Oral disease Notes

NOTES NOTES ORAL DISEASE GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES ▪ Infectious, inflammatory diseases; affect oral cavity, associated structures RISK FACTORS ▪ Poor oral hygiene, dehydration, concomitant illness, malnutrition DIAGNOSIS DIAGNOSTIC IMAGING X-ray ▪ See individual diseases CT scan ▪ Soft tissue inflammation extension SIGNS & SYMPTOMS ▪ Inflammation ▫ Redness, swelling, pain, loss of function, warmth ▪ Infection ▫ Fever, malaise, localized pain TREATMENT MEDICATIONS ▪ Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain ▫ For inflammation ▪ Antibiotics, antifungal medications ▫ For infection APHTHOUS ULCERS osms.it/aphthous-ulcers PATHOLOGY & CAUSES ▪ Painful lesions inside mouth; benign, noninfectious; AKA canker sores TYPES Minor ▪ Small (3–4mm), last 7–10 days, recur 3–4 times/year; if recurrent, > 4 times/year Major ▪ Lesions > 1cm, last 10–30 days 334 OSMOSIS.ORG Herpetiform ▪ Coalesce, recur frequently CAUSES ▪ Idiopathic; likely multifactorial; may be part of TH1 autoimmune response, hormonal factors influence epithelium thickness, connected to vitamin B12 deficiencies RISK FACTORS ▪ Stress, systemic autoimmune disorders (e.g. celiac), nutritional deficiencies, stopping smoking, oral cavity trauma (e.g. biting lips, dentures)

Chapter 39 Oral Disease COMPLICATIONS ▪ Recurrent aphthous stomatitis (Mikulicz ulcers), infection; may interfere with eating/ drinking SIGNS & SYMPTOMS ▪ Round/oval ulcerations in oral mucosa, white/yellow sharply demarcated center covered with fibrous membrane cap, surrounded by red erythematous margins; yellowish exudate ▪ Inside of cheeks, lips; under tongue; painful swallowing, if in back of throat Minor ▪ Small, mildly painful, annoying, round/ oval, disappear within seven days, resolve spontaneously, no scarring; more common on non-keratinized epithelium DIAGNOSIS OTHER DIAGNOSTICS ▪ Recurrence of ulcers TREATMENT MEDICATIONS ▪ Vitamin B12 supplementation ▪ Topical analgesics, corticosteroids, sucralfate suspension ▪ Anti-tumor necrosis factor (TNF)-alpha agents ▫ Recalcitrant, recurrent ulcers OTHER INTERVENTIONS ▪ Avoid triggers Major ▪ Larger, painful, recur more often, may scar Herpetiform ▪ Not herpes virus connected, vesicles coalesce into patches Figure 39.1 The clinical appearance of aphthous ulcers. OSMOSIS.ORG 335

DENTAL CARIES DISEASE osms.it/dental-caries DIAGNOSIS PATHOLOGY & CAUSES ▪ Odontogenic infections; tooth decay caused by acids produced by bacteria. ▪ Bacteria → plaque → ↓ pH → demineralization → caries CAUSES ▪ Streptococcus mutans, Streptococcus sabrinus, Lactobacillus spp. ▫ Metabolically produce acids RISK FACTORS ▪ Prolonged bottle use (baby bottle tooth decay), poor oral hygiene, sugar-rich foods, diabetes mellitus (DM), salivary gland disorders (e.g. Sjogren’s), medications that decrease salivation COMPLICATIONS ▪ Hematogenous spread of bacteria to heart valves, joints, implanted prosthetics ▪ Spread from enamel to tooth pulp, alveolar bone ▪ Abscesses ▪ Soft tissue infections in extraoral perforation ▪ Deep head, neck infections ▪ Jaw osteomyelitis ▪ Tooth loss DIAGNOSTIC IMAGING Odontogram ( jaw X-ray) ▪ Examine depth of lesions CT scan ▪ If widespread, soft tissue infection OTHER DIAGNOSTICS Clinical presentation ▪ Teeth discoloration, changes TREATMENT MEDICATIONS ▪ Topical/systemic antibiotics SURGERY ▪ Extraction of infected material, replacement with fillings OTHER INTERVENTIONS ▪ Dietary counselling, hygiene improvement SIGNS & SYMPTOMS ▪ Yellow/black teeth staining, enamel softening; appearance of pits, cracks ▪ If severe: tooth collapse ▪ If pulp affected: dull pain exacerbated by cold, soft food ▪ If root caries: lower, where teeth close together, food difficult to extract; more difficult to diagnose 336 OSMOSIS.ORG Figure 39.2 A dental cavity in the tooth of a ten-year-old boy.

