Oral Cavity Disorders PDF

ORAL CAVITY DISORDERS Rachel Elbing PA-C, MPH Augsburg Physician Assistant Studies © 2025  OBJECTIVES 1. Summarize the etiology, pathophysiology, clinical features, how diagnosis is established, potential complications and treatment for the cond...

ORAL CAVITY DISORDERS Rachel Elbing PA-C, MPH Augsburg Physician Assistant Studies © 2025  OBJECTIVES 1. Summarize the etiology, pathophysiology, clinical features, how diagnosis is established, potential complications and treatment for the conditions listed below: Leukoplakia Erythroplakia Oral lichen planus Oral candidiasis Gingivitis Glossitis Intraoral ulcers: aphthous ulcers, herpes stomatitis Sialadenitis Sialolithiasis Salivary gland tumors Sjogren Syndrome Mumps/Parotitis  LEUKOPLAKIA: ETIOLOGY & PATHOPHYSIOLOGY Etiology: Chronic irritation (dentures, tobacco, lichen planus) Rarely (2-6%) dysplastic or early invasive ________ carcinoma Pathophysiology: Hyperkeratotic response Rare malignancy  LEUKOPLAKIA: CLINICAL FEATURES = white patch on oral mucosa that cannot be removed by rubbing the mucosal surface This definition distinguishes leukoplakia from what other diagnosis? __________ Small to several cms in size  LEUKOPLAKIA: Ensure complete oral cavity exam DIAGNOSIS & TREATMENT Doesn’t resolve with elimination of friction (ie dentures) Early HEENT referral for dx & tx Dx: If enlarging, ulcerating or lesion with submucosal depth on palpation, incisional biopsy or exfoliative cytologic examination Tx: surgical excision, laser ablation, cryotherapy, retinoids, watchful waiting Avon, Sylvie Louise and Hagen B. E. Klieb. “Oral soft-tissue biopsy: an overview.” Journal 78 (2012): c75.  ERYTHROPLAKIA: ETIOLOGY & PATHOPHYSIOLOGY Etiology: 90% dysplastic or carcinoma! So very important to distinguish from leukoplakia… Pathophysiology: Dysplastic → malignant response generally in older patients with tobacco or EtOH use  ERYTHROPLAKIA: CLINICAL FEATURES = similar to leukoplakia but with definite erythematous component Fiery red, sharply demarcated erythematous patch on oral mucosa  ERYTHROPLAKIA: DIAGNOSIS & TREATMENT Complete HEENT exam → check lymph nodes (FNA is a quick diagnosis!) HEENT referral Dx: all lesions require bx Tx: surgical excision with clear margins Laser therapy with higher recurrence rates  RECALL CHECK: 5Ps of LICHEN PLANUS lichen planus ? Pruritic, planar (flat topped) Primary lesion flat topped papules w/ an irregular angulated border (purple, polygonal papules) Primarily scalp, extremities, nails & mucous membranes New lesions pink or white → classic lesion Whickham’s striae: white line lacy reticulated pattern New lesions at site of injury = _____________  ORAL LICHEN PLANUS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: autoimmune Pathophysiology: Chronic inflammatory disorder immune reaction T-cell mediated to epithelial cells Mucosal LP: white lacy or erosive patterns, often buccal mucosa/tongue/lip, rarely beyond Vermillion border, can include genitalia  ORAL LICHEN PLANUS: CLINICAL FEATURES Wickham Striae = most commonly presents as lacy leukoplakia but can be erosive Reticular, erythematous and erosive subtypes Can occur with other types of LP extraoral findings  ORAL LICHEN PLANUS: DIAGNOSIS & TREATMENT Dx: definitive dx requires bx Classic reticular pattern can be a clinical dx Tx: Topical corticosteroids first line Likely complication of this tx? _______ Good oral hygiene, minimize irritants  ORAL CANDIDIASIS: ETIOLOGY & PATHOPHYSIOLOGY AKA “__________” Etiology: Candida albicans Pathophysiology: Immune suppression results in fungal overgrowth Risk factors/groups: dentures, poor oral hygiene, DM, anemia, chemotherapy, corticosteroid use, antibiotic use, infants  ORAL CANDIDIASIS: CLINICAL FEATURES Creamy-white curd-like plaques Erythematous oral cavity Fluctuating throat/mouth discomfort Can be asx Can alter taste Easily removed with tongue depressor **These are the classic features of “pseudomembranous candidiasis”...just know there are other types as well  ORAL CANDIDIASIS: Dx: clinical dx DIAGNOSIS & TREATMENT Wet prep KOH prn Tx: Topical suspension: nystatin swish & swallow 5 ml (100,000 units/mL) tid Oral antifungals: fluconazole 100 mg daily x 7 days Tx underlying conditions (ie get DM control) Oral hygiene  GINGIVITIS: ETIOLOGY & PATHOPHYSIOLOGY MC: bacterial biofilm (i.e. dental plaque) Other causes: pregnancy, Vit C deficiency, drug-induced, necrotizing disease Dental plaque → gingivitis and can be reversed or → periodontitis  GINGIVITIS: CLINICAL FEATURES Healthy Gingiva: Pink, Gingivitis: Red, swollen, Periodontitis: gingival firm, no recession easily bleeding with inflammation with loss flossing/brushing of supportive connective tissue All pictures: © 2025 UpToDate, Inc. and/or its affiliates. All Rights Reserved.  