Outline Gingivitis and Periodontal Disease I. Introduction II. Gingival Disease III. Periodontal Disease 報告者 : 許修銘 IV. Extrinsic Stains & Calculus V. Summary 日期 : 93/07/20 1 I. Introduction (1) 2 I. Introduction (2) Gingiva of childhood Free Gingiva • Color: more reddish • Surface: less stippled • Probing depths around primary teeth • Coronal to the bottom of the gingival sulcus Attached Gingiva - 2mm - Proximal > facial & lingual • Extend apically where the free gingiva ends at the mucogingival junction • Alveolar bone in primary dentition - Trabeculae ¾, Calcification ¾ - Marrow space½ 3 I. Introduction (3) 4 I. Introduction (4) Gingivitis Bacterial Plaque • An inflammation involving only gingival tissues next to the tooth • Pediatric p’t: mild, reversible type • Major etiologic factors: uncalcified & calcified bacterial plaque • Soft bacterial deposits that firmly adhere to the teeth • Sequence of plaque formation (after brushing) - ~ 2 hrs: plaque begins to form 5 (coccus on thin pellicle) - ~ 5 hrs: plaque develop by cell division - ~ 24 hrs: rod-shaped bacteria appear - ~ 48 hrs: a mass of rods & filaments 6 1 II. Gingival Disease II-1. Simple Gingivitis II-1. Simple Gingivitis Eruption Gingivitis (1) II-2. Acute Gingival Disease • Absence of coronal contour protection of tooth during early stage of active eruption • Impingement of food on the gingiva causes the inflammatory process II-3. Chronic Nonspecific Gingivitis II-4. Chlorhexidine – Plaque-control agent II-5. Gingival Diseases Modified by Systemic Factors II-6. Scorbutic Gingivitis 7 II-1. Simple Gingivitis 8 II-1. Simple Gingivitis Eruption Gingivitis (2) Gingivitis Associated with Poor Oral Hygiene • Early gingivitis - quickly reversible • Treatment: good oral prophylaxis + oral hygiene instruction • Treatment: Mild eruption gingivitis → improved oral hygiene Painful pericornitis → counterirritant (Peroxyl) Pericornitis + swelling & lymph node involvement → antibiotic therapy 9 II-1. Simple Gingivitis 10 II-2. Acute Gingival Disease Allergy vs. Gingival Inflammation Herpes Simplex Virus Infection (1) • In the allergic children: gingival inflammation↑ during pollen seasons • Primary infection occurs in a child under 6 y/o • 99% are subclinical • P’ts with complex allergies who have symptoms for longer periods may be at higher risk for more adverse periodontal changes (Matsson & Moller, 1990) 11 12 2 II-2. Acute Gingival Disease II-2. Acute Gingival Disease Herpes Simplex Virus Infection (2) Herpes Simplex Virus Infection (3) • Acute herpetic gingivostomatitis - Active symptoms: fiery red gingiva, malaise, irritability, headache, pain when eating - Run a course of 10~14 days - Characteristic oral finding: ↓vesicles (yellow/white liquid-filled) ↓ulcers (painful, Ø 1~3mm) + whitish gray membrane • Acute herpetic gingivostomatitis - Palliative treatment: mild topical anesthetic vitamin supplement - Definitive therapy: analgesics 1 wk later (acetaminophen, ibuprofen) antiviral drug (acyclovir, famciclovir, valacyclovir) 2 wks later 13 II-2. Acute Gingival Disease 14 II-2. Acute Gingival Disease Herpes Simplex Virus Infection (4) Recurrent Apthous Ulcer (RAU) (1) • Recurrent herpes labialis (RHL) - Emotional stress, lowered tissue resistance, excessive exposure to sunlight - Treatment: Cereals, Seeds, Nuts, Chocolate antiviral drug lysine therapy (daily lysine doses of 1000mg / avoid eating arginine-rich foods) (Griffith, Norins & Kagan, 1978) • Recurrent apthous stomatitis (RAS) Dairy products, Yeast Canker sore • School aged children and adults • Persist for intervals of 4~12 days • Recurrent painful ulcerations - On the moist mucous - Round to oval crateriform base - Raised reddened margins 5 days later 15 II-2. Acute Gingival Disease 16 II-2. Acute Gingival Disease Recurrent Apthous Ulcer (RAU) (2) Recurrent Apthous Ulcer (RAU) (3) • Cause is unknown - Delayed hypersensitivity - Autoimmune responses - Precipitating factors: mirror trauma, stress - Nutritional deficiency (iron, vit. B12, folic acid) • Treatment: - Topical application of tetracyclines - Chlorhexidine mouthwash - Kenalog in orabase - Acyclovir - 5% Amlexanox oral paste (Aphthasol) 17 18 3 II-2. Acute Gingival Disease II-2. Acute Gingival Disease Acute Necrotizing Ulcerative Gingivitis (1) Acute Necrotizing Ulcerative Gingivitis (2) • • • • Vincent infection Young adult Rapid onset Characterized by painful necrotic ulcerative gingival lesions and affected interdental papilla • Borrelia vincentii, fusiform bacilli, spirochetes • Treatment: - Subgingival curettage, debridement - Mild oxidizing sol’n (H2O2) - Antibiotic therapy ↓local tx + OHI 19 II-2. Acute Gingival Disease 20 II-2. Acute Gingival Disease Acute Candidiasis Acute Bacterial Infections • Thrush, Candidosis, Moniliasis • Raised, furry, white patches (removed easily →bleeding underlying surface) ALL p‘ p‘t • Treatment: - Topical use of antifungal agent (Nystatin) • Acute streptococcal gingivitis - Painful, vivid, red gingivae - Enlarged papillae & gingival abscesses • Treatment: - Broad-spectrum antibiotics - Improved oral hygiene - Chlorhexidine mouthrinses 21 22 II-3. Chronic Nonspecific Gingivitis II-3. Chronic Nonspecific Gingivitis • Prevalence - Commonly seen during the pre- & teenage period • Features: - Rarely painful - long periods • Etiology: - Hormonal imbalance - Inadequate oral hygiene - Vitamin deficiency - Malocclusion - Faulty restoration - Mouth breathing • Thorough daily oral hygiene 9 Ms later 23 6 Ms later 24 4 II-4. Chlorhexidine – Plaque-control agent II-4. Chlorhexidine – Plaque-control agent • Chlorhexidine (CH) is a chlorophenyl biguanide with broad antimicrobial activity • Usage in dentistry: - Control of smooth-surface caries - Denture disinfectant - Plaque-control agent (0.12% CH gluconate mouthrinse) • Adverse side effects: - Mouth dryness & burning sensations - Desquamative lesions - Calculus & extrinsic stain accumulation - Negative systemic effect • Sound conventional plaque control measure + adjunctive use of CH as therapeutic mouthrinse 25 26 II-5. Gingival Diseases Modified by Systemic Factors II-5. Gingival Diseases Modified by Systemic Factors Endocrine System Genetic origin -Puberty Gingivitis • 11~14 y/o, ¾ with age • Bulbous interproximal papillae (ant. segment) • Treatment: - Improved oral hygiene Removing local irritants Adequate nutrition Gingivoplasty (severe case) -Hereditary gingival fibromatosis (HGF) (1) • • • • ↓local tx ↓gingivoplasty Elephantiasis gingivae Hereditary hyperplasia of the gums Autosomal dominant (chromosome 2p21) Gingiva: normal (at birth) →distinctive enlargement (primary teeth erupt) 27 II-5. Gingival Diseases Modified by Systemic Factors 28 II-5. Gingival Diseases Modified by Systemic Factors Genetic origin PhenytoinPhenytoin-Induced Gingival Overgrowth (1) (PIGO) • Slow, progressive, benign enlargement of the gingivae • Treatment: • Dilantin Hyperplasia • Features: - HGF (2) - Painless enlargement of interdental papillae & marginal gingiva - Does not occur in edentulous areas - Interdental lobulations coalesce at the midline→pseudopockets - Quadrant surgical removal of hyperplastic tissue (recur within a few months) - Apically positioned flap + CO2 laser 29 30 5 II-5. Gingival Diseases Modified by Systemic Factors II-5. Gingival Diseases Modified by Systemic Factors PhenytoinPhenytoin-Induced Gingival Overgrowth (2) • Treatment: - Professional prophylaxis & rigorous home care - Antiplaque rinses (0.12% CH gluconate) - Surgical removal (severe-2/3) gingivectomy internal bevel flap surgery - Positive-pressure appliance - Folic acid therapy ↓surgical • Drugs reported to cause gingival enlargement: - Phenytoin (Dilantin, anti-epileptic) - Cyclosporin (anti-rejection) - Nifedipine (calcium channel blocker) - Valproic acid - Phenobarbital 31 32 II-6. Scorbutic Gingivitis II-6. Scorbutic Gingivitis • Vit. C deficiency • Features: - Involving marginal tissues & papillae - Severe pain - Spontaneous hemorrhage • Treatment: - Complete dental care - Improved oral hygiene - Vit. C supplements 16 m/o ↓ascorbic acid 400mg/day 13 y/o → improved diet + OHI → 2 wks later 33 III. Periodontal Disease 34 III-1. Periodontitis in Children • Periodontitis is an inflammatory disease of the gingival and deeper tissues of the periodontium characterized by pocket formation and destruction of supporting alveolar bone • Alveolar bone crest (ABC)ÅÆCEJ - Normal: 1 ± 0.5 mm - Questionable bone loss: 2~3 mm - Definite bone loss: ＞3 mm III-1. Periodontitis in Children III-2. Premature Bone Loss III-3. Papillon-Lefèvre Syndrome III-4. Gingival Recession III-5. Self-Mutilation III-6. Abnormal Frenum Attachment 35 36 6 III-1. Periodontitis in Children III-1. Periodontitis in Children EarlyEarly-Onset Periodontitis (EOP) PrePre-pubertal Periodontitis (PP) (1) • Otherwise healthy • Categorized under Aggressive Periodontitis • Three different categories: - Localized juvenile periodontitis - Generalized juvenile periodontitis - Pre-pubertal periodontitis • Can be localized but usually occurs in generalized form • Onset is unknown but 4 y/o is when bone loss seen around molars