White Lesions Sumamry Not another white lesion! This lesson will help you differentiate between the many white lesions you will come across. Overview White lesions result from: Thickened keratin Necrotic epithelium Epithelial hyperplasia, Intracellular epithelial oedema Reduced vascularity of subjacent connective tissue. White/ yellow-white lesions may be due to fibrinous exudate A biopsy is required for any persistent and unexplained oral white patch in order to exclude cancer Key words¹ Keratosis Keratinisation of epithelium that is not usually keratinised The superficial cells of the stratified squamous epithelium are keratinised, Orthokeratosis anucleated and flattened More common in the oral mucosa. Superficial cells of the epithelium are ParakeratosisReviseDental.comkeratinised, flattened and have pyknotic nuclei. The granular cell layer isn't visible An abnormal quantity of keratin within the outer layer of the stratified squamous Hyperkeratosis epithelium that is usually keratinised Hyperplasia of stratum spinosum - prickle cell layer Acanthosis Increased thickness of epithelium Large and broad rete ridges Oedema Excess of watery fluid collecting in cells, tissues or cavities Decreased thickness of epithelium Atrophy Loss of rete ridges usually occur Dysplasia Mass of epithelial cells which are atypical Small red/ purple spots which are caused by bleeding into the oral mucosa - also Petechiae known as haemorrhage Similar to petechiae as they are caused by intradermal capillary bleeding Purpura Larger than petechiae and usually raised Differential diagnosis of a white lesion Hereditory Benign Intraepithelial Dyskeratosis (Witkop's disease) Dyskeratosis Congenita Frictional Keratosis Nicotinic Stomatitis Hairy leukoplakia Chemical burn Lichenoid reaction Squamous cell carcinoma - For information, please find in the Oral Cancer lesson Lichen planus Lupus erythematous Leukoplakia Proliferative Verrucous Leukoplakia Skin graft Pyostomatitis vegetans Submucous Fibrosis Geographic tongue (Benign Migratory Glossitis) - For information, please find in the Normal Variations of the Oral Cavity lesson Leukoedema - For information, please find in the Normal Variations of the Oral Cavity lesson White Sponge Naevus - For information, please find in the Normal Variations of the Oral Cavity lesson Pseudomembranous Candidiasis -For information, please find in the Fungal Infections and the Oral Cavity lesson Chronic Hyperplastic Candidiasis - For information, please find in the Fungal Infections and the Oral CavityReviseDental.com lesson Hereditary benign intraepithelial dyskeratosis (Witkop Disease) Aetiology and epidemiology Rare, autosomal dominant inheritance Early onset (within first year of life) Pathophysiology Three alleles for two linked markers exist on 4q35 chromosome Clinical features Asymptomatic, soft white folds and plaques of spongy mucosa On most oral surfaces apart from dorsum of the tongue Additionally: Bulbar conjunctivitis, conjunctival plaques at the corneal limbus Histopathology Epithelial hyperplasia and acanthosis are present within intracellular oedema Enlarged hyaline keratinocytes within superficial half of epithelium Diagnosis Biopsy usually to confirm diagnosis Management No treatment, condition is self-limiting and benign Dyskeratosis congenita Aetiology and epidemiology X-linked and autosomal, both dominant and recessive forms are recognised Patients undergo premature aging and have a predisposition to malignancy Manifestations appear in first 10 years of life Pathophysiology X-linked dyskeratosis encodes a protein called dyskerin, which is abnormal Clinical features Mucosal erosions and leukoplakia may develop ApproximatelyReviseDental.com 30% of the leukoplakia progress to oral cancer in 10-30 years Reticulated skin hyperpigmentation of the upper chest and dysplastic nail changes are characteristic Rapidly progressing periodontal disease, thrombocytopenia and aplastic anaemia may also be seen Histopathology Hyperkeratosis with epithelial atrophy Varying severity of dysplasia Diagnosis History, clinical presentation and biopsy Management Careful observation and biopsy of suspicious areas to detect any malignant change Dental implications Rapidly progressing periodontal disease Focal (Frictional) hyperkeratosis Aetiology and epidemiology Chronic rubbing or friction against oral mucosa Pathophysiology Due to irritation, a protective hyperkeratotic white lesions forms: analogous to a callous on the skin Clinical features Depending on the cause, may be well-demarcated or diffused Homogeneously white, may have a thickened corrugated appearance Lips, lateral margins of the tongue, buccal mucosa along the occlusal line and edentulous alveolar ridges are mostly affected Histopathology Hyperkeratosis