GINGIVITIS: DIAGNOSIS & TREATMENT Dx: Clinical diagnosis Can utilize radiographs for periodontal disease Prevention: Prevent plaque build up (_________) Tx: Debridement by dental professional and oral hygiene routine at home Chlorhexidine mouthrinses  GINGIVITIS: OTHER CAUSES Necrotizing ulcerative gingivitis “Trench Mouth” Painful acute inflammation and necrosis often with bleeding Halitosis Fever Cervical lymphadenopathy 38 year-old male, HIV-positive with necrotizing Necrotizing ulcerative periodontitis periodontitis before (panel A) and two months after (panel B) active treatment that included scaling and root planing, use of systemic Common in patients with HIV antibiotic (amoxicillin combined with metronidazole), and use of 0.12% chlorhexidine Rapid attachment loss and bone loss gluconate. Courtesy of Antonio Moretti, DDS, MS. © 2025 UpToDate, Inc. and/or its affiliates. All Rights Reserved. AND FOR FUN… © 2025 UpToDate, Inc. and/or its affiliates. All Rights Reserved.  GLOSSITIS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: nutritional deficiencies _______, drug reactions, dehydration, irritations, autoimmune Pathophysiology: Inflammation of the tongue → loss of filiform papillae  GLOSSITIS: CLINICAL FEATURES Red, smooth surfaced tongue Rarely painful (glossodynia: burning and pain of tongue) Can have geographic tongue  GLOSSITIS: DIAGNOSIS & TREATMENT Dx: clinical dx Bx prn Tx: ID causative agent & tx underlying condition Nutritional consult Can ppx nutritional replacement if unable to ID  INTRAORAL ULCERS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: Aphthous ulcers: unknown, likely association with HHV 6 Herpes stomatitis: HSV Pathophysiology: Aphthous ulcers: trauma/stress can predispose viral eruption Herpes stomatitis: HSV-1 infection, lies dormant in trigeminal ganglia (CN ___) & reactivates  INTRAORAL ULCERS: CLINICAL FEATURES Aphthous ulcers: = “canker sore” Ulceration of freely moving, nonkeratinized mucosa (ie buccal, not gingiva or palate) Single or multiple Recurrent often Painful, small round ulcerations with yellow-gray fibrous center surrounded by red halo  INTRAORAL ULCERS: CLINICAL FEATURES Herpes stomatitis: Mild Initial burning → lesions Most common on attached gingiva and lip junction but can be throughout oral mucosa Small vesicles that rupture & form scabs In immunocompromised, can be frequent & severe  INTRAORAL ULCERS: Dx: clinical dx DIAGNOSIS & TREATMENT Tx: Aphthous ulcers: Self limited >1cm and debilitating, consider topical/oral steroids Herpes stomatitis: Self limited Acyclovir or valacyclovir to decrease duration & risk of postherpetic pain Which med would you choose? When would it need to be initiated?  SIALADENITIS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: Bacterial → MC S aureus Pathophysiology: Dehydration or chronic illness (ie Sjogrens) predispose to ductal obstruction often via a mucus plug → stasis → secondary infection  ANATOMICAL REVIEW Parotid gland drains via ________ duct Stensen’s Duct: Whartons’s Duct: Submandibular & sublingual glands drain via __________ duct  SIALADENITIS: CLINICAL FEATURES Usually affects parotid or submandibular glands Acute gland swelling and pain PE: tenderness and erythema of duct, may be able to massage pus Which gland is impacted from the duct above?  SIALADENITIS: DIAGNOSIS & TREATMENT Dx: clinical dx US/CT in absence of clinical improvement Tx: IV/PO abx Swelling resolution takes 2-3 weeks Increase salivary flow: hydration, warm compresses, sialogogues (ie lemon drops) Risk of suppurative sialadenitis: life-threatening form, may require operative I&D  SIALOLITHIASIS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: unknown but stagnation of salivary flow & elevated calcium levels contribute Why is this Pathophysiology: more common in Calculus formation secondary to submandibular inflammation, injury, bacteria as nidus gland?  