<div> <div style="background-color: #424242; padding: 20px;"> <p style="color: white; font-size: 2em;">**PHYSICAL &**</p> <p style="color: white; font-size: 2em;">**CHEMICAL**</p> <p style="color: white; font-size: 2em;">**INJURIES**</p> <p style="color: white; font-size: 1em;">Dr Lalima Tiwari</p> <p style="color: white; font-size: 1em;">Oral Medicine Specialist</p> <p style="color: white; font-size: 1em;">Clinical Senior Lecturer</p> </div> <img src="image.png" alt="Abstract black and white line graphic background."> </div>  Presented by: - **Dr. Lalima Tiwari** - Oral Medicine Specialist - Clinical Senior Lecturer A dark gray rectangular box with white text displaying the title "PHYSICAL & CHEMICAL INJURIES" and the presenter's details, Dr Lalima Tiwari, Oral Medicine Specialist and Clinical Senior Lecturer. The background features a black and white abstract pattern of wavy horizontal lines. Learning objectives **1. Describe the repertoire of physical and chemical injuries that can affect the oral hard and soft tissues.** **2. Describe the repertoire of responses of oral soft tissues to trauma.** **3. Discuss the aetiology, pathogenesis, the clinical and histopathologic features and the diagnosis and treatment of:** * Frictional keratosis * Linea alba * Morsicatio buccarum * Traumatic ulceration * Burns **4. Discuss exfoliative cheilitis.** **5. Discuss the aetiology, pathogenesis, the clinical and histopathologic features and the diagnosis and treatment of:** * Amalgam tattoos and other localized exogenous pigmentations * Smoker’s melanosis * Drug related discoloration of oral mucosa **6. Explain oral complication of radiation therapy.** 1. Describe the repertoire of physical and chemical injuries that can affect the oral hard and soft tissues. 2. Describe the repertoire of responses of oral soft tissues to trauma. 3. Discuss the aetiology, pathogenesis, the clinical and histopathologic features and the diagnosis and treatment of: - Frictional keratosis - Linea alba - Morsicatio buccarum - Traumatic ulceration - Burns 4. Discuss exfoliative cheilitis. 5. Discuss the aetiology, pathogenesis, the clinical and histopathologic features and the diagnosis and treatment of: - Amalgam tattoos and other localized exogenous pigmentations - Smoker’s melanosis - Drug related discoloration of oral mucosa 6. Explain oral complication of radiation therapy.  1. Describe the repertoire of physical and chemical injuries that can affect the oral hard and soft tissues. 2. Describe the repertoire of responses of oral soft tissues to trauma. 3. Discuss the aetiology, pathogenesis, the clinical and histopathologic features and the diagnosis and treatment of: - Frictional keratosis - Linea alba - Morsicatio buccarum - Traumatic ulceration - Burns 4. Discuss exfoliative cheilitis. 5. Discuss the aetiology, pathogenesis, the clinical and histopathologic features and the diagnosis and treatment of: - Amalgam tattoos and other localized exogenous pigmentations - Smoker’s melanosis - Drug related discoloration of oral mucosa 6. Explain oral complication of radiation therapy. The image displays a circular diagram illustrating various types of physical and chemical injuries. At the center is a blue circle labeled "Physical and chemical injuries," with six surrounding teal arrows pointing inward, each labeled with a specific injury type: Thermal injury, Acidic and alkaline products, Traumatic occlusion, Sharp occlusal anatomy, Medications, and Radiation induced. The diagram visually categorizes these injury types as contributing factors to the central concept. # **Frictional keratosis** * **Represents increased keratin production in response to $\text{chronic mechanical irritation}$** Frictional keratosis represents increased keratin production in response to chronic mechanical irritation. 1. **Benign alveolar ridge keratosis on retromolar pad, present bilaterally** 2. **Benign alveolar ridge keratosis of previously extracted teeth** Image courtesy of Al masyad A, Li C, Woo SB; 2020  #### Clinical Variations 1. Benign alveolar ridge keratosis on retromolar pad, present bilaterally 2. Benign alveolar ridge keratosis of previously extracted teeth Three intraoral photographs showing benign alveolar ridge keratosis on the retromolar pad, present bilaterally, and keratosis in the area of previously extracted teeth. The images highlight the affected areas with red circles, showing white or pale lesions on the gingival tissue adjacent to dental prostheses and edentulous sites. Image courtesy of Van der Waal, 2015   *(Content consists of clinical imagery documentation)* A close-up photo showing frictional keratosis on the gingiva, characterized by a pink, slightly raised lesion with a smooth surface adjacent to the teeth. A clinical photo depicting verrucous leukoplakia on the gingiva, featuring a white, warty lesion with a rough texture on the gum tissue. Frictional keratosis on left lateral tongue Non-homogenous leukoplakia on left lateral tongue Image courtesy of Yang S, Lee Y, Chang L, Luo C. 2021   #### Differential Observations - Frictional keratosis on left lateral tongue - Non-homogenous leukoplakia on left lateral tongue Close-up photo showing frictional keratosis on the left lateral tongue, characterized by a rough, white lesion with a textured surface, located near the teeth and under the tongue. Close-up photo of non-homogenous leukoplakia on the left lateral tongue, displaying an irregular white patch with a slightly raised and uneven surface, situated on the tongue's lateral aspect. **Histopathology** * Orthokeratosis or hyperparakeratosis (1) * Shaggy keratin surface * Prominent granular cell (2) * Intracellular oedema – ballooned cells in spinous layer (3) * Acanthosis (4) * Lack of inflammation in superficial connective tissue (5) * Features of dysplasia absent Image courtesy of Muller S, 2019  #### Microscopic Features - Orthokeratosis or hyperparakeratosis - Shaggy keratin surface - Prominent granular cell layer - Intracellular oedema – ballooned cells in spinous layer - Acanthosis - Lack of inflammation in superficial connective tissue - Features of dysplasia absent A histopathological image showing a