Chapter 39 Oral Disease Figure 39.3 An orthopantomogram demonstrating dental cavities of the left mandibular second and third molar teeth. GINGIVITIS osms.it/gingivitis PATHOLOGY & CAUSES ▪ Type of periodontal disease; inflammation of gums ▪ Pathogenic bacteria tunnel between microcolonies on tooth to surface in order to bring in steady supply of food → form hard mass (dental calculus) → bacterial plaque formation → enter gingival sulcus → gingivitis ▪ Immune response delivers blood to damaged tissue → provides nutrients for bacteria → immune response activates osteoclasts → dissolves bone → tooth loosening ▪ Non-infectious systemic factors → gingival overgrowth, inflammation ▫ Hormonal shifts (e.g. during pregnancy) ▫ Drug-induced (e.g. phenytoin, calcium channel blockers) ▫ Malnutrition-induced (e.g. vitamin C deficiency) ▫ Non-plaque-induced (rare, associated with genetics, allergy, trauma) COMPLICATIONS ▪ Periodontitis, tooth loss, receding gums SIGNS & SYMPTOMS ▪ Redness, swelling, bleeding after brushing/ flossing ▪ May be asymptomatic in early infection DIAGNOSIS DIAGNOSTIC IMAGING X-ray ▪ Evaluate bone level, sulcus becomes deeper as periodontal pocket expands OTHER DIAGNOSTICS Physical exam ▪ Swollen/bleeding gums, probe gingival sulcus to determine depth RISK FACTORS ▪ Poor dental hygiene, older age OSMOSIS.ORG 337

TREATMENT MEDICATIONS ▪ Antibiotics for severe infections SURGERY ▪ Removal of infected tissue if severe Figure 39.4 An individual with a severe case of gingivitis. The gums are swollen and hemorrhagic. There is visible plaque covering the free gingival margin of both maxillary incisors. LUDWIG'S ANGINA osms.it/ludwigs-angina PATHOLOGY & CAUSES ▪ Bilateral infection of submandibular space (sublingual, submylohoid) CAUSES ▪ Spread from infection of 2nd/3rd mandibular molars, pericoronitis, parotitis, peritonsillar abscess ▪ Mandibular fracture, piercings ▪ Causative agents polymicrobial from mouth flora, dominated by Streptococcus viridans; staphylococci, bacteroides also common RISK FACTORS ▪ DM, hypertension, HIV infection, immunosuppression COMPLICATIONS ▪ Airway obstruction, mediastinitis, necrotizing cellulitis, sepsis, asphyxia 338 OSMOSIS.ORG SIGNS & SYMPTOMS ▪ Infection ▫ Fever, chills, malaise, pain ▪ Stiff neck, dysphagia, individual leans forward to expand airway, no lymphadenopathy, bilateral, sudden aggressive spread, enlarged tongue, drooling ▪ Critical symptoms ▫ Stridor, cyanosis ▪ No abscess formation DIAGNOSIS DIAGNOSTIC IMAGING CT scan ▪ Rule out abscess formation (occurs late in disease) ▪ Chest CT scan ▫ Mediastinitis