Thickening of granular cell layer A few chronic inflammatory cells may be seen in the subjacent connective tissue Diagnosis History, clinical presentation and biopsy if not cause known Management Removal of the cause Smokeless tobacco-associatedReviseDental.com lesions Aetiology and epidemiology Snuff (particulate, finely divided, or shredded tobacco) appears to much more likely cause oral lesions than chewing tobacco Tobacco-containing preparations are generally of a higher pH (alkaline) and often mixed with other ingredients e.g. betel nut, lime, camphor, spice Pathophysiology Oral mucosa responds with inflammation and keratosis Altered cell signalling and subsequent cell damage have been demonstrated Dysplastic changes may follow with a risk of malignant change Clinical features White asymptomatic lesions develop in the immediate area where the tobacco was placed, most commonly mucobuccal fold mandible Mucosa develops a granular to wrinkled appearance Advanced cases, a heavy folded character may be seen Histopathology Slight to moderate parakeratosis Superficial epithelium may demonstrate vacuolisation or oedema Slight to moderate chronic inflammatory cell infiltrate Epithelial dysplasia may develop Diagnosis Clinical presentation, history Biopsy not necessarily required unless lesions persistent after discontinuation of smokeless tobacco use Management Discontinuation of smokeless tobacco use Dental implications These patients will have acceleration of periodontal disease Nicotinic stomatitis Aetiology and epidemiology Pipe and cigar smoking Pathophysiology Inflammation surrounding the minor salivary gland excretory ducts Clinical features Initial erythematous change followed by keratinisation of the palate Red dots surrounded by white keratotic rings appear Histopathology Epithelial hyperplasia, hyperkeratinization ChronicReviseDental.com inflammatory cell infiltration of sub epithelial connective tissue Excretory ducts show squamous metaplasia Diagnosis History and clinical presentation Management Smoking cessation Smokers Palate Hairy leukoplakia Aetiology and epidemiology 20% of patients with hairy leukoplakia have AIDS Pathophysiology HasReviseDental.com been associated with Epstein-Barr Virus Candidal infections co-exist in approximately half of the cases Clinical features Unilateral or bilateral on the margins of the tongue but can develop at other sites e.g. buccal and labial mcuosa Well-demarcated white lesion Varies from a flat and plaque-like to a papillary/ filiform or corrugated lesion Histopathology Viral inclusions or peripheral displacement of chromatin with a resultant smudgy nucleus Marked hyperparakeratotic surface with irregularities and ridges C.albicans hyphae often seen extending into the superficial epithelium Cells show ballooning degradation and perinuclear clearing in the spinous cell layer Very low numbers of subepithelial inflammatory cells Diagnosis Biopsy can be taken for histopathological examination however it is preferable to substantiate the diagnosis with electron microscopy or DNA-hybridisation Management Lesion responds to antiviral therapy and does not respond to antifungal therapy Chemical burn Aetiology and epidemiology Commonly caused due to the application of aspirin to the site of a toothache or on the fitting surface of the denture Pathophysiology The low pH of aspirin causes erythema and tissue necrosis Clinical features White, friable slough that can be easily removed leaving a bed of erythema and ulceration Histopathology Areas of focal coagulative necrosis of the epithelium Ulceration Intra and extra-cellular oedema Sub-epithelial acute inflammatory infiltrate Diagnosis Clinical examination and history. No biopsy required Management Remove application of chemical Use of antiseptic mouthwash to keep mouth clean Dental implications AssessmentReviseDental.com of toothache if present Lichenoid reaction Aetiology and epidemiology Caused typically by a restorative dental material, most commonly amalgam or an adverse reaction from systemic drug therapy e.g. NSAIDs, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, oral hypoglycaemic agents and antimalarials Pathophysiology Delayed-type Hypersensitivity reaction to a component within the dental material e.g. mercury within amalgam Clinical features Asymmetry and involvement of the palate distinguish it from lichen planus Reaction will be adjacent to the restoration is related to a restorative material Histopathology Nearly identical to lichen planus Acanthosis and inflammatory exocytosis, with perivascular inflammation Inflammation generally extends deeper into the lamina propria than oral lichen planus Diagnosis Histopathological examination from a biopsy can help suggest lichenoid reaction over lichen