cross-section of skin tissue with various labeled features. The image displays orthokeratosis or hyperparakeratosis (1) at the surface, prominent granular cells (2), intracellular edema with ballooned cells in the spinous layer (3), acanthosis (4), and a lack of inflammation in the superficial connective tissue (5). The tissue is stained to highlight cellular structures, with the labels corresponding to the text on the left. Frictional keratosis | Diagnosis: | | | :--- | :--- | | | **• Need to distinguish from other oral potentially malignant disorders** | | | • History: Is the patient aware of trauma? Any indication of possible mechanical trauma? Can the trauma be addressed? | | | • Clinical: Appearance. Address the trauma – eliminate after source of irritation eliminated | | | • Investigations: Biopsy of suspicious lesions (persistent) or when limited clinical information available| | Treatment: | | | :--- | :--- | | | • Address the trauma | | | • Review in 2 weeks, lesion eliminated | | | • Chronic irritation may require habit awareness techniques | | | • Lesions do not undergo malignant transformation |  #### Diagnostic Process - **Differential Diagnosis:** Need to distinguish from other oral potentially malignant disorders. - **History:** Determine if the patient is aware of trauma or if there is any indication of mechanical trauma that can be addressed. - **Clinical Assessment:** Evaluate appearance; eliminate the source of irritation and monitor for resolution. - **Investigations:** Perform a biopsy for persistent suspicious lesions or when clinical information is limited. #### Treatment Protocols - Address and eliminate the source of trauma. - Review the patient in 2 weeks to ensure the lesion is eliminated. - Chronic irritation may require habit awareness techniques. - Note: These lesions do not undergo malignant transformation. A two-column table detailing the diagnosis and treatment of frictional keratosis. The 'Diagnosis' section lists criteria such as distinguishing from other oral potentially malignant disorders, assessing history and clinical appearance, and considering biopsy for suspicious lesions. The 'Treatment' section outlines addressing trauma, reviewing in two weeks, using habit awareness techniques for chronic irritation, and notes that lesions do not undergo malignant transformation. <img src="image_of_buccal_mucosa_showing_linea_alba.jpg"> **Linea Alba** * "white line" * Common alteration of the buccal mucosa associated with pressure, irritation or sucking trauma from teeth * Due to parafunctional habits: cheek biting, clenching, teeth grinding * Asymptomatic, horizontal linear white keratotic line/ridge on the buccal mucosa approximating the occlusal plane (often bilateral) * Can be seen with scalloping of lateral border of tongue $\to$ associated with bruxism * Often mistaken for leukoplakia * Histopathology: hyperkeratosis overlying normal oral mucosa, on occasion intracellular oedema * Usually clinical diagnosis * No treatment required, no complications documented with it's development * Spontaneous regression may occur Image courtesy of Neville B, Damm D., 2016  #### Clinical Characteristics - Also known as "white line." - Common alteration of the buccal mucosa associated with pressure, irritation, or sucking trauma from teeth. - Etiology: Parafunctional habits such as cheek biting, clenching, or teeth grinding. - Presentation: Asymptomatic, horizontal linear white keratotic line/ridge on the buccal mucosa approximating the occlusal plane (often bilateral). - Associated Findings: Can be seen with scalloping of the lateral border of the tongue, often associated with bruxism. - Differential: Often mistaken for leukoplakia. #### Histopathology and Management - **Histopathology:** Hyperkeratosis overlying normal oral mucosa; occasional intracellular oedema. - **Diagnosis:** Usually a clinical diagnosis. - **Management:** No treatment required; no complications documented. Spontaneous regression may occur. A close-up intraoral photograph showing a horizontal white keratotic line on the buccal mucosa, characteristic of linea alba. The image also displays a tooth with a dental restoration and the surrounding gingival tissue. # **Morsicatio buccarum** * Chronic bite keratosis * Benign, trauma-induced lesion of the oral mucosa * Aetiology: chronic trauma to non-keratinized mucosa * Parafunctional habits; nibbling, sucking on mucosa, rubbing along denture hardware/orthodontic appliances * Pathogenesis: parakeratosis and benign epithelial hyperplasia #### Overview and Etiology - Also known as chronic bite keratosis. - Benign, trauma-induced lesion of the oral mucosa. - **Aetiology:** Chronic trauma to non-keratinized mucosa. - Parafunctional habits: nibbling, sucking on mucosa, rubbing along denture hardware or orthodontic appliances. - **Pathogenesis:** Parakeratosis and benign epithelial hyperplasia. **a** Irregular, shaggy macerated appearance of the left buccal mucosa typical for cheek biting (morsicatio mucosae). **b** Photomicrograph showing marked hyperparakeratosis with a shaggy appearance with surface fissures and clefts. The epithelium is acanthotic with ballooned cells. Bacterial colonies are present on the keratin surface without an inflammatory response Image courtesy of Muller S, 2019   #### Clinical and Microscopic Appearance - **Clinical:** Irregular, shaggy macerated appearance of the buccal mucosa typical for cheek biting (morsicatio mucosae). - **Histopathology:** - Marked hyperparakeratosis with a shaggy appearance. - Surface fissures and clefts. - Acanthotic epithelium with ballooned cells. - Bacterial colonies present on the keratin surface without an inflammatory response. A clinical photograph showing an irregular, shaggy macerated appearance of the left buccal mucosa, typical for cheek biting (morsicatio mucosae). A photomicrograph displaying marked hyperparakeratosis with a shaggy appearance, surface fissures, and clefts. The epithelium is acanthotic with ballooned cells, and bacterial colonies are present on the keratin surface without an inflammatory response. # Traumatic ulceration * Reactive oral ulcers: trauma affecting mucosal lining of