Clin Med: Mouth, Pharynx, Laryngx

Aphthous Ulcers (Canker Sores)

Common, painful, recurrent oral ulcers occurring on nonkeratinized mucosa (such as labial/buccal mucosa, floor of mouth, ventral tongue, or soft palate) with an idiopathic or multifactorial etiology linked to local trauma, emotional stress, or nutritional deficiencies in iron, folate, or vitamin B12. Clinically, they present as round or oval ulcers with a yellow-gray base and an erythematous halo without preceding vesicles, categorized as minor (

Necrotizing Ulcerative Gingivitis (Trench Mouth)

Polymicrobial anaerobic bacterial infection of the gingiva occurring in susceptible patients due to predisposing factors like poor oral hygiene, smoking, psychological stress, malnutrition, or immunosuppression. Clinically, it presents with severe gingival pain, spontaneous bleeding, "punched-out" necrosis of the interdental papillae covered by a gray-white pseudomembrane, foul breath (halitosis), and potential fever or cervical lymphadenopathy.

Herpetic Gingivostomatitis

Primary oral infection caused by Herpes Simplex Virus-1 (HSV-1) occurring most commonly in children, characterized by an abrupt onset of fever, malaise, and cervical lymphadenopathy. Pathophysiology involves viral replication causing diffuse, painful gingivitis and widespread vesicles that rupture into shallow ulcers across both keratinized and nonkeratinized oral mucosa; recurrent disease presents milder as herpes labialis (cold sores) preceded by a prodrome of burning or tingling.

Mucocele

Common, benign mucus-filled lesion of a minor salivary gland, most frequently caused by mechanical trauma or duct rupture (such as lip biting) on the lower lip. Clinically, it presents as a painless, soft, fluctuant, translucent or bluish swelling that may fluctuate in size or spontaneously rupture.

Ranula

Mucocele located specifically in the floor of the mouth, resulting from mucus extravasation from the sublingual gland. Clinically, it presents as a soft, fluctuant, bluish unilateral swelling beneath the tongue, classified as simple (confined to the floor of the mouth) or plunging (extending through or around the mylohyoid muscle into the neck), with larger lesions causing interference with speech or swallowing.

Glossitis

Inflammation or atrophy of the tongue tissue characterized by the loss of filiform papillae. Pathophysiology is commonly driven by nutritional deficiencies (iron, vitamin B12, folate), oral candidiasis, xerostomia, local irritation, or celiac disease, presenting clinically as a smooth, glossy, erythematous ("beefy red") tongue that causes burning, tenderness, or sensitivity.

Burning Mouth Syndrome (Glossodynia)

Chronic neurosensory pain condition characterized by a burning, tingling, or painful sensation of the oral mucosa (most commonly the anterior tongue, lips, or palate) in the setting of a completely normal physical oral examination. Pathophysiology is primary/idiopathic (most common in peri- and postmenopausal women), requiring a diagnosis of exclusion that rules out secondary causes such as candidiasis, xerostomia, nutritional deficiencies, diabetes, or thyroid disease.

Fissured Tongue

Common, benign structural variant of the tongue characterized by multiple grooves or fissures on the dorsal surface, increasing in frequency with age. It presents as an asymptomatic finding, though food and cellular debris trapped within the fissures can lead to localized irritation or halitosis.

Black Hairy Tongue

Benign, temporary condition caused by hyperkeratosis, elongation, and impaired shedding of filiform papillae on the dorsal tongue. Pathophysiology involves the elongated papillae trapping bacteria, yeast, food debris, and pigments—frequently triggered by poor oral hygiene, tobacco use, antibiotic therapy, xerostomia, or staining drinks—presenting clinically as yellow, brown, green, or black discoloration of the tongue that may cause halitosis or altered taste.

Angular Cheilitis (Perleche)

Inflammatory condition of the oral commissures (corners of the mouth) triggered by chronic moisture accumulation and saliva maceration, leading to secondary infection with Candida albicans or Staphylococcus aureus. Risk factors include ill-fitting dentures, drooling, xerostomia, iron or B-vitamin deficiencies, or diabetes, presenting clinically with painful erythema, cracking/fissuring, scaling, and crusting at the corners of the mouth.

Geographic Tongue (Benign Migratory Glossitis)

Common, benign inflammatory disorder of the tongue characterized by localized loss of filiform papillae. Clinically, it presents as smooth, erythematous areas surrounded by slightly raised white or cream borders that continuously alter their shape, size, and location over time, remaining largely asymptomatic or causing burning sensitivity with spicy or acidic foods.

Oral Hairy Leukoplakia

Opportunistic mucosal lesion caused by the reactivation of latent Epstein-Barr Virus (EBV) in immunosuppressed individuals, classically associated with HIV infection. Clinically, it presents as painless, white, corrugated or "hairy" plaques along the lateral borders of the tongue (unilateral or bilateral) that cannot be wiped or scraped off.

