Oral Lesion Terminology: Graduate Oral Pathology PDF

GRADUATE ORAL PATHOLOGY DBPG 1612 Fall 2023 Kalu U.E. Ogbureke, BDS, MSc, JD, DMSc, FDSRCS, FDSRCPS(G), FDSRCSEdin, FRCPath Diplomate, American Board of Oral & Maxillofacial Pathology (ABOMP) Diplomate, American Board...

GRADUATE ORAL PATHOLOGY DBPG 1612 Fall 2023 Kalu U.E. Ogbureke, BDS, MSc, JD, DMSc, FDSRCS, FDSRCPS(G), FDSRCSEdin, FRCPath Diplomate, American Board of Oral & Maxillofacial Pathology (ABOMP) Diplomate, American Board of Medical Malpractice (ABMM) Diplomate American Board of Legal Medicine (ABLM) Professor Department of Diagnostic and Biomedical Sciences SOD 5363 Tel. 713-486-4406 Email. [email protected] ORAL LESIONS: DESCRIPTIVE TERMINOLOGY Present in limited but recognizable ways: – A. Blister  Vesicle  Bulla – Erosion  Ulcer – Plaque  Patch – Pustule (pus) – Papule  Nodule  Tumor  ORAL EPITHELIUM: Functions Physical barrier 1.organisms & toxins Chemical barrier 1. “Acid Mantle” pH 2. “slime layer” Hydrophobic barrier 1. Keeps H2O out. 2.Keeps H2O in. Temperature Flexible  ORAL EPITHELIUM: Regions 1. Stratum corneum 2. Stratum granulosum, a. Keratohyaline b. Desmosomes 3. Stratum spinosum, a. MCG (lamellar) b. Desmosomes 4. Basal Cell layer 5. Lamina propria  MACULE Flat, non palpable, non-elevated lesion. Color different from that of surrounding skin. Black, purple, blue, brown, red, yellow and white lesions. Usually < 1 cm. Examples: – Actinic Lentigo; Amalgam Tattoo; Melanotic macule; Café au lait;Blue Nevus; Lichen Planus; Melanoma  PLAQUE Usually < 1 cm subtle surface changes. Examples: – Lichen Planus – Melanoplakia – Hairy nevus – Vitiligo – Lupus; Melanoma  PATCH Lesion > than 1 cm. Examples: – Seborrheic keratosis – Leukoplakia – Lichen Planus – Melanoma – Denture Hyperplasia – Psoriasis – Spreading Basal Cell – Atopia (dermatitis)  PAPULE I small, solid, elevated lesion usually < 1 cm with about equal diameter and depth. May present with rough, pebbly/fine scales on lesion.  PAPULE II SUPERFICIAL Dermis/lamina propria is not depressed or PENETRATED by lesion. May present with a “stalk” as a form of attachment.  PAPULE III Example: – Metabolic Sarcoidosis Squamous cell Basal cell – Infiltrates Hemangioma Granuloma – “PEBBLY” Congenital nevus Intra-dermal nevus  NODULES I Papules that grow become nodules. Nodules that grow become tumors. Inflammatory type. Neoplastic type. Solid tissue mass. > than 1 cm size. Push down dermis.  NODULES II Examples – Epidermal cyst – Ganglion cyst – Lipoma – Neurofibroma – Any cancer form – Skin tag – Fibroma Sarcoid nodule – Keloid  VESICLE AND BULLA 1.< than 1 cm. 2.Serum or 3.Lymph 4.Thin epi cover. 5. Lesion called a Bulla if size is greater then 1 cm  VESICLE & BULLA: Examples I INTRA-EPIDERMAL/EPITHELIAL: A. Acantholysis Basement membrane intact: Impetigo Frictional blisters. Pemphigus foliaceus Pemphigus vulgaris. Darier’s Disease. B. Viral Blisters. Herpes.  VESICLE & BULLA: Examples II SUB-EPIDERMAL/EPITHELIAL – Pemphigoid. – Lupus. – Sunlight Disease. – Linear IgA Disease. – Epidermolysis. – Bollous Drugs Rx’s. – Uticaria  PUSTULE A fluid filled sack that contains cloudy and or purulent material. – Infection related. – Painful – Points to infection. – < then 1 cm. – Usually elevated.  PUSTULE: Examples Acne. Pustular psoriasis. Folliculitis. Pustular candidiasis. Extra-Oral abscess. Periodontal. Endodontic. Blastomycosis  ULCERS, FISSURES AND CRACKS A. Follows blister. B. Follows pustule. C. Epidermis lost: 1. Primary Barrier lost. 2. MCG function lost. 3. Infection Potential 4. Painful. 5. Immune weakness.  ULCERS, FISSURES AND CRACKS: Examples I Aphthous ulcers ANUG / ANUP Virus infections Angular chelitis Pemphigus Pemphigoid Lupus Cancer forms  KERATIN HORNS Diagnosis?  