mouth * Self-inflicted * Mechanical trauma - sharp margins of teeth, prosthesis, denture flange, self-biting, factitious injuries * Ulcer: complete loss of epithelium which exposes the underlying connective tissues * Clinical presentation: * Mechanical: areas or erythema surrounding a central removable, yellow fibrinopurulent membrane * Can develop a rolled white border of hyperkeratosis immediately adjacent the area of ulceration * Can affect any oral mucosal surface - tongue, lips, buccal mucosa * Riga-Fede disease: 1 week - 12 month old children * Associated with natal teeth * Anterior ventral surface of tongue most common site of involvement * Can be associated with other neurologic conditions including cerebral palsy, Tourette syndrome * Diagnosis: * History * Clinical presentation * Identify trauma * Resolve spontaneously once causative factor has been identified and removed (10-14 days) #### Overview and Clinical Presentation - Reactive oral ulcers caused by trauma affecting the mucosal lining. - **Etiology:** - Self-inflicted or mechanical trauma (sharp tooth margins, prostheses, denture flanges, self-biting, factitious injuries). - **Definition:** Complete loss of epithelium exposing underlying connective tissues. - **Clinical Features:** - Areas of erythema surrounding a central removable, yellow fibrinopurulent membrane. - Possible rolled white border of hyperkeratosis adjacent to the ulcer. - Can affect any surface: tongue, lips, buccal mucosa. - **Riga-Fede Disease:** - Occurs in children (1 week to 12 months old). - Associated with natal teeth; most common on the anterior ventral surface of the tongue. - May be associated with neurologic conditions (e.g., cerebral palsy, Tourette syndrome). #### Diagnosis - Based on history and clinical presentation. - Identify the source of trauma. - Lesions should resolve spontaneously within 10-14 days once the causative factor is removed. Normal mucous membrane | Epithelium | |---| | Lamina propria | **(a) external trauma of different nature (mechanical, thermal, chemical, radiant),** **Mucosal ulcer** Complete breach of epithelium Image courtesy of Contemporary Oral Medicine, 2019   #### Structural Changes - **Normal Mucous Membrane:** Comprised of epithelium and lamina propria. - **External Trauma:** Can be mechanical, thermal, chemical, or radiant in nature. - **Mucosal Ulcer:** Defined by a complete breach of the epithelium. A labeled diagram showing a normal mucous membrane with the epithelium and lamina propria clearly marked, serving as a reference for the subsequent illustrations. A flowchart diagram illustrating the progression from a normal mucous membrane to a mucosal ulcer, with intermediate stages showing external trauma and a complete breach of the epithelium, labeled as (a), (b), (c), and (d). Image courtesy of Contemporary Oral Medicine, 2019   *(Content consists of illustrative diagrams of mucosal breaches)* A clinical photograph showing a traumatic ulcer on the tongue caused by a sharp tooth, with the surrounding tissue appearing inflamed and the ulcer presenting as a well-defined, pale lesion. A clinical photograph depicting oral squamous cell carcinoma on the tongue, characterized by an irregular, ulcerated lesion with a raised border and necrotic tissue, indicating malignancy. Fig. 8-8 **Riga-Fede Disease.** Newborn with traumatic ulceration of anterior ventral surface of the tongue. Mucosal damage occurred from contact of tongue with adjacent tooth during breastfeeding. Image courtesy of Neville B, Damm D., 2016  #### Riga-Fede Disease Case Example - Observed in newborns as traumatic ulceration of the anterior ventral surface of the tongue. - Mucosal damage typically occurs from contact of the tongue with adjacent teeth during breastfeeding. A close-up photograph of a newborn's mouth showing a traumatic ulceration on the anterior ventral surface of the tongue, identified as Riga-Fede Disease. The mucosal damage is caused by contact with an adjacent tooth during breastfeeding, as indicated by the caption. # **Histopathology** Figure 1. Low-power microscopic image shows a traumatic ulcer of the lateral tongue. A hypertrophic squamous epithelium (arrows) is immediately adjacent to the ulcer, showing an abrupt transition. Note the extension of the inflammatory infiltrate into the muscle at the bottom of the photo. Figure 2. Intermediate-power microscopic view demonstrates the fibrinopurulent exudate and very abrupt "traumatic" edge to the epithelium. Inflammation fills the stroma. Figure 3. Higher-power view shows the granulation tissue with a mixed inflammatory infiltrate, including eosinophils with associated vessels. Image courtesy of Thompson L., 90    #### Microscopic Observations - **Low-power view:** Shows a traumatic ulcer (e.g., lateral tongue) with hypertrophic squamous epithelium immediately adjacent to the ulcer, showing an abrupt transition. Inflammatory infiltrate may extend into underlying muscle. - **Intermediate-power view:** Demonstrates fibrinopurulent exudate and an abrupt "traumatic" epithelial edge. Inflammation fills the stroma. - **High-power view:** Shows granulation tissue with a mixed inflammatory infiltrate, including eosinophils and associated vessels. Low-power microscopic image showing a traumatic ulcer of the lateral tongue with hypertrophic squamous epithelium adjacent to the ulcer, indicating an abrupt transition and inflammatory infiltrate extending into the muscle. Intermediate-power microscopic view demonstrating fibrinopurulent exudate and a very abrupt 'traumatic' edge to the epithelium, with inflammation filling the stroma. Higher-power view showing granulation tissue with a mixed inflammatory infiltrate, including eosinophils and associated vessels. Traumatic Ulcer * Management: * Identify trauma * Resolve spontaneously once causative factor has been identified and removed (10-14 days) * Chlorhexidine gel, mouthrinse * Lignocaine gel * Antinflammatory mouthrinse (Difflam) * **Review after treatment, if lesion persists, further investigations are warranted including biopsy to rule out malignancy** * Unique chronic traumatic ulcer: Traumatic ulcerative granuloma with stromal