Gingival Hyperplasia

Overgrowth and structural enlargement of the gingival tissue. Pathophysiology involves chronic tissue inflammation, altered extracellular matrix regulation during pregnancy, or drug-influenced tissue responses to phenytoin, cyclosporine, or calcium channel blockers (especially nifedipine), presenting clinically as swollen, enlarged gingiva that may cover tooth crowns and worsen with dental plaque accumulation.

Gingivitis

Reversible inflammatory disease of the gingival tissue caused by bacterial dental plaque accumulation. Pathophysiology involves localized mucosal inflammation without loss of periodontal tissue attachment or alveolar bone, presenting clinically with swollen, erythematous gingiva that bleeds upon brushing, flossing, or probing.

Periodontitis

Chronic inflammatory disease affecting the deep supporting structures of the teeth, developing from untreated dental plaque accumulation. Pathophysiology involves progressive destruction of the periodontal ligament and alveolar bone resorption—exacerbated by smoking and poorly controlled diabetes—presenting clinically with gingival recession, deep periodontal pocket formation, tooth mobility, and eventual tooth loss.

Dental Caries

Localized destruction of calcified tooth tissue caused by dental plaque bacteria metabolizing dietary carbohydrates into organic acids. Pathophysiology involves progressive acid demineralization of enamel and dentin leading to structural cavitation, presenting clinically with sensitivity to temperature or sweets, localized tooth pain, and potential progression to pulpal necrosis or abscess.

Dental Abscess

Localized collection of pus arising from an odontogenic infection secondary to advanced dental caries, pulpal infection, periodontal disease, or dental trauma. Clinically, it presents with severe, localized tooth pain, gingival swelling with fluctuance or purulent drainage, facial edema, fever, and risk of deep neck space complications (signaled by red flags like trismus, dysphagia, drooling, or floor-of-mouth swelling).

Ludwig's Angina

Rapidly progressive, life-threatening cellulitis involving the bilateral submandibular, sublingual, and submental spaces, typically originating from an odontogenic infection of the mandibular second or third molars. Pathophysiology involves rapid soft-tissue infection spreading through floor-of-mouth anatomical planes, presenting clinically with firm, "woody" submandibular swelling, an elevated and indurated floor of the mouth forcing the tongue upward, severe dysphagia, drooling, trismus, fever, and rapid upper airway obstruction.

Leukoplakia

Potentially malignant white mucosal patch or plaque that cannot be wiped or scraped off and cannot be characterized clinically or pathologically as any other disease. Pathophysiology involves chronic irritation from tobacco, alcohol, or mechanical friction causing mucosal hyperkeratosis, dysplasia, or carcinoma, presenting as an asymptomatic white lesion on high-risk oral sites (lateral/ventral tongue, floor of mouth) or vocal folds (causing hoarseness).

Erythroplakia

Well-demarcated red oral patch or lesion that cannot be attributed to any other specific condition. Pathophysiology demonstrates a significantly higher prevalence of severe epithelial dysplasia, carcinoma in situ, or invasive squamous cell carcinoma compared to leukoplakia, presenting as an asymptomatic red patch on high-risk sites including the floor of the mouth, ventral/lateral tongue, or soft palate.

Oral Lichen Planus

Chronic, immune-mediated inflammatory disease of the oral mucosa. Pathophysiology involves T-cell-mediated destruction of basal keratinocytes, presenting clinically as bilateral, symmetric lacy white lines (Wickham striae) on the buccal mucosa (reticular form, often asymptomatic) or painful, burning erythematous, erosive, and ulcerative mucosal lesions that carry a long-term risk of malignant transformation.

Oral SCC

Primary malignant neoplasm arising from the oral mucosal epithelium, strongly linked to tobacco use, heavy alcohol consumption, and chronic mucosal irritation. Pathophysiology involves malignant cell invasion into surrounding tissue, presenting early as a subtle red/white patch or nonhealing ulcer and progressing to an indurated mass, pain, bleeding, dysphagia, loose teeth, or cervical lymphadenopathy.

Oropharyngeal SCC

Malignant epithelial neoplasm localized to the palatine tonsils, base of tongue, soft palate, or posterior pharyngeal wall, strongly driven by high-risk Human Papillomavirus infection (especially HPV-16) as well as tobacco and alcohol use. Clinically, it presents as a painless cervical neck mass (often the initial presenting sign), unilateral tonsillar enlargement or asymmetry, persistent sore throat, odynophagia, or referred otalgia with a normal ear examination.

Acute Bacterial Sialadenitis

Acute bacterial infection of a major salivary gland, most commonly affecting the parotid gland via Staphylococcus aureus. Pathophysiology is driven by retrograde bacterial invasion secondary to salivary stasis, dehydration, duct obstruction (sialolithiasis), or anticholinergic medications, presenting clinically with acute, painful, erythematous, tender glandular swelling, fever, pain worsening during meals, and purulent drainage expressible from the salivary duct orifice upon massage.

Viral Parotitis (Mumps)

Systemic viral infection caused by the mumps virus leading to acute inflammation of the parotid glands. Clinically, it presents with prodromal fever, malaise, and headache followed by painful, frequently bilateral parotid gland swelling positioned anterior and inferior to the ear and extending toward the jaw line.

