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INTRODUCTION
Periodontal disease is defined as the disease of supporting tissue of the teeth caused by specific microorganism [group of specific organism], malocclusion, chronic trauma resulting in progressive destruction of the periodontal ligament & alveolar bone with pocket formation, recession or both.
CLASSIFICATION
Periodontitis
[A] Chronic periodontitis (slow onset) Localized Generalized [B] Aggressive periodontitis (early onset)
Localized aggressive periodontitis
(New term for localized juvenile periodontitis) Generalized aggressive periodontitis (New term for generalized juvenile periodontitis)
Leukocyte disorders Neutropenia Chediak-Higashi syndrome Leucocyte adhesion deficiency syndrome Papillon-Lefevre syndrome Down syndrome
Diabetes mellitus Hypophosphatasia Histiocytosis X Ehlers-Danlers syndrome Juvenile hyaline fibromatosis of gingiva Acquired immunodeficiency syndrome Virus-associated hemophagocytic syndrome Malnutrition
Hypophosphatasia Leucocyte adhesion defect Papillon-lefevre syndrome Down syndrome Chediak-Higashi syndrome Langerhans cell histiocytosis Acute leukemia Insulin-dependent diabetes mellitus
Mucogingival defects
Localized gingival recessions
PREPUBERTAL
PERIODONTITIS
Localized
Generalized
Affected site harbours actinobacillus actinomycetemcomitan, prevotella intermedia & porphyromonous gingivalis
Treatment
Local debridement Antibiotic therapy Improved oral hygiene
TREATMENT Antibiotic therapy Extraction of affected teeth SEQUELAE Prepubertal periodontitis involving primary teeth will advance to periodontitis of permanent dentition
LOCALISED TYPE -- It appears to be self limiting & affects mainly permanent first molars & Incisors in adolescents -- Bone loss is rapid & is not commensurate with amount of local Irritants present such as plaque & calculus
ETIOLOGY -- Susceptible individuals has both functional defects involving Neutrophils & high virulent strains of actinobacillus actinomycetemComitans & bacteriodes species
CLINICAL FEATURES -- More common in young adults involving permanent dentition Occurs in presence of marked gingival inflammation & gross plaque Accumulation ETIOLOGY:-- Subgingival plaque from affected site harbours high percentage Of porphyromonas gingivalis
TREATMENT
Medical debridment -- Antiobiotic therapy TETRACYCLINE 1gm/day FOR 14 TO 21 DAYS OR AMOXICILLIN 1gm/day + METRONIDAZOLE 750mgm/day FOR 7 DAYS
ORAL MANIFESTATION:-
(i) Gingival enlargement with ulceration (ii) Thinning of lamina dura (iii) Destruction of periodontal ligament (iv) Tooth migration
(i) Alveolar bone loss around primary level (ii) Severe ulcerative gingivitis
CYCLIC NEUTROPENIA
HYPOPHOSPHATASIA:-
It is characterised by low serum alkaline phosphatase & reciprocal change in urine phosphoethanol amine level
ORAL MANIFESTATION:-
(i) Premature mobility & loss of primary teeth [Incisors are affected more than molars] (iI) Acementogenesis (iii) Dentinal dysplasia (Iv) Enlarged pulp chamber
HISTOCYTOSIS X
It is non lipidreticuloendotheliosis marked by multiple hard & soft tissue lesions containing histocytes & eosinophils
ORALMANI
ACRODYNIA
It is also called pinks or swifts diseases
ETIOLOGY
DIABETES MELLITUS & CHRONIC GRANULOMATOUS DISEASES Patient is more susceptible to periodontal desiases because of decreased immunity
DOWN SYNDROME:It is a genetic condition arising form trisomy of chromosome 21.Patient is susceptible to periodontal diseases because of specific immune defect involving t lymphocyte
The greater metabolic activity in children in whom anabolism is dominant over catabolism may offer the peridontium greater resistance to break down The oral flora is different in children,late establishment of spirochetes and bacteroides which have been associated with the development of gingivitis in children may delay the onset of periodontal disease The composition and metabolism of plaque found in children may be responsible for its reported lower irritation potential