eosinophilia (TUGSE) * Deep pseudoinvasive inflammatory reaction that is slow to resolve #### Clinical Management - Identify and remove the source of trauma. - Lesions typically resolve spontaneously within 10-14 days after removal of the cause. - **Supportive Therapies:** - Chlorhexidine gel or mouthrinse. - Lignocaine gel for pain. - Anti-inflammatory mouthrinse (e.g., Difflam). - **Follow-up:** Review after treatment; if the lesion persists, further investigations (including biopsy) are required to rule out malignancy. #### Chronic Variants - **Traumatic Ulcerative Granuloma with Stromal Eosinophilia (TUGSE):** A unique chronic traumatic ulcer characterized by a deep pseudoinvasive inflammatory reaction that is slow to resolve. # Burns * **Thermal burns:** * Injury with extreme temperatures * Hot foods/drinks, microwavable foods, * Cryogenic burns from very cold foods, * E-cigarette explosions * Injury of tissue, result in sloughing of epithelium and exposure of highly vascularized connective tissue = accounts for erythematous appearance <img src="image.png" alt="Intraoral photograph showing a traumatic ulcer on the gingiva or buccal mucosa, likely caused by a thermal burn from pizza, as indicated by the caption."> Traumatic ulcer from thermal burn (pizza) Jadhav et al., 2022  Oral burns result from tissue injury that causes sloughing of the epithelium and exposure of vascularized connective tissue, leading to an erythematous appearance. #### Etiology and Effects - **Causes:** Hot foods/drinks, microwavable foods, cryogenic burns (very cold foods), and e-cigarette explosions. - **Presentation:** Often presents as a traumatic ulcer (e.g., on the gingiva or buccal mucosa) following contact with extreme temperatures. Intraoral photograph showing a traumatic ulcer on the gingiva or buccal mucosa, likely caused by a thermal burn from pizza, as indicated by the caption. The image displays a red, inflamed area with exposed tissue, consistent with a thermal injury. # **Burns** * **Chemical Burns:** * Acids or alkaline nature * Acids: Bind to epithelium and denature the proteins of the cells = coagulative necrosis of the cells $\to$ coagulum limits the penetration of the acid * Alkaline substance: Dissolve protein and collagen leading to saponification of fatty tissue and liquefactive necrosis $\to$ does, not limit tissue penetration = alkaline substances potential to cause more extensive damage than acids = deeper penetration of chemical * Prolonged contact can cause systemic effects due to absorption Fedele S. 2010: #### Mechanisms of Injury - **Acids:** Bind to epithelium and denature proteins, causing coagulative necrosis. The resulting coagulum limits further acid penetration. - **Alkaline Substances:** Dissolve protein and collagen, leading to saponification of fatty tissue and liquefactive necrosis. These do not limit tissue penetration and can cause more extensive, deeper damage than acids. - **Systemic Effects:** Prolonged contact may lead to systemic absorption of the chemical agent. Table 1 Reported toxic agents linked to chemical oral burns From: Fedele S. 2010: **Traumatic chemical oral ulceration: a case report and review of the literature** | CHEMICAL TOXIC SUBSTANCES | UTILISATION/COMM | | :--- | :--- | | **DENTAL MATERIALS**| | | Cavity varnish$^{6}$ | Restorative dental material (liquid/gel) | | Dentine bonding agent$^{7}$ | Restorative dental material (liquid) | | Phosphoric acid etching solutions$^{8}$ | Restorative dental material (gel/liquid) | | Iodine$^{9}$ | Antiseptic (liquid) | | Phenol (carbolic acid)$^{9}$ | Antiseptic (liquid) | | Trichloroacetic acid$^{10}$ | Astringent for gingival retraction (liquid) | | Ferric sulphate$^{11}$ | Astringent for gingival retraction (liquid) | | Chromic acid$^{12}$ | Antiseptic (therapeutic agent) (liquid) | | Hydrofluoric acid$^{13,14}$ | Porcelain and metal etching (liquid) | | Sodium hypochlorite$^{15,16,17,18,19,20}$ | Root canal irrigant (liquid) | | Calcium hydroxide$^{21,22}$ | Used in restorative dentistry (cement) | | Formocresol$^{21,12}$ | Endodontic treatments (pulp medicament) (liquid) | | Paraformaldehyde$^{9}$ | Devitalising agents (liquid) | | Arsenic$^{23}$ | Devitalising agents (paste) | | | **MEDICATIONS** | | Chlorpromazine$^{15}$ | Antipsychotic drug | | Promazine$^{15}$ | Antipsychotic drug | | Aspirin$^{24,25,26,27,28,29,30,31,32,33}$ | Non opioid analgesic | | Alendronate$^{34,35}$ | Bisphosphonate | | | **NON-PHARMACEUTICAL SUBSTANCES** | | Mouthwashes$^{36,37,38,39,40}$ | Antiseptic oral cavity (liquid) | | Hydrogen peroxide$^{31,32,41,42,43}$ | Antiseptic (liquid) | | Gasoline$^{15}$ | Petroleum - derived mixture used ad fuel (liquid) | | Rubbing alcohol$^{15}$ | 68.5-71.5% vol/vol of absolute alcohol (liquid) | | Battery acid$^{44}$ | Sulphuric acid and water (liquid) | | Minard's liniment$^{44}$ | Relief from pain (liquid) | | Arrack$^{45}$ | Strong distilled spirit (liquid) | | Silver nitrate$^{46}$ | Chemical cauterisation | | Denture cleansers$^{47,48}$ | Substances for cleaning dentures (tablet) | | Fresh fruit and fruit juices$^{49,50}$ | Liquid | | Garlic$^{51}$ | Culinary and medicinal uses (vegetable) | | | **DRUGS** | | Cocaine$^{2,3,4}$ | Recreational drug | | MDMA$^{52}$ | Recreational drug | | Amphetamine$^{53}$ | Recreational drug |  #### Toxic Agents Linked to Chemical Burns **Dental Materials** - Cavity varnish, Dentine bonding agents, Phosphoric acid etching solutions - Iodine, Phenol (carbolic acid), Chromic acid (antiseptics) - Trichloroacetic acid, Ferric sulphate (astringents) - Hydrofluoric acid (porcelain/metal etching) - Sodium hypochlorite (root canal irrigant) - Calcium hydroxide, Formocresol, Paraformaldehyde, Arsenic (restorative/endodontic agents) **Medications** - Antipsychotics: Chlorpromazine, Promazine - Analgesics: Aspirin - Bisphosphonates: Alendronate **Non-Pharmaceutical Substances** - Mouthwashes, Hydrogen peroxide - Gasoline, Rubbing alcohol, Battery acid - Minard's liniment, Arrack (distilled spirit) - Silver nitrate (cauterization) - Denture cleansers, Fresh fruit/juices, Garlic **Recreational Drugs** - Cocaine, MDMA, Amphetamine Table 1 titled 'Reported toxic agents