Sialolithiasis

Formation of a stone or calculus within a salivary gland duct system, most commonly obstructing the submandibular gland (Wharton's duct). Pathophysiology involves mechanical duct obstruction impeding salivary outflow, presenting clinically with recurrent, episodic pain and gland swelling specifically triggered by eating/meals, which resolves between meals and may feature a palpable stone in the floor of the mouth.

Salivary Gland Tumors

Neoplasms arising in the major or minor salivary glands, where the majority occur in the parotid gland and are benign (pleomorphic adenoma being the most common). Benign tumors present as slow-growing, painless masses, whereas malignant tumors present with rapid growth, pain, tissue fixation, cervical lymphadenopathy, and facial nerve weakness or paralysis (CN VII palsy representing a critical red flag for malignancy).

Xerostomia

Subjective sensation of dry mouth resulting from reduced salivary flow. Pathophysiology is most frequently drug-induced (anticholinergics, antihistamines, antidepressants, diuretics) or caused by autoimmune destruction (Sjögren syndrome) or head/neck radiation therapy, presenting clinically with dry, sticky mucosa, difficulty chewing/swallowing/speaking, rampant dental caries, oral candidiasis, cracked lips, and altered taste.

Torus Palatinus

Benign, non-neoplastic bony exostosis located along the midline of the hard palate (or lingual mandible as torus mandibularis). Pathophysiology involves slow, outward cortical bone growth, presenting clinically as a hard, immobile, painless mass covered by normal mucosa that is typically discovered incidentally.

Dysphonia (Hoarseness)

Abnormality of voice quality, pitch, loudness, or vocal effort resulting from disrupted vocal fold vibration or incomplete closure. Etiologies range from acute viral laryngitis, voice overuse, and benign vocal fold lesions to vocal cord paralysis or laryngeal malignancy, requiring evaluation via laryngoscopy if persistent beyond 4 weeks or accompanied by red flag symptoms like stridor, neck mass, dysphagia, or hemoptysis.

Stridor

High-pitched, harsh breath sound generated by turbulent airflow passing through a narrowed upper airway. Pathophysiology depends on obstruction anatomical level

Laryngopharyngeal Reflux (LPRD)

Inflammatory laryngeal condition caused by retrograde flow of gastric contents into the upper aerodigestive tract. Pathophysiology involves direct pepsin and acid irritation of sensitive supraglottic mucosa, presenting clinically with chronic hoarseness, frequent throat clearing, a globus sensation ("lump in the throat"), chronic cough, and excess throat mucus, often without classic esophageal heartburn.

Peritonsillar Abscess (Quinsy)

Localized collection of pus between the tonsillar capsule and surrounding pharyngeal constrictor muscle, developing as a polymicrobial complication of acute tonsillitis. Clinically, it presents with severe unilateral sore throat, high fever, odynophagia, drooling, trismus, a "hot potato" muffled voice, unilateral peritonsillar swelling, and displacement of the uvula away from the affected side.

Epiglottitis

Rapidly progressive, life-threatening inflammation and edema of the epiglottis and supraglottic structures, historically caused by Haemophilus influenzae type b (Hib) in children and currently by Streptococcus species or S. aureus in adults. Pathophysiology involves acute bacterial infection causing marked supraglottic tissue swelling that rapidly occludes the upper airway, presenting clinically with abrupt onset of high fever, severe sore throat, odynophagia, drooling, muffled voice, inspiratory stridor, and leaning forward in a tripod posture to maintain airway patency.

Benign Vocal Fold Lesions

Non-neoplastic structural alterations of the vocal fold covering. Includes vocal nodules (bilateral, symmetric fibrous thickenings caused by chronic phonotrauma/overuse in singers or teachers), vocal polyps (usually unilateral fluid-filled or vascular lesions following acute vocal trauma), and vocal cysts (unilateral subepithelial retention or epidermoid cysts), all presenting with persistent dysphonia, hoarseness, and vocal fatigue.

Vocal Cord Paralysis

Impairment of vocal fold mobility caused by injury to the vagus nerve (CN X) or recurrent laryngeal nerve. Pathophysiology stems from surgical trauma (thyroid/neck surgery), thoracic/mediastinal malignancy, intubation, or neck trauma; unilateral involvement presents with a breathy, hoarse voice and aspiration risk, whereas bilateral involvement causes inspiratory stridor and severe airway obstruction representing a life-threatening emergency.

SCC of the Larynx

Primary malignant neoplasm arising from the laryngeal epithelium, accounting for >90% of laryngeal cancers and strongly associated with tobacco use and alcohol consumption. Pathophysiology involves progressive epithelial dysplasia advancing to invasive carcinoma, presenting clinically with persistent/progressive hoarseness as the cardinal early symptom, with advanced disease causing dysphagia, odynophagia, referred otalgia, neck mass, hemoptysis, weight loss, or stridor