W30 BDS10013 White Patches (Lecture)_46f950923c574c7b00c73da0ec6b682f.pdf

Loading...
Loading...
Loading...
Loading...
Loading...
Loading...
Loading...

Transcript

BDS10013 Oral White Patches Aims: The aim of this lecture is to detail the histopathology of causes of white patches of an infectious and/or immunological aetiology Objectives: On completion of this lecture, the student should be able to: Understand the histopathological aspects of oral lichen planu...

BDS10013 Oral White Patches Aims: The aim of this lecture is to detail the histopathology of causes of white patches of an infectious and/or immunological aetiology Objectives: On completion of this lecture, the student should be able to: Understand the histopathological aspects of oral lichen planus and related disease, oral hairy leukoplakia, lupus erythematosus and chronic hyperplastic candidiasis Understand the use of immunohistochemistry for the diagnosis of oral hairy leukoplakia White lesions Why do some lesions appear white? Here are the main histopathologic changes causing the white colour of the most common oral white lesions These are the most common oral white lesions classified according to etiology HEREDITARY Leukoedema White Sponge Nevus Hereditary Benign Intraepithelial Dyskeratosis Dyskeratosis Congenita INFECTIOUS Oral Hairy Leukoplakia Candidiasis Immune mediated diseases Oral lichen planus Lichenoid reaction Lupus erythematosus  REACTIVE & INFLAMMATORY Linea Alba (White Line) Frictional (Traumatic) Keratosis Cheek Chewing Chemical Injuries of the Oral Mucosa Actinic Keratosis (Cheilitis) Smokeless Tobacco–Induced Keratosis --Nicotine Stomatitis DYSPLASIA & NEOPLASIA Leukoplakia Oral squamous cell carcinoma Miscellaneous lesions Fordyce’s granules Geographic tongue Hairy tongue They could be classified according to clinical appearance, as follows Flat Plaques, Solitary Frictional (Traumatic) Keratosis Leukoplakia Actinic Cheilitis Smokeless Tobacco–Induced Keratosis Squamous cell carcinoma Pseudomembranous Lesions Chemical burns Candidiasis Verrucous/Rippled Plaques Proliferative verrucous Leukoplakia Verrucous carcinoma Hairy leukoplakia Flat Plaques, Bilateral or Multifocal Leukoedema White Sponge Nevus Oral lichen planus Lacey White Lesions Oral lichen planus Lichenoid reactions Lupus erythematosus Papular Lesions Koplik spots of measles Fordyce’s granules Stomatitis nicotina Also, They could be classified clinically into: White oral mucosal patches Non adherent -Pseudomembranous candidosis (thrush) -Drug-associated necrotic debris (for example, aspirin, cocaine) Adherent -White sponge naevus -Geographic tongue -Frictional keratosis -Lichen planus -Lupus erthymatosus -Oral hairy leukoplakia HEREDITARY Leukoedema White Sponge Nevus Hereditary Benign Intraepithelial Dyskeratosis Dyskeratosis Congenita Leukoedema  It is a common condition of unknown cause, it may represent a variation of normal rather than a disease  Blacks are affected more than whites, whites usually show milder presentation of leukoedema Clinical features  Asymptomatic, diffuse translucent, greyish white appearance of the bilateral buccal mucosa.  On stretching the mucosa, the lesion disappears. Leukoedema Histopathological features An increase in thickness of the epithelium with broad and elongated rete ridges Intracellular edema of the spinous layer These vacuolated cells appear large and have pyknotic nuclei. The epithelial surface is frequently parakeratinized Leukoedema Treatment Leukoedema is a benign condition, and no treatment is required. The diagnosis is confirmed by disappearance of the lesion when stretched INFECTIOUS Oral Hairy Leukoplakia Candidiasis Oral hairy leukoplakia (OHL)  OHL is caused by Epstein Barr virus (EBV),  it is commonly seen in HIV patients and is a sign of severe immunosuppression and advanced disease.  Also, OHL may be seen in immuno-compromised patients such as transplant recipients  Discovery of OHL in “normal” patients mandates a thorough evaluation to rule out immunocompromise. Oral hairy leukoplakia (OHL) Clinical features  OHL appears as white mucosal plaque that does not rub off.  Mostly occur on the lateral border of the tongue  It ranges from faint, white vertical streaks to thickened, furrowed areas of leukoplakia with a shaggy surface  The lesions may extend to cover the entire dorsal and lateral surfaces of the tongue. Oral hairy leukoplakia (OHL) Histopathological features The epithelium exhibits a bandlike zone of lightly stained cells with abundant cytoplasm (“balloon cells”) in the upper spinous layer Thickened parakeratin with surface corrugations or thin projections. The epithelium is acanthotic Oral hairy leukoplakia (OHL) Histopathological features The superficial epithelial cells reveals nuclear clearing and peripheral margination of chromatin termed nuclear beading, caused by extensive EBV replication that displaces the chromatin to the nuclear margin. Dysplasia is not noted. Heavy candidal infestation in the parakeratin layer Oral hairy leukoplakia (OHL) Histopathological features Multiple methods could be used to demonstrate o EBV including PCR and immunohistochemistry (the brown dots in the following photomicrograph reveals presence of EBV in the nuclei of infected epithelial cells) Candidiasis  Candidiasis is the most common oral fungal infection in humans, caused by the yeast-like fungal organism Candida albicans  It has a variety of clinical manifestations making the diagnosis difficult at times.  