linked to chemical oral burns' from Fedele S. 2010, listing various chemical toxic substances categorized under dental materials, medications, non-pharmaceutical substances, and drugs, with their utilization or comments. | | | |---|---| | **Aspirin induced chemical burn noted on the buccal mucosa, with noted residual aspirin present on teeth** Image from: McKinney R et al. 2022 | **Extensive ulceration of the palate and lateral aspects of tongue secondary to deliberate application of sulphuric acid** Image from: Fedele S et al., 2010 |   #### Clinical Examples - **Aspirin Burn:** Noted on the buccal mucosa, often with residual aspirin tablets present on adjacent teeth. - **Sulphuric Acid Burn:** Extensive ulceration of the palate and lateral aspects of the tongue, often associated with deliberate application. A photo showing an aspirin-induced chemical burn on the buccal mucosa, with residual aspirin visible on the teeth. The image is from McKinney R et al., 2022. A photo depicting extensive ulceration of the palate and lateral aspects of the tongue due to deliberate application of sulphuric acid. The image is from Fedele S et al., 2010. # Burns <table> <tr> <td style="background-color: #36598E; color: white;">**Diagnosis:**</td> <td style="background-color: #36598E; color: white;">**Histopathology:**</td> <td style="background-color: #36598E; color: white;">**Treatment:**</td> </tr> <tr> <td> <ul> <li>Clinical history and features</li> <li>History demonstrating chronological correspondence between potential causative agent and onset of ulceration aids diagnosis</li> <li>Histopathological examination of lesional and perilesional tissue is rarely indicated unless difficult to obtain adequate history</li> </ul> </td> <td> <ul> <li>Areas of focal coagulative necrosis of epithelium</li> <li>Ulceration</li> <li>Intra - and extra-cellular oedema</li> <li>Sub-epithelial acute inflammatory infiltrate</li> </ul> </td> <td> <ul> <li>Identify and remove toxic agents</li> <li>Mild to moderate tissue damage heal spontaneously within 7 - 15 days without scarring</li> <li>Palliative and symptomatic treatment: gentle plaque control, topical anaesthetic</li> <li>Severe tissue damage: non-potent topical corticosteroid (e.g. triamcinolone) in protective carboxymethylcellulose vehicle may be helpful, bland diet</li> <li>Lesions with extensive exposure may require local debridement and antibiotic therapy</li> </ul> </td> </tr> </table> Fedele S. 2010:  #### Diagnosis - Based on clinical history and features. - Chronological correspondence between the causative agent and ulcer onset is key. - Histopathology is rarely indicated unless the history is difficult to obtain. #### Histopathology - Focal coagulative necrosis of the epithelium. - Ulceration. - Intra- and extra-cellular oedema. - Sub-epithelial acute inflammatory infiltrate. #### Treatment - Identify and remove the toxic agent. - Mild to moderate damage typically heals within 7-15 days without scarring. - **Palliative Care:** Gentle plaque control, topical anaesthetics, and a bland diet. - **Severe Cases:** Non-potent topical corticosteroids (e.g., triamcinolone) in a protective vehicle; extensive lesions may require debridement and antibiotic therapy. A flowchart diagram titled 'Burns' with three main sections: Diagnosis, Histopathology, and Treatment. Each section contains bullet points detailing clinical features, histopathological findings, and therapeutic approaches for burn injuries. The diagram uses blue arrow-shaped headers to connect the sections in a sequential flow. # Exfoliative cheilitis * Rare inflammatory dermatologic condition * Unknown aetiology * Associated with underlying stress/anxiety, parafunctional/factitial habits including lip licking and chewing * Characterized by chronic excessive production and subsequent desquamation of a thick keratin scale * Clinical features: * Symptoms: sensitivity and burning of lips * Female * Involvement of upper and lower lip vermillion * Scaling, peeling, erythema, crusting, burning, bleeding * Can be confused with allergic contact cheilitis and atopic cheilitis - history of contact with allergen or positive allergy or patch test Almazrooa et al. 2013 #### Overview - A rare inflammatory dermatologic condition of unknown etiology. - Often associated with stress, anxiety, or parafunctional habits (lip licking/chewing). - Characterized by chronic excessive production and desquamation of a thick keratin scale. Fig. 1. A 79-year-old woman (patient 14) with exfoliative cheilitis involving both lips before (a) and after (b) 1 month of treatment with pimecrolimus ointment, showing partial response. Fig. 2. A 77-year-old woman (patient 8) with exfoliative cheilitis involving primarily the lower lip before (a) and after (b) 1 month of treatment with pimecrolimus ointment, showing partial response. Almazrooa et al. 2013   #### Clinical Presentation - **Demographics:** Predominantly affects females. - **Symptoms:** Sensitivity and burning of the lips. - **Signs:** Scaling, peeling, erythema, crusting, and bleeding involving the upper and lower lip vermillion. - **Differential Diagnosis:** Must be distinguished from allergic contact cheilitis and atopic cheilitis via history or patch testing. A 79-year-old woman (patient 14) with exfoliative cheilitis involving both lips, showing before (a) and after (b) 1 month of treatment with pimecrolimus ointment, demonstrating a partial response. A 77-year-old woman (patient 8) with exfoliative cheilitis involving primarily the lower lip, showing before (a) and after (b) 1 month of treatment with pimecrolimus ointment, demonstrating a partial response. # Exfoliative cheilitis * Histopathology: parakeratosis or hyperkeratosis, benign epithelial hyperplasia, acute or chronic inflammation and fibrosis, superficial fungal or bacterial microorganisms * Management: difficult * Topical treatments include * Corticosteroids * Antibacterial and antifungal ointments * Sunscreen * Herbal products * Petroleum jelly * 2-3% salicylic acid ointment * 0.1% tacrolimus ointment * Cryotherapy with liquid nitrogen * Systemic treatments: antidepressants, antifungal agents, corticosteroids <img src="image_of_histopathology_slide.png" alt="Histopathology slide showing epithelial layers."