin’s lymphoma

12.   Linear Gingival Erythema

Aptheous Ulcer

HPV

Group 3. ODHIS assumed associated with immune suppression

More commonly observed

1.       Angular candidiasis

2.       Herpes labialis

3.       Intra-oral herpes

4.       Minor aphthous ulcers

Rarely reported

1.       Bacillary epithelioid angiomatosis

2.       Tuberculosis

3.       Deep-seated mycosis (except histoplasmosis)

4.       Molluscum contagiosum

5.       Varicella Zoster Virus (VZV)

6.       HSV Labialis

7.       Intra-oral Herpes

8.       Minor Aphthous Ulcers

Angular Chelitis with candidosis

Group 4. Therapeutically-induced oral diseases

Side-effect

·         Melanotic hyperpigmentation

·         Ulcers

·         Hyposalivation

·         Lichenoid drug reaction

·         Neutropenia-induced ulcers

·         Thrombocytopenia

·         Lypodystrophy-associated oral changes

·         Perioral paresthesia

·         Steven Johnson’s?

·         Exfoliative cheilitis?

Resistance-induced disease

·         Different Candida spp and strains

·         HSV

Antiretrovirals and Adverse Reactions

Antiretroviral Drugs

Indinavir

Saquinavir

Amprenavir

Nevirapine

Delavirdine

Efavirenz

Stavudine

Didanosine

Recurrent HSV

Adverse reactions of antiretroviral drugs

Oral ulcers

Stevens Johnson’s

Taste changes

Dryness

Perioral paresthesia

Thrombocytopenia

Ulcers – Medication Induced

Recurrent HSV

Group 5. Emerging oral diseases

1.       Human papilloma virus, several HPV types (may be associated with immune reconstitution)

2.       Erythema migrans

3.       Variants of Non-Hodgkin’s Lymphoma (NHL B-cell types)

4.       Epithelial neoplasms

5.       Aggressive interproximal dental caries

6.       Condyloma Accuminatum

7.       Squamous Cell Carcinoma