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Dental and periodontal pathology and odontogenic infections - Coggle…
Dental and periodontal pathology and odontogenic infections
Infant Oral Assessment, and early assessment
Steps
Medical and dental history, examination, provide caries risk assessment and appropriate caries prevention plan, provide anticipatory guidance
Intraoral soft tissues, and compare and contrast mucosa gingiva
Oral Environment
Diverse Normal flora, warmth, moisutre
Surfaces in the oral cavity allow microorganisms to adhere and form biofilms
Highly organized communities of microorganisms that hold the community together, form plaque
Relevant in initiation of oral disease states, acid released buts pressure on biofilm, and sucrose is main driver
Oral Mucosa
Organization
Lining Mucosa (non-keratinized)
Mobile areas of the epithelium (soft palate, ventral surface of the tongue, floor of mouth, and mucosal surfaces)
Masticatory Mucosa: Keratinized
Gingiva, hard palate, dorsal surface of tongue
Specialized Mucosa:
Dorsal tongue and lingual papillae
Gingiva
Attached gingiva: Firm densed tightly bound to underlying periosterum, tooth adn bone
Fre gingiva: part that surrounds tooth and is not directly attached
Dental Caries
Process
Formation of protein coating (Pellicile) on tooth
Allows bacteria to adhere
fermentation of dietary carbohydrate lowers pH
acids released from bacteria demineralize tooth enamel
saliva cannot penetrate plaque to neurtralize the acid to remineralize surface
caries progress with breakdown of dentinwhihc erodes, reaches pulp and causes pain
Multifactorial
Susceptible tooth surface: poor oral hygiene
specific microorganisms: S. Mutans bacteria
fermentable carbohydrates: Cariogenic diet, sweetened beverages
time: prologned exposure
Early childhood Caries
Definition
presence of 1+ decayed, missing, or filled tooth surfaces in any primary tooth in a child 71 months of age or younger
Characteristics: S. Mutans, Vertically tranmsision, preventable via proper oral hygiene and dietary habits
Determinants: Bacterial Acquisition, oral hygiene status, prolonged exposure to fermentable carbohydrates
Clinical presentation
Early Lesions
Develops on smooth surfaces, and appears as chalky white decalcification
Advancing
Virulent caries with rapid progression, enamel chips away as lesions advance
Rampant
Progressively involves molar and cuspid teeth, maxillary and mandibular lesions present
Severe
Pulpal involvement, abscess, fistula, risk for cellulitis
Complications
Odontogenic Infection: Decayed teeth with dental abscess
Facial Cellulitis: Infection spreading into surrounding tissues
Treatment
has unique challenges, advanced behaviour management, and substantial costs
Moving from surgical treatment to chronic disease management
Chemotherapeutics and interventions to suppress microial flora, remineralizing agents, and inhibit demineralization
Fluoride varnish: Stabilise early lesions and slow progression of active carries
Interim therapeutic restorations: Place fluoride releasing restorative material, regular follow up care
Silver diamine Fluoride: Arrest caries progression, antimicrobial and mineralizing agent
Oral Lesions
Primary Herpetic Gingivostomatitis
Initial exposure to the herpes simplex virus, small vesicles coalesce and rupture
Mangement: Maintain hydration and nutritional intake
Neonatal Cysts
Small white papules that is present in newborns
Epstein Pearls (median palatal raphe), Bohn's nodules (remnants of salivary glands, hard palate and junction), Dental lamina (crest of alveolar ridge)
Management: None
Natal or neonatal Teeth
Within 30 days erupt, lower incisors, normal primary teeth
Maintain if stable and monitor for changes
Riga Fede Ulceration
Traumatic ulceration of ventral surface of tonuge caused by rubbing on newly erupted sharp incisal edges of mandibular incisiors
Management: Refer to pediatric dentist for reducing and smoothing of teeth
Eruption Cyst
Fluctuant fluid cyst may appear prior to eruption
Management: Monitor for tooth eruiption, incision is contraindicated
Aphthous Stomatitis
Single or multiple superficial erosions
Management: Palliative, lesions heal uneventfully
Periodontal Disease
Gingivitis: Most common and mild form of periodontal disease, tissue irritation, redness, swelling
Cause
Oral bacteria intereact with sugars and starches that form plaque, and if remains on teeth forms calculus
Types
Hyperemic: Increased blood flow to tissue, secondary to poor poral hygiene
Hyperplastic: Overgrowth due to hyperplastic or hypertrophic often induced my medication (CCB, Anti-epileptic medications, immunosuppressive drugs)
Periodontitis: At the gingival crevice (sulcus), epithelium is attached to the tooth, bacteria accumulate, disrupt attachment, periodontal tissues are infected and inflamed
Causes
Calculus serves as a reservoir for bacteria, the longer plaque and calculus remain the more damage is expected
Persistent inflammation ultimately leads to tissue destruction and pocket formation between teeth and gums
Pocket depth advances with disease progression, resulting in tissue and bone loss, tooth instability, and ultimately tooth loss
Bacterially induced: A. Actinomycetemocomitans, P. Gingivalis, P. Intermedia, B. Forsythus (Gram -ve anaerobic)
Inflammatory: Destroys connective tissue and alveolar bone
Common over age of 65
Pathogenesis
Difficulty to access to remove plaque, calculus and bacteria
Anaerobic bacteira that produce endotoxin (LPS)
Inflammatory mediators results in breakdown of conenctive tissue and bone loss
Symptoms
Red/Shiny guyms, gingival bleeding, painless,t ender on palpation, swollen discolored gums, halitosis, recession, mobility of teeth, abscess/purulence
Examination
Tone, texture, color contour, probing (bleeding/attachment levels), Calculus/Plaque, gum recession, furcations, tooth mobility, radiographs (bone loss)
Treatment
Active therapy
Minor cases (non-surgical) - Scaling/root planning
Advanced cases: Surgical, periodontal surgery and extractions
Allows for better access, decreases probling depth, can regenerate los tissues, and eliminate active infection
Supportive Therapy
Maintenance: Good Oral hygiene, regular professional monitoring
Halitosis
20% of population has some degree of bad breath
Miyazaki Classification
Genuine halitosis: physiology, pathologic
Pseudohalitosis, Halitophobia
Sources
Tongue, periodontal disease, Dental caries, recent oral surgery, food impaction, oral infection, poor hygiene, smoking, garlic and dairy diet, dry mouth
Main Cause: Putrefaction of sulfur containing amino acids in dietary and salivary protein by anaerobic gram-negative bacteria found in biofilms
Treatment
Tongue brushing/scraping, chewing gum, gargling, proper oral hyginee and profession care, furhter asssesment
Loss of primary teeth
Usually occurs around 6 years of age with loss of incisors
Premature exfoliation is an important diagnostic event that warrants prompt investigations to see into: Toxicities, metabolic disorders, malignancies, syndromes