> Almazrooa et al. 2013  #### Histopathology - Parakeratosis or hyperkeratosis. - Benign epithelial hyperplasia. - Acute or chronic inflammation and fibrosis. - Presence of superficial fungal or bacterial microorganisms. #### Management Strategies Management is often difficult and includes: - **Topical Treatments:** Corticosteroids, antibacterial/antifungal ointments, sunscreen, petroleum jelly, 2-3% salicylic acid, 0.1% tacrolimus, or pimecrolimus ointment. - **Procedures:** Cryotherapy with liquid nitrogen. - **Systemic Treatments:** Antidepressants, antifungal agents, or corticosteroids. A histopathology slide showing epithelial layers with parakeratosis or hyperkeratosis, benign epithelial hyperplasia, and acute or chronic inflammation, consistent with exfoliative cheilitis. The image displays a purple-stained tissue section with distinct cellular layers, highlighting the pathological features mentioned in the text. <a></a> **Amalgam tattoo and other exogenous pigmentation** * **Amalgam tattoo** * Implantation of dental amalgam in oral mucosa * Mucosal abrasion can be contaminated by amalgam dust within oral fluids * Broken amalgam pieces fall into extraction sites * Endodontic root fill procedures can be left within soft tissue at surgical sites * Metallic particles can be driven through oral mucosal from pressure of high speed air turbines Image courtesy of Neville B, Damm D, 2016  #### Amalgam Tattoo Mechanisms - Implantation of dental amalgam into the oral mucosa. - Contamination of mucosal abrasions by amalgam dust in oral fluids. - Broken amalgam pieces falling into extraction sites. - Amalgam left in soft tissue during endodontic root fill procedures. - Metallic particles driven into mucosa by high-speed air turbine pressure. A close-up clinical photograph showing an amalgam tattoo on the oral mucosa, characterized by a dark, bluish-gray pigmentation adjacent to teeth, illustrating the implantation of dental amalgam in the tissue. Amalgam tattoo and other exogenous pigmentation * Clinical Features: * Macules or slightly raised lesions * Black, blue, grey * Well-defined, irregular or diffuse borders * Lateral spread can occur for several months after pigmentation * Any mucosal surface - gingiva, alveolar mucosa, buccal mucosa * Radiographic features: metallic fragments can be seen visibly - densely radiopaque    #### Clinical Presentation - **Appearance:** Macules or slightly raised lesions; black, blue, or grey in colour. - **Borders:** Well-defined, irregular, or diffuse. - **Progression:** Lateral spread can occur for several months after initial pigmentation. - **Sites:** Any mucosal surface, including gingiva, alveolar mucosa, and buccal mucosa. #### Radiographic Features - Metallic fragments appear as densely radiopaque spots on radiographs. Clinical photograph showing a patient's mouth with amalgam tattoo on the gingiva, characterized by a black pigmented lesion near a dental restoration, illustrating the clinical features of exogenous pigmentation. Radiographic image showing a dental X-ray with a radiopaque metallic fragment, demonstrating the radiographic feature of amalgam tattoo where metallic debris is visible within the oral tissues. Close-up clinical photograph of a dark pigmented lesion on the gingiva adjacent to a tooth with an amalgam restoration, exemplifying the clinical presentation of an amalgam tattoo. Amalgam tattoo and other exogenous pigmentation * Cosmetic tattooing - vermilion border of upper and lower lips * Intentional tattooing - maxillary labial gingival in African countries * Histopathology: * Pigmented fragments of metal within connective tissue * Scattered, large, dark, solid fragments or numerous fine, black, or dark-brown granules may be seen * Silver salts of dental amalgam preferentially stain reticulin fibers, especially those encircling nerves and vascular channels * Diagnosis: * Obtain radiograph and demonstrate metallic fragments * Biopsy to rule out melanoma * Treatment: no treatment required, or can be removed surgically if cosmetic issue <img src="image1.png"> <img src="image2.png"> <img src="image3.png"> Image courtesy of Neville B, Damm D., 2016    #### Other Exogenous Pigmentation - **Cosmetic Tattooing:** Often on the vermilion border of the lips. - **Intentional Tattooing:** Maxillary labial gingiva (observed in some African countries). #### Histopathology - Pigmented metal fragments within connective tissue. - Appearance ranges from large, dark, solid fragments to fine black/dark-brown granules. - Silver salts stain reticulin fibers, particularly those around nerves and vessels. #### Diagnosis and Treatment - **Diagnosis:** Use radiographs to demonstrate metallic fragments; biopsy may be necessary to rule out melanoma. - **Treatment:** No treatment is required unless removal is requested for cosmetic reasons. Close-up photo of the upper and lower teeth showing dark pigmentation along the gingival margin, consistent with an amalgam tattoo, with a darkened area on the labial gingiva. Photo of a tattoo on the inner lip with the word 'INSANITY' written in dark ink, illustrating intentional tattooing in the oral cavity. Histopathological image showing pigmented fragments of metal within connective tissue, with dark granules scattered in the tissue, demonstrating the microscopic appearance of an amalgam tattoo. <img src="image.png" alt="Image of oral pigmentation on gums"> **Smoker's melanosis** * Oral pigmentation increased significantly in heavy smokers * Exposure to polycyclic amines (e.g., nicotine and benzpyrene) has been shown to stimulate melanin production by melanocytes that also are known to bind strongly to nicotine. * Melanin production in the oral mucosa of smokers serves as a protective response against some of the harmful substances in tobacco smoke. Image courtesy of Neville B, Damm D., 2016  #### Pathogenesis - Oral pigmentation increases significantly in heavy smokers. - Exposure to polycyclic amines (e.g., nicotine and benzpyrene) stimulates melanin production by melanocytes. - Melanin production serves as a protective