Clinical presentations include 1.Pseudomembranous 2.Chronic atrophic (erythematous) 3.Denture stomatitis 4.Inflammatory papillary hyperplasia 5.Angular chelitis 6.Median rhomboid glossitis 7.Hyperplastic (candidal leukoplakia) 8.Mucocutaneous 9.Endocrine-candidiasis syndrome Candidiasis  The best recognized form of candidal infection is pseudomembranous candidiasis. Also known as thrush,  It is characterized by the presence of adherent white plaques that resemble curdled milk on the oral mucosa  The white plaques are composed of tangled masses of: ♦hyphae ♦desquamated epithelial cells ♦debris  These plaques may be removed by scraping them with a tongue blade or rubbing them with a dry gauze.  The underlying mucosa may appear normal or erythematous. Candidiasis Pseudomembranous candidiasis may be seen in Infants due to the underdeveloped immune systems.  Patients due to  Administration of broadspectrum antibiotics, which will eliminate the competing bacteria  Impairment of the patient’s immune system as in leukemic patients and HIV patients Candidiasis  The term chronic hyperplastic candidiasis (candidal leukoplakia) is used to describe a white patch that cannot be removed by scraping [least common form]  It is believed that this condition represents candidiasis that is superimposed on a preexisting leukoplakia  The diagnosis is confirmed by the presence of candidal hyphae and complete resolution after antifungal therapy Candidiasis Histopathologic Features The candidaI organism can be seen microscopically in either an exfoliative cytologic preparation or in tissue sections obtained from a biopsy specimen. The candidal hyphae are embedded in the parakeratin layer and penetrate into the viable cell layers of the epithelium Candidal hyphae show bright magenta color by PAS stain Candidiasis Histopathologic Features 3-Small collections of neutrophils (microabscesses) are seen in the parakeratin layer and the superficial spinous cell layer Increased thickness of parakeratin on the 1. surface elongation of the epithelial rete ridges. 2- Chronic inflammatory cell infiltrate in the underlying connective tissue Immune mediated diseases Oral lichen planus Lichenoid reaction Lupus erythematosus Lichen planus  Lichen planus is a relatively common, chronic dermatologic disease that often affects the oral mucosa. [Lichens are primitive plants and the term planus is Latin for flat]  It is an immunologically mediated mucocutaneous disorder.  A variety of medications induce lesions that are clinically similar to lichen planus known as lichenoid mucositis Lichen planus Clinical features    Most common clinical type is the reticular type, usually occurs bilaterly on the buccal mucosa Oral lesions are characterized by fine lacelike network of white lines (Wickham striae) Also, the lateral and dorsal tongue, the gingivae, the palate, and vermilion border may be involved Lichen planus Histopathological features Rete ridges are pointed showing saw tooth shape Intense band like lymphocytic infiltrate hyperkeratosis Degenerated keratinocytes may be seen in the interface between epithelium and connective tissue have been termed Civatte bodies. Lichen planus Histopathological features  The histopathologic features of lichen planus are characteristic but may not be specific, because other conditions, such as lichenoid drug reaction, lichenoid amalgam reaction, oral graft-versus-host disease (GVHD) and lupus erythematosus (LE) may also show a similar histopathologic pattern. Lupus Erythematosus (LE) LE is a classic example of an immunologically mediated condition. There are 3 forms: Systemic LE (SLE) is a serious multisystem disease with a variety of cutaneous and oral manifestations. Chronic cutaneous LE (CCLE) affects the skin and oral mucosa, and the prognosis is good. Subacute cutaneous LE (SCLE) is third form of the disease, which has clinical features intermediate between those of SLE and CCLE. Lupus Erythematosus (LE) Oral manifestations Lesions may appear as lichenoid areas Or show varying degrees of ulceration, pain, erythema, and hyperkeratosis They usually affect the palate, buccal mucosa, and gingivae. Involvement of the vermilion zone of the lower lip may be seen (lupus cheilitis) Lupus Erythematosus (LE) Oral manifestations Other oral complaints include xerostomia, stomatodynia, candidiasis, periodontal disease, and dysgeusia Confirming the diagnosis of SLE depends on both clinical and laboratory findings Lupus Erythematosus (LE) Histopathological Features Hyperkeratosis Alternating