Soft tissue oral lesions in children


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Soft tissue oral lesions in children

  1. 1. SOFT TISSUE ORAL LESIONS IN CHILDREN Chinthamani Laser Dental Clinic
  2. 2. Drug induced gingival hyperplasia (PIGO) Also known as phenytoin induced gingival overgrowth.  Dilantin hyperplasia. ETIOLOGY: Multifactorial a) Disturbance in adrenocortical function b) Local response to metabolic products of phenytoin in saliva c) Direct action on phenytoin on fibroblast.  It is related to the efficacy of oral hygiene and, thus to the amount of plaque, and inadequate amounts of antimicrobial factors in the oral cavity could contribute to greater plaque accumulation. 
  3. 3. Clinical features        Appears as early as 2 to 3 weeks after initiation of drug therapy, peaks at 18 to 24 months. Painless enlargement of interproximal gingiva. The buccal & anterior segment are more affected than the lingual & posterior segments. Gingiva appears pink and firm Does not bleed on probing. Lesion is purely fibrotic in nature or… Secondary infection superimposes and combined type of inflammatory enlargement ensues.
  4. 4. Clinical features   As interdental lobulations grow, clefting becomes apparent at the midline of tooth. Lobulations coalesce at the midline forming pseudopockets and covering most of crown tooth
  5. 5. TREATMENT Symptomatic treatment: -Antihistamines -Topical steroids -Folic acid -Ascorbic acid -Topical antibiotics -Alkaline mouth washes  Vigorous gingival massage coupled with efficient tooth brushing and gum stimulators. 
  6. 6. Treatment      Surgical approach: Gingivectomy with periodontal knives. Laser Electrosurgery Internal bevel flap surgery
  7. 7. CONDITIONED ENLARGEMENTS Occurs when the systemic condition of the patient exaggerates or distorts the normal response to the dental plaque.  Includes: Pubertal gingivitis Non-specific Nutritional Allergic 
  8. 8. Hormonal (pubertal gingivitis) ETIOLOGY:  Hormonal changes    Direct effect on perio. tissue metabolism Permeability of the vascular system Microbiota react specifically to availability of hormones in oral fluids.
  9. 9. Clinical features      Circumpubertal enlargement Sex: both in males and females Appears in areas of local irritation Size of gingival enlargements far exceeds that usually seen in comparable local factors. After puberty, the enlargement undergoes a spontaneous reduction.. But does not disappear until local factors are removed.
  10. 10. Treatment  Removing sources of irritation  Scaling  Curettage  Surgical removal in severe cases
  11. 11. NUTRITIONAL(SCURVY) ETIOLOGY  Deficiency of vitamin c
  12. 12. Clinical features       Gingiva : -bluish red -soft and friable -smooth shiny surface Spontaneous hemorrhage on slight provocation Surface necrosis with pseudomembrane formation Enlarged tissue cover the clinical crown Typical foul breath with fusospirochetal stomatitis Superinfection leading to ulceration and necrosis of papillae
  13. 13. Treatment     Ingestion of vit. C tablets Diet rich in citrus fruits Oral prophylaxis Maintainence of good oral hygiene
  14. 14. Non specific enlargements (granuloma pyogenicum)      The lesion varies from a discrete spherical , tumour like mass with a pendulated attachment to a flattened , keliod like enlargement with a broad base. Bright red , Either friable or firm, surface ulceration Purulent exudation
  15. 15. Treatment   Removal of lesion Eliminating irritating local factors
  16. 16. Allergic (plasma cell gingivitis)   The use of drugs may evoke an allergic rasponse manifested as an inflammatory reaction. May be associated with generalised allergic response.  The gingival and buccal mucosa on the left side show pronounced erythema and slight swelling. Diffuse ulcerations can also be seen.
  17. 17. The inflammatory infiltrate is composed predominately of plasma cells (He x 400).
  18. 18. Treatment   Stoppage of drugs generally reverses this condition. Anti – allergic drugs are of help.
  19. 19. Juvenile periodontitis Uncommon form of severe periodontal disease belonging to a group termed as an  EARLY ONSET AGGRESSIVE PERIODONTAL DISEASE.  Described by Wannenmacher(1938)  Age: teenagers  3 types of disease: a) chronic slowly progressive b) fairly generalized c) acute progressive and more general 
  20. 20. Etiology PMN dysfunction Susceptibility to infection A. Actinomycetemcomitans Serum amplification leukotoxin antibody neutralisation Local PMN & macrophage destruction Accelerated disease
  21. 21. Clinical features Loss of attachment Bone loss(3-4 times) Mobility of teeth Denuded root surface Periodontal abscess
  22. 22. Clinical features (cont.)     Teeth involved: permanent incisors and first molars. The attack sequence appear to follow eruption chronology. Most striking feature : Lack of clinical inflammation despite the presence of deep pockets. Starts as a localized form if not treated generalized form
  23. 23. Clinical features (cont.)     Advanced bone loss in the primary dentition does exit but without destinctive localization. Every third case presents with lymphadenopathy Clinically only thin layer of plaque is present Classically, distolabial migration of the maxillary incisors Diastema formation
  24. 24. Radiographic findings •A full mouth series of radiographs would be beneficial in this case rather than routine bite wing x-rays. • Bilateral bone loss is discovered around all first molars and incisors. • Vertical bony defects are Characteristic in LJP.
  25. 25. Treatment       Root resection Subgingival irrigation with iodine and hydrogen peroxide. Scalling and root planing Tetracycline is antibiotic of choice Oral hygiene maintainence Bone grafting
  26. 26. Preoperative and post operative
  27. 27. Papillon lefevre syndrome Described by : Papillon and Lefevre  Characterized by hyperkeratosis of palms and soles + precocious periodontal destruction and shedding of the deciduous and permanent dentition. ETIOLOGY:  Suggested to be due to 1. Defective local vitamin A metabolism 2. Deep subgingival flora assocaited with PLS is composed of great no. of motile, gram –ve anaerobic rods , including bacteroids gingivalis and capnocytophagia. 3. Cellular immune defect with a decreased stimulation of lymphocytes. 4. Now generally accepted as the homozygosity of autosomal recessive genes. 
  28. 28. Clinical features a)   Skin lesions: start b/w first and fourth year after birth. Hyperkeratotic lesions of palms and soles bilaterally. Hyperkeratosis is usually progressive and becomes dry and scaly.
  29. 29. Clinical features b)        Dental signs and symptoms: Swollen gingiva, migration and mobility of teeth Pockets Fetor-ex-oris Painless exfoliation By 3.5 to 4.5 years all the deciduous teeth are lost. Eruption of permanent enhanced Disease progress recycles & by ages 13-14 & all permanent teeth
  30. 30. Radiographic findings    Severe horizontal alveolar bone loss. Alveolar bone and basal bone resorbs beyond apices of roots. Incomplete root resorption.
  31. 31. Treatment   Vitamin C metabolites (retinoids):are involved in regulation of growth and differentiation of the epithelial cells. Profound effect on keratinization by dec. the total keratin content of the keratinocytes. Antbiotics
  32. 32. 044-43800059 , 92 83 786 776