response against harmful substances in tobacco smoke. A close-up photograph of oral pigmentation on the gums, illustrating smoker's melanosis. The image shows dark brown to black pigmentation on the gingival tissue surrounding the teeth, with the text on the right explaining that this pigmentation increases in heavy smokers due to exposure to polycyclic amines in tobacco smoke. # **Smoker's melanosis** * **Histopathology:** * Increased melanin pigmentation of the basal cell layer of surface epithelium, similar to melanotic macule * Incontinent melanin pigmentation seen in superficial connective tissue * Scattered melanophages * **Diagnosis:** * Smoking history * Clinical presentation * Medical history – rule out Peutz-Jeghers syndrome, drug related pigmentation, endocrine disturbance * Biopsy * **Management:** * Cessation of smoking leads to gradual disappearance of lesion over 3 year period Neville B, Damm D., 2016 #### Histopathology - Increased melanin pigmentation in the basal cell layer of the epithelium. - Incontinent melanin pigmentation in superficial connective tissue. - Presence of scattered melanophages. #### Diagnosis and Management - **Diagnosis:** Based on smoking history and clinical presentation. Medical history is used to rule out Peutz-Jeghers syndrome, drug-related pigmentation, or endocrine disturbances. Biopsy may be performed. - **Management:** Cessation of smoking leads to the gradual disappearance of the lesion over approximately 3 years. **Drug related discolouration of the oral mucosa** * Medications stimulate melanin production by melanocytes * Deposition of drug metabolites is responsible for colour change | Drug | Spread | Location | Colouring | Duration | Reported incidence | Route of administration | |---|---|---|---|---|---|---| | Afamelanotide | Generalised | Lips | - | - | 4% | Subcutaneous | | Abacavir sulphate / Lamivudine/ Zid- ovudine | Generalised | Oral mucosa | - | - | - | Oral | | Amitriptyline | Generalised | Lingual dorsum | Black | - | - | Oral | | Subcitrate of bismuth potassium, metronidazole and tetracycline | Generalised | Lingual dorsum | Darkening | Temporary | <1% | Oral | | Bremelanotide | Localised | Gum | Hyperpigmen- tation | Temporary /permanente dose dependant | 1% | Subcutaneous | | Chlorhexidine gluconate | Generalised | Lingual dorsum Yellow/ brown | Individual factors Concentration Duration of treatment | >56% | Topical use | | Chloroquine | Generalised | Lingual dorsum Mucosa oral Hard palate | Blue / grey | Duration of treatment Interruption of treatment | ---- | Oral | | Estrogens conjugate | Generalised | Lips Gum Floor of the mouth | Brown | Long duration | ---- | Intravenous Oral Vaginal | | Ethylsuccinate of erythromycin / Sulfisoxazol acetyl | Generalised | Lingual dorsum | Brown /black | Few days | ---- | Oral | | Hydroxychloroquine | Generalised | Gum | Blue / greyish | After 6 days of treatment | ---- | Oral | | Hidroxyurea | Localised focal bilateral | Lateral borders of the tongue | Brown | After one year of treatment | ---- | Oral | | Imatinib | Generalised | Hard palate | Blue / dark blue/ grey | After 10-13 years | ---- | Oral | | Levodopa/ Bensera- zide | Generalised | Lingual dorsum | - | - | ---- | Oral | | Linezolid | Generalised | Lingual dorsum | - | Disappearance after a month of treatment | ---- | Intravenous oral | | Minocycline | Generalised/ Localised | Lips Oral mucosa, Hard palate Gum | Blue/ black/ grey | Dose dependant Length of treatment Age Autoimmune disease | 22.5% | Intravenous Oral Subgingival Topical | | Palifermine | Localised | Lingual dorsum (painful maculas) Oral mucosa | - | Two months after interruption Non-recurrent | 17% | Intravenous | | Peginterferon a2b | Generalised | Lingual dorsum | Dark brown | Improvement after 6 months of interruption of treatment | ---- | Oral | | Prussian blue | Generalised | Oral mucosa | Greyish- blue /black | - | ---- | Oral | | Perimetamina | Generalised | Hard palate | Hyperpigmen tation | After 6 months of interruption | ---- | Oral | | Silver nitrate | Generalised | Lingual dorsum Oral mucosa | Greyish-blue /black | Permanent | ---- | Topical | | Zidovudine | Localised (macula) | Oral mucosa | - | Appeared after 8 months of treatment Dissapeared after 2 months | ---- | Intravenous Oral | Neville B, Damm D., 2016, Table from: Mallagray-Montero et al., 2022  #### Mechanisms - Medications may stimulate melanin production by melanocytes or result in the deposition of drug metabolites. #### Common Causative Agents - **Antimalarials/Rheumatologic:** Chloroquine, Hydroxychloroquine (Blue/grey on palate/gingiva). - **Antibiotics:** Minocycline (Blue/black/grey), Linezolid, Tetracycline. - **Hormonal:** Conjugated Estrogens (Brown on lips/gingiva). - **Antipsychotics:** Chlorpromazine, Promazine. - **Other:** Zidovudine, Imatinib, Silver nitrate, Chlorhexidine (Yellow/brown staining). A detailed table listing various drugs and their effects on oral mucosa discoloration, including drug name, spread, location, colouring, duration, reported incidence, and route of administration. The table is sourced from Neville B, Damm D., 2016, and references Mallagray-Montero et al., 2022. Minocycline-related discolouration Neville B. Damm D., 2016   #### Minocycline-Related Discolouration - Minocycline can cause distinct blue, black, or grey discolouration of the lips, oral mucosa, hard palate, and gingiva. The effect is often dose-dependent and related to the length of treatment. Close-up intraoral photo showing dark grey discoloration on the floor of the mouth, consistent with minocycline-related staining, with surrounding healthy oral mucosa and teeth. Close-up intraoral photo displaying extensive dark discoloration on the gingival and buccal mucosa, with a clear contrast between the stained areas and the adjacent healthy tissue, illustrating minocycline-related discoloration. Drug related discolouration of the oral mucosa | **Histopathology:** | **Diagnosis** | **Management:** | | :--- | :--- | :--- | | • Dark brown granulated pigments in lamina propria | • Medical history | • No long-term problems | | • Infiltration of fibroblasts and macrophages in subepithelial