atrophy and thickening of the spinous cell layer Degeneration of the basal cell layer Subepithelial lymphocytic infiltration These features may also be seen in oral lichen planus: however, LE can be distinguished by the presence of patchy deposits on staining by PAS stain Miscellaneous lesions Fordyce’s granules Geographic tongue Hairy tongue Geographic tongue (glossitis areata exfoliativa, erythema migrans, benign migratory glossitis) It is a condition of unknown etiology Some investigators believe that it represents the oral manifestation of psoriasis (common chronic disease characterized by patches of abnormal red, itchy & scaly skin) Geographic tongue Clinical features Each patch has a life history of about one week after which it disappears, & reappear at another area It begins as a circular or oval smooth red areas with elevated yellowish border on anterior 2/3 of tongue Filiform papillae disappear & fungiform are retained It usually occur on the anterior 2/3 of the tongue but mucosal sites other than the tongue may be involved The elevated yellowish border is due to hyperplasia of the filiform papillae The smooth red areas are due to atrophy of filiform papillae Geographic tongue Histopathological features Hyperparakeratosis, acanthosis, and elongation of the epithelial rete ridges  Collections of neutrophils (Munro abscesses) within the epithelium Intense neutrophil and lymphocytic infiltrate in the underlying connective tissue [The intense neutrophilic infiltrate may be responsible for the destruction of the superficial portion of the epithelium, thus producing an atrophic, reddened mucosa as the lesion progresses] Geographic tongue Treatment & prognosis The condition is completely benign No treatment is required Patients may complain of tenderness or a burning sensation with hot or spicy foods In such cases, topical corticosteroids will be helpful Hairy Tongue It is characterized by extensive proliferation of the filiform papillae & marked accumulation of keratin on of the dorsal surface of the tongue resulting in hair like appearance The condition represents an increase in decrease in normal OR keratin keratin production desquamation Hairy Tongue It varies in colour from yellowish to various shades of brown or black. The colour is due to: extrinsic factor from OR foods or drugs chromogenic bacteria. Clinical significance Bad taste Halitosis Gagging sensation Hairy Tongue Histopathology Elongation and marked hyperkeratosis of the filiform papillae Treatment: brushing the tongue mildly by the toothbrush or the use of commercial “tongue scrapers” Fordyce granules  Are sebaceous glands occurring on the oral mucosa which normally develop in relation to hair follicles  They are considered as an ectopic condition Sebaceous glands in skin Fordyce granules Clinical appearance The spots are single or multiple pinhead-sized papules Most frequently in the buccal mucosa in the molar region, on the lips, just behind the oral commissure The overlying mucosa may be smooth or may be slightly elevated. Fordyce granules Histopathology Presence of sebaceous follicles, either lying free beneath the epithelial surface, or related to the surface directly or through a well formed duct which may be blocked with keratin. They are not, related to hair follicles. Key points  leukoedema disappears on stretching the mucosa, and requires no treatment  Oral hairy leukoplakia is caused by Epstein Barr virus and commonly seen in HIV patients  Candidiasis is the most common oral fungal infection in humans, caused by Candida albicans, commonly appera as white patch that can be rubbed off  lichen planus is commonly seen as fine lacelike network of white lines (Wickham striae) bilaterly on the buccal mucosa A variety of medications induce lesions that are clinically similar to lichen planus known as lichenoid mucositis  Geographic tongue represents the oral manifestation of psoriasis Fordyce granule is an ectopic condition due to presence of sebaceous glands in mucous membrane Aims: The aim of this lecture is to detail the histopathology of causes of white patches of an infectious and/or immunological aetiology Objectives: On completion of this lecture, the student should be able to: Understand the histopathological aspects of oral lichen planus and related disease, oral hairy leukoplakia, lupus erythematosus and chronic hyperplastic candidiasis Understand the use of immunohistochemistry for the diagnosis of oral hairy leukoplakia Reading material: Students are advised to review any relevant teaching provided in the first year. In addition, they are advised to read relevant sections of the following texts: Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp 53-57 Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 261-269 Gandolfo S, Scully C, Carrozzo M. Oral Medicine, Churchill Livingston, 2006 pp 49, 101, 108 Felix D, Luker J, Scully C. Oral Medicine: Update for the Dental Team, Dental Update Books 2015 pp 18, 41-45 Thank you

Use Quizgecko on...
Browser
Browser