Oral Mucosal “Coloration” The oral mucosa represents the first part of the digestive tract and is exposed to various exogene noxes Exposition of longer duration can lead to reactive changes that need to be differentiated from malignancies  Diagnostic Approach to Evident White Lesions Try to remove local factors that could have contributed to the lesion commence anti-inflammatory treatment for two weeks, if lesion remains: biopsy a diagnosis based on clinical appearance alone is usually not sufficient to determine the histological nature of the tissue  “White” Lesions: The “Abnormal” Normal Fordyce Granules White Sponge Nevus Frictional Keratosis Leukoedema Cheek/Tongue Biting Linea Alba Chemical Burns White Sponge Nevus Geographic Tongue Hairy Tongue  Fordyce Granules Variation of Normal Fordyce Granules Normal sebaceous glands— ectopic Evident in 80% of population Most often in adults  Fordyce Granules II Fordyce granules may be Facts: found on: – May also be found in hair – Lower lip follicles of the skin – Equally affect both male – Buccal mucosa and females – Patients may have a few or – Often bilaterally hundreds. symmetrical – Asymptomatic—painless  Fordyce Granules: Histology Sebaceous glands Rounded cells Clear, granular cytoplasm  White Sponge Nevus Inherited condition Mutation of keratin genes Autosomal dominant inheritance pattern Rare  White Sponge Nevus II Similar to cheek chewing in clinical appearance Hyperkeratosis Widespread keratinization of the buccal mucosa  Leukoedema Variation of normal Equal sex predilection More common in African Americans Does not rub off Disappears when stretched  Geographic Tongue Affects 2 to 3% of population Rare in children Female predilection Inflammatory  Geographic Tongue II Patterns change—usually visible on the dorsal and ventral tongue areas. Atrophic, denuded patches Concentric rings (yellow or white)  Frictional Keratosis Physical irritation Whitish plaques Physical irritation is not considered leukoplakia Adaptive response is a callus (over production of keratin).  Linea Alba Localized Friction Occurs along the line of occlusion on buccal mucosa Frictional keratosis May indicate bruxism  Cheek (Tongue) Chewing Also called morsicatio Morsicatio Buccarum labiorum on labial Physical irritation Over production of keratin Can be confused with white sponge nevus Chronic trauma Patients should be shown the area and encouraged to stop.  Nicotine Stomatitis Heavy smokers – Reverse smoking – White keratinized tissue – Minor salivary gland duct openings appear red. – May lead to carcinoma – Smoking cessation  Hairy Tongue May be caused by – Antibiotics – Radiation therapy – Smoking – Peroxide use – Overgrowth of oral flora  Hairy Tongue II Hairy tongue represents the elongation of filiform papillae. Occurs on the dorsal tongue Hair-like projections may be white or brown. Candida albicans is occasionally found. Chlorhexidine gluconate is sometimes prescribed. Use tongue cleaner and debridement with toothbrush.  Hairy Leukoplakia Infected by EBV Secondary to immunosuppression May appear with organ transplant patients Does not rub off  Chemical and Thermal Burns Caustic chemicals cause burns on mucosa. Examples include aspirin placed on a tooth to relieve the pain, home remedies, phenols, silver nitrate, and hydrogen peroxide. Necrosis of the epithelium causes a white color.  Coagulation Necrosis Necrosis of the surface epithelium from a chemical burn. Cells within the epithelium no longer have a nuclei. ORAL PREMALGNANT LESIONS (OPL)  Red/White Oral Mucosal lesions White lesions: Red lesions: Leukoplakia Erythroplakia Lichen Varicosity Leukoedema Hemangioma Morsicatio buccarum Purpura (Petechiae, Ecchymosis) White Sponge Nevus Sturge-Weber Angiomatosis Fordyce’s Granules Hereditary Hemorrhagic Telangiectasia  ORAL PREMALIGNANT LESIONS (OPLs) LESIONS WITH HIGHER THAN NORMAL PROPENSITY FOR TRANSITION TO CANCERS WITH TIME, IN THE ABSENCE OF ADEQUATE INTERVENTION *Leukoplakia: clinically inexplicable white patch 3-15% will transition to oral cancer *Erythroplakia: clinically inexplicable red patch  Most are histologically diagnosed epithelial dysplasia or worse  Much higher chance of progression to carcinoma  Biopsy is mandatory *Clinical terms implying no specific histopathology and therefore of no pathological diagnostic value Oral cancers  Frequently, such lesions develop in areas of the oral cavity where they are not obvious to the patient (sulcus glosso- alveolaris, dorsal