and perivascular areas | • Clinical history | • Discontinuing mediation results in gradual fading of areas of hyperpigmentation | | | • Clinical examination +/- biopsy | | Neville B, Damm D., 2016, Mallagray-Montero et al., 2022  #### Histopathology - Dark brown granulated pigments in the lamina propria. - Infiltration of fibroblasts and macrophages in subepithelial and perivascular areas. #### Diagnosis and Management - **Diagnosis:** Established through medical history, clinical examination, and occasionally biopsy. - **Management:** No long-term health problems are associated. Discontinuing the medication typically results in the gradual fading of hyperpigmentation. A table detailing the histopathology, diagnosis, and management of drug-related discoloration of the oral mucosa. The table is divided into three columns: Histopathology lists dark brown granulated pigments in lamina propria and infiltration of fibroblasts and macrophages; Diagnosis includes medical history, clinical history, and clinical examination with or without biopsy; Management states no long-term problems and that discontinuing medication results in gradual fading of hyperpigmentation. # Oral complication of radiotherapy * Cancer patients undergoing radiation therapy of head and neck encounter acute and chronic change to their soft tissue Neville B, Damm D., 2016, Sroussi H et al., 2017 Cancer patients undergoing radiation therapy for the head and neck encounter both acute and chronic changes to their oral soft tissues. <img src="image1.png" /> **Mucositis** * Acute response to treatment * 80% of patients treated with head and neck radiation * Occurs in first 2-3 weeks of radiation treatment, Peak near end of treatment and continue for 2-4 weeks post radiation treatment Neville B, Damm D., 2016, Sroussi H et al., 2017  #### Acute Radiation Response - Affects approximately 80% of patients receiving head and neck radiation. - Typically occurs within the first 2-3 weeks of treatment. - Symptoms peak near the end of treatment and may continue for 2-4 weeks post-radiation. A close-up photograph of oral mucositis, showing inflamed and ulcerated mucosal tissue in the mouth, with redness and white patches indicative of the condition. This image is used to illustrate the clinical presentation of mucositis, which is described in the adjacent text as an acute response to head and neck radiation treatment. # **Oral complication of radiotherapy** * **Candidiasis** * Associated with mucosal pain, taste change, dysphagia * Pseudomembranous and erythematous candidiasis, angular cheilitis * **Neurosensory disorders: mucosal pain and taste dysfunction** * Can be related to inflammation, ulceration, mucosal atrophy, mucosal neuropathy * Compounded by dry mouth * Mucosal sensitivity may persist long after clinical mucositis resolves * RT can cause neuroepithelial damage causing dysgeusia, or mucosal sensitivity (75% of cases) * Management: analgesics: topical, (NSAIDs), mild opioid combinations, Centrally acting medications, LLLT * Improvement of taste usually 3-6 months post-RT, but in some instances continue Neville B, Damm D., 2016, Sroussi H et al., 2017 #### Candidiasis - Associated with mucosal pain, taste changes, and dysphagia. - Presents as pseudomembranous or erythematous candidiasis, and angular cheilitis. #### Neurosensory Disorders - **Mucosal Pain and Taste Dysfunction:** Related to inflammation, ulceration, atrophy, or neuropathy; compounded by dry mouth. - **Dysgeusia:** RT can cause neuroepithelial damage; taste improvement usually occurs 3-6 months post-RT, though some cases persist. - **Management:** Analgesics (topical, NSAIDs, mild opioids), centrally acting medications, and Low-Level Laser Therapy (LLLT). # **Oral complication of radiotherapy** * **Xerostomia and salivary gland dysfunction** * Salivary glands are very sensitive to RT * Changes occur within 1 week of commencing treatment * Dramatic decrease in saliva flow noted during first 6 weeks of treatment * Management: Symptomatic - salivary replacements * **Caries** * Cervical location, secondary to salivary gland dysfunction * Caries prevention * **Post-radiation fibrosis** * Trismus due to fibrosis in masticatory muscles limit function * < 35 mm mouth opening * TheraBite Jaw Motion Rehabilitation System can be used, or LLT Neville B, Damm D., 2016, Sroussi H et al., 2017  #### Salivary and Structural Complications - **Xerostomia:** Salivary glands are highly sensitive; flow decreases dramatically within the first 6 weeks of RT. Management is symptomatic (salivary replacements). - **Radiation Caries:** Typically occurs at the cervical location due to salivary dysfunction; requires rigorous prevention. - **Post-radiation Fibrosis:** Can lead to trismus (mouth opening < 35 mm) due to fibrosis of masticatory muscles. Management includes the TheraBite system or LLLT. A clinical photograph showing the oral cavity of a patient with post-radiation fibrosis, displaying reduced mouth opening and visible dental caries. The image illustrates the effects of radiotherapy on salivary glands and masticatory muscles, consistent with the text describing trismus and xerostomia. Oral complication of radiotherapy * **Osteoradionecrosis** * Nonvital irradiated bone that persists longer than 3 months in the absence of local neoplastic disease   #### Osteoradionecrosis (ORN) - Defined as nonvital irradiated bone that persists for longer than 3 months in the absence of local neoplastic disease. A clinical photo showing oral tissue with exposed bone, illustrating osteoradionecrosis, a complication of radiotherapy. The image depicts nonvital irradiated bone that persists longer than three months. An X-ray image showing radiographic evidence of osteoradionecrosis, highlighting nonvital irradiated bone. This image supports the diagnosis of a complication from radiotherapy, as described in the accompanying text. * Thank you! * **Lalima.Tiwari@uwa.edu.au** #### Contact Details For further inquiries or information regarding this presentation, please contact: - **Email:** Lalima.Tiwari@uwa.edu.au Thank you for your time and attention. 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