Chapter 39 Oral Disease LAB RESULTS TREATMENT ▪ Blood culture MEDICATIONS OTHER DIAGNOSTICS ▪ Ultrasound-guided needle aspiration ▪ Empiric broad-spectrum antibiotics with beta-lactamase activity SURGERY ▪ Surgical drainage, if abscess identified on CT scan OTHER INTERVENTIONS Airway management ▪ Fiberoptic nasal intubation, emergent tracheostomy may be necessary ORAL CANDIDIASIS osms.it/oral-candidiasis PATHOLOGY & CAUSES ▪ Opportunistic infection of oral mucosal membranes by Candida spp. (e.g. Candida albicans) ▪ AKA thrush TYPES Pseudomembranous ▪ Whitish plaques on oral mucosa (most common); can be scraped off to reveal erythematous surface Atrophic (denture stomatitis) ▪ Red lesions without plaques Hyperplastic (rare) ▪ Non-scrapable plaques RISK FACTORS COMPLICATIONS ▪ Spread into pharynx, disseminated candidiasis SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ ▪ May be asymptomatic Cottony feeling in mouth; lesions Pain/tenderness in oral cavity Painful swallowing (odynophagia) Decreased sense of taste Angular cheilitis DIAGNOSIS LAB RESULTS ▪ Microbiological analysis of scrapings; Gram stain; KOH preparation; biopsy ▪ Young age, dentures, xerostomia, antibiotics, DM, malnutrition ▪ Immunosuppression due to corticosteroids, chemotherapy, HIV/AIDS OSMOSIS.ORG 339

TREATMENT MEDICATIONS ▪ Topical antifungal agents (e.g. nystatin suspension, clotrimazole troches, systemic fluconazole) Figure 39.5 Oral candidiasis in a child who had taken antibiotics. PAROTITIS osms.it/parotitis PATHOLOGY & CAUSES ▪ Parotid gland inflammation ▪ Salivary stasis → seeding of parotid (Stensen) duct by microorganisms → infection, inflammation CAUSES ▪ Bacterial: S. aureus, most common ▪ Viral: mumps, influenza, coxsackie, Epstein– Barr virus (EBV) ▪ Autoinflammatory: sarcoidosis as part of Mikulicz syndrome RISK FACTORS ▪ Surgery, dehydration, salivary gland stones, poor oral hygiene, medications that decrease salivation (e.g. anticholinergic, 340 OSMOSIS.ORG sympathomimetics) COMPLICATIONS ▪ Spread to deep head, neck structures; septic jugular thrombophlebitis; septic osteomyelitis; sepsis; respiratory obstruction; facial nerve palsy SIGNS & SYMPTOMS ▪ Systemic manifestations ▫ Fever, chills ▪ Periauricular, mandibular pain, swelling; trismus, dysphagia; purulent drainage ▪ Viral ▫ No discharge, prodrome followed by swelling lasting 5–10 days

Chapter 39 Oral Disease DIAGNOSIS DIAGNOSTIC IMAGING ▪ Sample purulent exudate, ultrasound guided needle aspiration; culture, Gram stain Ultrasound ▪ Increased blood flow through gland, enlargement, nodules CT scan ▪ Extension of inflammation to surrounding tissues LAB RESULTS ▪ Complete blood count (CBC) ▪ Increased amylase without underlying pancreatitis ▪ Viral shows leukocytosis, increased IgM against mumps Figure 39.6 The clinical appearance of parotitis of the left parotid gland. There is a marked swelling just anterior to the left ear. TREATMENT MEDICATIONS ▪ Hydration; IV antibiotics ▪ Vaccination ▫ Mumps prevention PERIODONTITIS osms.it/periodontitis PATHOLOGY & CAUSES ▪ Inflammation, destruction of supporting structures around teeth, wasting of bone ▪ Dysbiosis (disturbed bacterial symbiosis) more extreme than in gingivitis ▪ Orange-complex of bacteria (Fusobacterium nucleatum, Prevotella intermedia), red-complex of bacteria (Tannerella forsythia, Treponema denticola, Porphyromonas gingivalis) → immune response → more blood flow to damaged tissue → provides nutrients for bacteria → more damage to gingiva, periodontal ligament → activated osteoclasts in bone → tooth loosening ▪ Severity based on ligament loss ▪ Porphyromonas gingivalis impairs immune cells, kills bacteria → pathogenic bacteria overgrow ▪ Necrotizing ulcerative periodontitis (NUP) ▫ Extreme loss of periodontal attachment, alveolar bone; associated with immunosuppression (e.g. HIV/AIDS; chemotherapy, severe malnutrition); may be associated with enteric bacteria, yeast OSMOSIS.ORG 341