and lateral tongue, oral vestibule, retromolar area) Therefore, thorough intraoral examination – twice a year recommended  Leukoplakia White lesions on the mucosa which will not rub of and cannot be classified as any other disease (WHO 1978) It is a clinical descriptive term, not a histological diagnosis  Leukoplakia: Etiology Combination of extrinsic local factors and intrinsic predisposing factors Initiation through chemical or mechanical irritation: – chemical: alcohol, tobacco – mechanical: sharp tooth or crown margins, irritating denture clasps  Leukoplakia: Histologic Features Leukoplakia usually shows hyperkeratosis or acanthosis with or without dysplasia (20% show dysplasia) white colour change is the sign of hyperkeratosis  Hyperorthokeratosis Abnormal increase in thickness of the orthokeratin layer or stratum corneum  Hyperparakeratosis Parakeratin: persistence of nuclei or nuclear remnants in the keratin layer Presence of parakeratin, where it is not usually found, or a thickening of the parakeratin layer is called hyperparakeratosis  Acanthosis Abnormal thickening of the stratum spinosum (spinuous layer) may or may not be associated with hyperorthokeratosis or hyperparakeratosis  Dysplasia Abnormal epithelial changes that signal potential transition to malignancy – Mild: affects only basal 1/3 of epithelium – Moderate: affects half of epithelial layer – Severe: more than 2/3 of epithelium affected – Carcinoma in situ (CIS): the whole thickness of epithelium is involved but the basement membrane is intact  Criteria for Dysplasia Irregular stratification or loss of polarity of the cells in the epithelium Increased mitoses Nuclear hyperchromatism Increased nuclear/cytoplasmatic ratio Nuclear Pleomorphism abnormal keratinization “The more dysplastic the lesion is, the higher the chance of malignant transformation of the lesion into a carcinoma.” Clinical appearance - homogeneous and non- homogeneous Leukoplakia Homogeneous: non-palpable, faintly translucent white discoloration non-homogeneous: – verrucous or nodular – speckled: hyperkeratotic white areas and red areas – errosive: fissuring and ulcer formation Erosions and ulceration are strong clinical indications/signs of malignant transformation  Sites of predilection Lateral and ventral tongue floor of the mouth alveolar ridge mucosa corner of the mouth less frequently: – soft palate – lip  4-6% of leukoplakias progress to squamous cell carcinoma within 5 years High risk sites of malignancy: – floor of the mouth – lateral and ventral tongue – lips Differential diagnosis Nicotine Stomatitis Candidiasis Hairy Leukoplakia Leukoedema White sponge naevus Fordyce granules  Nicotine Stomatitis Palate initially becomes diffusely erythematous and eventually turns grayish white secondary to hyperkeratosis multiple keratotic papules with depressed red centers correspond to dilated and inflamed excretory duct openings of the minor salivary glands  Candidiasis White plaque exposing shallow erosions when whipped off  Hairy leukoplakia Oral sign of HIV infection Viral origin likely (Epstein-Barr virus) Frequently associated with Candida albicans Proliferative Verrucous Leukoplakia Aggressive form of leukoplakia High incidence of oral cancer Progressive Tendency to form on the gingiva  Lichen planus Common skin disease with oral manifestation (ca 30% of cases) or oral lesions without cutaneous signs Most likely immunologic disorder in which T lymphocytes destroy the basal cell layer of the affected epithelium Malignant potential is controversial  Lichen planus Frequently affected sites: – buccal mucosa – dorsal tongue less frequently affected: – lips – palate – gingiva – floor of mouth  Lichen planus Four appearances of oral lichen planus: – striated (reticular) – atrophic – erosive – plaquelike  Lichen planus  Lichen planus  Lichen planus  Erythroplakia Definition – persistent red patch that cannot be characterized clinically as any other condition redness of the lesion is a result of atrophic mucosa overlying highly vascular submucosa  Erythroplakia Most erythroplakia are histologically diagnosed