SIALOLITHIASIS: CLINICAL FEATURES Postprandial pain & local swelling Can be painless swelling PE: may be able to visualize or palpate stone  SIALOLITHIASIS: Dx: clinical dx DIAGNOSIS & TREATMENT US/CT in absence of clinical improvement, concern for malignancy Tx: HEENT referral Dilate/incise duct to remove stones close to orifice Sialoendoscopy: for distal/larger stones Risk secondary infection  SALIVARY GLAND TUMORS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: no single predominant factor RF: radiation, smoking, viral infections (EBV, HIV, HPV), environmental exposures Pathophysiology: Majority in parotid gland & majority benign Pleomorphic adenomas MC Warthin tumors  SALIVARY GLAND TUMORS: CLINICAL FEATURES Usually asymptomatic mass in superficial gland If involves facial nerve, what sxs would you expect?  SALIVARY GLAND TUMORS: DIAGNOSIS & TREATMENT Dx: CT/MRI is replacing sialography FNA bx Tx: Parotidectomy or submandibular gland excision May skip FNA & proceed directly to surgical mgmt Postoperative radiation if larger high-grade cancer  SJOGREN SYNDROME: ETIOLOGY & PATHOPHYSIOLOGY Etiology: systemic autoimmune disorder MC in middle-aged females Pathophysiology: Immune dysfunction of lacrimal & salivary glands Primary or secondary (association with another Rheumatic dx)  SJOGREN SYNDROME: CLINICAL FEATURES Dry eyes and dry mouth Ocular sx: burning, itching, FB sensation, inability to wear contact lenses Xerostomia: “cotton mouth” sensation, difficulty swallowing dry foods, dental caries +/- rheumatoid arthritis or other connective tissue dx Dryness can involve nose, throat, larynx, bronchi, vagina, & skin  SJOGREN SYNDROME: DIAGNOSIS & TREATMENT Dx: Rheumatoid factor & antinuclear antibodies (ANA) common Schirmer test: measures quantity of tears secreted CBC to evaluate systemic activity Lip bx: lymphoid foci in accessory salivary glands Parotid bx: atypical presentations to r/o neoplasm  SJOGREN SYNDROME: TREATMENT Multidisciplinary referrals: Rheumatologist, Ophthalmologist, dentist Alleviate symptoms, ID systemic manifestations & prevent complications Eyes: Artificial tears Cyclosporine (Restasis) Mouth: Hydration Gum chewing/hard candy… Pilocarpine & cevimeline → stimulate saliva production PO hygiene  MUMPS/PAROTITIS: ETIOLOGY & PATHOPHYSIOLOGY Etiology: Paramyxovirus respiratory droplet spread Pathophysiology: 12-15 days exposure → onset Rapid spread in congregate settings 1/3 subclinical infection but still transmissible  MUMPS/PAROTITIS CLINICAL FEATURES Painful, swollen salivary glands (usually parotid) +/- F/C Can lead to trismus Can involve ________, pancreas & meninges PE: parotid tenderness with overlying facial edema  MUMPS/PAROTITIS: DIAGNOSIS & TREATMENT Dx: Clinical diagnosis ↑ IgM diagnostic Mild leukopenia, lymphocytosis may occur Tx: Symptomatic: topical compresses, antipyretics Vaccination prevention (MMR) Isolation until swelling subsides  DISEASES OF ORAL CAVITY AND PHARYNX Etiology/ Management/ Disease Clinical Features Diagnosis Pathophysiology Treatment Chronic irritation White patch; CAN History/exposure Elimination/monitoring; Leukoplakia NOT be removed biopsy if concerning features Erythroplakia Oral Lichen Planus Oral Candidiasis Glossitis Sialadenitis Sialolithiasis  CASE # 1 New grad PA is working 60 hrs/wk in general surgery and develops non-specific jaw swelling. She takes a Benadryl and wakes up the following morning with significantly worsened left lower jaw swelling with trismus. She is afebrile and otherwise asx. What is the most likely diagnosis? Why does the work history matter? Why did it get worse overnight?  CASE # 2 You are rounding on a patient POD # 1 s/p superficial parotidectomy. What type of neurological exam would you perform? What deficit is most likely to occur?  BOARD QUESTION A 4 year old presents with a sore throat, fever and rash. The rash developed today and appears on physical exam as a fine, punctuate erythematous lesions that blanch on pressure. The lesions are located on the face, along the skin folds, and on chest, back, and buttocks. The oropharynx is erythematous with enlarged tonsils. Palatal petechiae and strawberry tongue are also noted. Which of the following is the most likely diagnosis? a. Kawasaki’s disease b. Scarlet fever c. Rubeola d. Rubella  REVIEW Which is more likely to result in a malignancy? Leukoplakia or erythroplakia Physical exam technique to differentiate oral candidiasis from oral lichen planus? How would you differentiate an aphthous ulcer vs. herpetic stomatitis? Difference between sialadenitis & sialolithiasis? QUESTIONS?