CAUSES ▪ Poor oral hygiene; red-, orange-complex bacteria RISK FACTORS OTHER DIAGNOSTICS ▪ Clinical exam ▫ Probe teeth pockets, test for bleeding, depth TREATMENT ▪ DM, smoking, Ehler–Danlos syndrome COMPLICATIONS ▪ Tooth loss, infection spread to soft tissues of head, neck, sinusitis; hematogenous dissemination to heart valves (prosthetic/ native), joints, etc. SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ Redness, swelling, tender to palpation Halitosis Bleeding during teeth brushing Teeth loosening Periodontal pockets widen MEDICATIONS ▪ Systemic antibiotics (if severe) SURGERY ▪ Removal of infected tissue (if severe) OTHER INTERVENTIONS ▪ Prevent plaque formation ▫ Daily brushing, flossing; antimicrobial agents (e.g. mouthwash) ▪ Scaling, root planing ▫ Remove plaque ▪ Topical fluoride DIAGNOSIS DIAGNOSTIC IMAGING Panoramic dental X-ray ▪ Bone loss around tooth SIALADENITIS osms.it/sialadenitis PATHOLOGY & CAUSES ▪ Inflammation of salivary glands ▫ Parotid (most common), sublingual, submandibular; unilateral ▪ Decreased flow of saliva → deposits settle in walls of salivary duct → duct blocked → flow of saliva slowed → deposits of calcium, phosphorous, etc. precipitate → form small concretions (microsialoliths) → grow into sialoliths → stones block duct → bacteria moves from mouth up, around blockage, into salivary duct → 342 OSMOSIS.ORG inflammation, tissue swelling CAUSES ▪ Bacterial: Staphylococcus aureus (most common), Streptococcus viridans, Haemophilus influenzae ▪ Viral: mumps, HIV RISK FACTORS ▪ Decreased salivary flow (dehydration, illness, anticholinergic medications, Sjogren’s syndrome) ▪ Risk increases with age

Chapter 39 Oral Disease LAB RESULTS ▪ Lab culture of pus ▫ Gentle compression of gland OTHER DIAGNOSTICS ▪ Clinical presentation TREATMENT MEDICATIONS ▪ Antibiotics SURGERY Figure 39.7 An individual holding their own salivary duct stone following surgical removal. Salivary duct stones predispose individuals to sialadenitis. ▪ Surgical gland removal ▫ If disease recurrent OTHER INTERVENTIONS ▪ Hydration, warm compress, glandular massage, sialogogues SIGNS & SYMPTOMS ▪ Acute sialadenitis ▫ Fever, chills, abscess formation ▫ Pain, swelling, redness of skin overlying affected gland ▫ Less saliva → dry mouth → bad taste (pus leaking out of affected duct) ▫ Severe: painful to open mouth ▪ Chronic sialadenitis ▫ Less painful, gland enlarges following meals, no overlying redness of the skin ▫ Associated with conditions linked to chronic decreased salivary flow (e.g. Sjogren’s syndrome), due to inflammation, salivary duct fibrosis, altering glandular tissue, composition of saliva DIAGNOSIS Figure 39.8 A submandibular sialogram demonstrating a salivary duct stone; a risk factor for sialadenitis. DIAGNOSTIC IMAGING Ultrasound ▪ Abscess, salivary stone, tumor OSMOSIS.ORG 343

Figure 39.9 The histological appearance of sialadenitis at low power. The acini are surrounded by dense fibrosis and display patchy lymphocytic infiltrates. 344 OSMOSIS.ORG