epithelial dysplasia or worse Much higher chance of progression to carcinoma Biopsy is mandatory  Actinic Cheilitis Clinical lesion of the lower lip caused by excessive solar radiation damage Precancerous condition Biopsy recommended  Lentigo maligna Mostly in persons above age 50 on sun exposed skin Oral lesions predominantly on palate and buccal mucosa Transformation into lentigo-maligna-melanoma after several years  Oral Squamous Cell Carcinoma Most common malignant tumor of oral cavity male to female ratio 3:1 usually beyond 4th decade in life contributing factors: tobacco and alcohol (also: lack of oral hygiene, mechanical irritation, sunlight, viruses)  Oral Squamous Cell Carcinoma Well differentiated, moderately differentiated and poorly differentiated tumors can be distinguished (prognostic marker) about 80% of tumors show keratinization  Oral Squamous Cell Carcinoma - Clinical Signs relatively painless mass or ulcer (suddenly ill fitting denture) non healing extraction socket sudden loosening of teeth initially painless, relative sudden onset, fast progressing  Oral Squamous Cell Carcinoma Predilection sites: floor of the mouth lateral border of tongue mandible > maxilla (retromolar area, alveolar mucosa) lower lip > upper lip  Carcinoma of the lip Male to female ratio 8:1 beyond 6th decade in life in 90% of cases lower lip affected etiology: UV light, mechanical and chemical factors (tobacco) generally good prognosis because tumour metastasizes late  Carcinoma of the Floor of the Mouth most frequent localization of OSCC early metastasis into regional lymph nodes fair prognosis, is getting worse, if tumor is further posterior  Carcinoma of the tongue Lateral and ventral tongue commonly affected base of tongue is problematic due to late detection of tumor and poor prognosis symptom: difficulty swallowing  Carcinoma of the alveolar mucosa Verrucous form with cauliflower appearance is most common Early infiltration of bone Clinical sign of painless tooth loosening and non healing extraction socket  TAKE HOME APPROACH! Oral Squamous Cell Carcinoma If an ulceration or other lesion of unclear origin is present in the oral cavity: try to remove possible contributing factors (mechanical trauma ect.), start anti-inflammatory treatment for one week If the lesion does not resolve, a biopsy is indicated PIGMENTED LESIONS: (red, Purple, Blue/Black. Brown, ETC)  Oral Mucosal lesions: Coloration Red-white lesions Pigmented lesions speckled Erythroplakia Melanoplakia Ephelis (Freckle) Squamous Cell Carcinoma Tobacco associated Lichen planus Pigmentation (Smokers Lupus Erythematosus Melanosis) Lichenoid Drug Reactions Nevus Candidiasis (Candidal Malignant Melanoma Leukoplakia, Antibiotic Sore Mouth, Denture Stomatitis) Peutz-Jeghers Syndrome Addisons’s Disease Amalgam Tattoo  Important Factors in Assessment The Medical History What medications is the person taking? The duration, location, clinical appearance, self- reported drugs, radiographic appearance, past pathology reports, and patient self-history  Melanocytes Functions Oral pigmentation – Produce melanin to – Due to the number of protect the skin from melanocytes harmful rays of the sun – Due to the amount of melanin produced – Due to the – Some individuals incorporation of a produce more and foreign substance in some produce less. the oral and perioral The numbers of tissues melanocytes can vary as well.  Traumatic or Inflammatory Lesions Most commonly caused by trauma, chronic friction to the tissues, thermal changes, and chronic inflammation  Ethnic Tattooing History 60-year-old Arabian woman who has a lip tattoo to ward off “bad spirits” and to guard against “bad luck.”  Amalgam Tattoo (Focal Argyrosis) Amalgam fragments within the tissues Endodontics, restorative work force particles into the tissues Amalgam Tattoo II  Titanium Tattoo May produce blue/gray pigments Squamous cell carcinoma should be considered in implants that are failing.  Intentional Tattoo Tattooing and piercing are often seen together. Oral tattooing is less frequently seen.  