and / or incisors • Onset to alveolar destruction is rapid 37 38 III-1. Periodontitis in Children III-1. Periodontitis in Children PrePre-pubertal Periodontitis (PP) (2) PP (3) • Etiology: - Leukocyte chemotactic defect - Gingival pockets Actinobacillus actinomycetemcomitans Porphyromonas (Bacteroides) gingivalis • Treatment: - Early Dx, dental curettage & prophylaxis, OHI, extraction of hopeless primary teeth - Antibiotic: Amoxicillin or Tetracycline 4.5 y/o → dietary counseling + excellent oral hygience 8 yrs later 39 40 III-1. Periodontitis in Children III-1. Periodontitis in Children Localized juvenile periodontitis (LJP) (1) Localized juvenile periodontitis (LJP) (2) • Features: - Localized bone loss around permanent incisors & first molars - Little or no plaque or tissue inflammation - Progression is 3-4 times faster than adult • Etiology: - Aa is the etiologic microbial species - Neutrophil chemotactic defect 12 y/o 41 42 7 III-1. Periodontitis in Children III-1. Periodontitis in Children Generalized Juvenile Periodontitis (GJP) EOP Treatment • Severe periodontitis Rapidly progressive periodontitis • Occurs around puberty • Features: - Rapid affects the entire periodontium - Plaque deposition & marked inflammation • Etiology: - Porphyromonas gingivalis - Neutrophil chemotactic defect • General rules - Early Dx, antibiotics, infection-free • Treating LJP (Keyes technique/1985) - Scaling & root planing + irrigation with saturated salt sol’n & 1% chloramine-T - Systemic tetracycline (1g/day) for 14 D - Home care: soda/3% H2O2 + salt irrigations • Treating GJP: less predictable 43 44 III-2. Premature Bone Loss III-3. Papillon-Lefèvre Syndrome • Systemic– but rare in the primary dentition • Local factors: trauma, periodontitis • Related systemic disease • Precocious Periodontosis • Genetic disorder: chromosome 11q14-q21 • Features: - Palmar & plantar hyperkeratosis - Premature loss of primary & permanent teeth • Treatment: - Antibiotic therapy - Extraction of affected teeth - Hypophosphatasia - Papillon-Lefèvre syndrome - Histiocytosis X - Agranulocytosis - Leukocyte adherence deficiency - Neutropenias - Leukemias - Diabetes mellitus - Scleroderma - Fibrous dysplasia - Acrodynia - Down syndrome - Chdiak-Higashi syndrome 45 46 III-4. Gingival Recession III-3. Papillon-Lefèvre Syndrome 2.5 y/o 17.5 y/o • Etiology: 3 y/o 3~6 y/o: tetracyclines for ear infections 47 - Narrow band of attached gingiva Alveolar bony dehiscence Impinging frenum attachment Tooth prominence Toothbrush trauma Orthodontic tooth movement Oral habits Periodontitis Pseudorecession (extrusion of teeth) • Elimination of the stimulus & f/u 4~8 wks 48 8 III-6. Abnormal Frenum Attachment III-5. Self-Mutilation • Etiology - Local dental factors - Emotional problem • Normal frenum attachment usually terminating at the mucogingival junction • Abnormal/high frenum: inadequate attached gingiva in the insertion area 6 y/o • Seldom has there been any correlation between a maxillary frenum problem and recession 49 III-6. Abnormal Frenum Attachment 50 III-6. Abnormal Frenum Attachment Frenectomy & Frenotomy • Indications: - Persistent gingival inflammation - Progressive gingival recession - Midline diastema after 3│3 eruption - Inhibit tongue touching 1│1 . 51 IV. Extrinsic Stains & Calculus 52 IV-1. Extrinsic Stains & Deposits • Extrinsic staining – readily removed and have no effect on the enamel • Pigmentation is associated with an active chemical change in tooth structure e.g. 8% SnF2 → light brown ~ black IV-1. Extrinsic Stains & Deposits IV-2. Calculus 53 54 9 IV-1. Extrinsic Stains & Deposits IV-1. Extrinsic Stains & Deposits Green Stain Orange Stain • Result of the action of chromogenic bacteria on the enamel cuticle. • Gingival third of labial surface • Roughened surface → recurrence • Occurs less frequently and is easier to remove than green stain • Associated with poor oral hygiene • Gingival third 55 IV-2. Calculus IV-1. Extrinsic Stains & Deposits Black Stain • • • • 56 • Calcified dental plaque=Dental Calculus • Caries↓→Calculus↑ • Supragingival calculus - M│M buccal surfaces - 21│12 lingual surfaces Less common Difficult to remove A line following the gingival contour Relatively free from caries amelogenesis imperfecta 57 V. Summary 58 Thanks for Your Attention • The predominant form of periodontal disease in pediatric p’t is nonspecific gingivitis • Development of EOP: genetic factor, bacteria, systemic disease • Plaque & calculus is an important factor in the development of gingival & periodontal disease The End 59 60 10