Lead-Line Stain Referred to as Burtonian line Lead poisoning in children (plumbism) Blue, gray, or black line in premolar region  Minocycline Stain Black bone staining Ingestion of minocycline Semisynthetic tetracycline —1960s Used to treat acne  AZT Pigmentation Used in the treatment of AIDS—zidovudine May cause pigmentation of the nails, tongue, and other oral tissues  Tobacco-Associated Melanosis Light brown pigmentation  Betel Quid Use Considered premalignant Use of quid Mixture of tobacco, areca nut, flavoring, slaked lime Arecoline is a substance found in areca nuts. Released when chewed or ground. Areca nut has a fibrous core that is chewed and produces a red color that stains the teeth/tissues. Highly addictive and produces a sense of euphoria Betel Quid and Areca Nut Use  Submucous Fibrosis Submucous fibrosis Premalignant Oral constriction Fibroblasts promote thick bands. Cumulative  The Nevus Intradermal nevus or intramucosal nevus—in oral tissue Compound nevus Junctional nevus  Blue Nevus Second most frequently seen melanocyte, orally Usually occur on the palate  Blue Nevus (cont.) Pigmented deep blue to purple cells  Oral Melanotic Macule (Focal Melanosis) Childhood or 20 to 30 years old Intraoral lesions usually occur in those older than 40. 3% of population Lip is most common (AKA: ephelides pl.).  Oral Melanotic Macule (cont.) Lentigo maligna—atypical melanocytes Usually in older population  Laugier-Hunziker Syndrome Functional alteration of the melanocytes that induce increased synthesis of melanosomes and transport to the basal cell layer  Laugier-Hunziker Syndrome (cont.) Pigmented macules 1 to 5 mm May affect most cutaneous areas Mean age is 52. Median age is 42.  Laugier-Hunziker Syndrome (cont.) Pigmented buccal mucosa/palate, lips are often affected. Nail striation may be confused with melanoma.  Oral Melanoma Occur most often in males in the 50-year-old age group May be confused with other pigmented lesions Poor prognosis  Malignant Melanoma Proliferation of melanocytes Spreading laterally through tissue  Basal Cell Carcinoma Usually occurs on the upper 2/3 of the face Rolled borders with a waxy-type appearance Pearly iridescent-type surface  Squamous Cell Carcinoma May occur on any skin surface. Lower lip is a prime area. Vermillion border is lost—no definition. Small lines running from the lips are increased from sun damage.  Actinic Keratosis Most common type of precancerous skin lesion May appear as an early melanoma Referral to a dermatologist is needed.  Actinic Cheilitis Caused by solar damage. Also called solar cheilitis. Smoking is a risk factor. Scaling, peeling appearance  Benign Skin Lesions Acrochordon Skin tag Stalk-like or pedunculated Flesh colored  Solar Lentigo Benign macules caused by sun exposure. AKA: liver spots and age spots.  Psoriasis Red, plaque-like lesions covered with a white thin scale, appearing pearly, iridescent appearance Etiology: genetic, environmental, and trauma  Seborrheic Keratoses Benign but may appear as melanoma or warts Caused by overproduction of sebum by the sebaceous glands  Graft Versus Host Disease Occurs in association with organ or bone marrow transplantation The oral cavity may be involved in 80% of cases.  Impetigo Caused by Staphylococcus aureus and streptococci organisms  Red and Blue (Purple) Lesions of the Oral Cavity  Petechiae, Ecchymoses, and Purpura Petechiae Pinpoint size 1 to 2 mm May indicate blood disorders May be caused by trauma or disease  Purpura Larger than a petechiae Over 2 mm Caused by trauma, systemic disease as well  Ecchymoses The larger of the three hemorrhages Greater than 2 cm Will not blanch with diascopy  Hypersensitivity Foods—flavoring Environment Dental products − Toothpaste, mouthrinse − Amalgam or crown materials  Hypersensitivity (cont.) Lichenoid Reactions Lichenoid Reaction Medications Contact with tissue of dental products Contact with tissues of amalgam  Hereditary Hemorrhagic Telangiectasia Also known as Osler- Rendu-Weber disease Dilated blood vessels Spider veins May bleed profusely Nosebleeds  SUMMARY! Any red/purple/blue coloration of the oral mucosa/mouth must be accounted for (diagnosis)!