1.Anatomy of the periodontium in children Gingiva Marginal gingiva For children,marginal gingival tissue around the primary dentition are more highly vascular contain fewer connective tissue than tissues around the permanent teeth.

2. Attached gingiva The width of attached gingival is less variable in the primary dentition, there is less mucogingival problem in the primary dentition Junctional epithelium There continue to be an apical shift when the teeth are fully erupted. the gingival margins are frequently at different levels on adjacent teeth that are at different stages of eruption. Sometimes it gives an erroneous appearance that gingival recession has occurred around those teeth that have been in the mouth longest. Stability is achieved at 12 years for 1 2 3 5 6, 16 years for the other teeth. 3. Periodontal ligament Periodontal ligament space is wider in children It is less fibrous and more vascular Cementum Thinner Alveolar bone Thinner cortical plates Larger marrow spaces Greater vascularity Fewer trabeculae 4. Gingival conditions Acute gingivitis Chronic gingivitis Gingival overgrowth Factitious gingivitis Mucogingival problems 5. Primary herpetic gingivostomatitis Definition: An acute infectious disease of the gingiva caused by the herpesvirus Pathogeny: Herpes simplex viruses Herpes simplex viruses (HSVs) Two types exist: type 1 (HSV-1) and type 2 (HSV-2). Both are closely related but differ in epidemiology Type-1 Gingivostomatitis Type-2 Genitalia Transmission: HSV-1 is transmitted chiefly by contact with infected saliva Infected saliva from an adult or another child is the mode of infection. HSV-2 is transmitted sexually or from a mother's genital tract infection to her newborn. 6. Prevalence: HSV infection appears to have increased worldwide in the last 2 decades, making it a major public health concern. Many primary infections are asymptomatic, Herpes simplex infections are asymptomatic in as many as 80% of patients, Symptomatic infections may be characterized by significant morbidity and recurrence. Moreover, infections can cause life-threatening complications, particularly in immunocompromised hosts. 7. Clinical features: Age: 6 months to 3 years Incubation period 1 week Prodrome: Febrile illness Headache, malaise, oral pain Cervical lymphadenopathy 8. Symptom Gingivitis: Gingivitis is the most striking feature, with markedly swollen, erythematous, friable gums Vesicular lesions: Vesicular lesions develop on oral mucosa ,lip and tongue can occur anywhere in the oral cavity, on the perioral skin, on the pharynx Diagnosis: According to Clinical features,History and age 9. Prognosis Oral lesions heal without scarring Course: Acute disease lasts 5-7 days, and the symptoms subside in 2 weeks. Viral shedding from the saliva may continue for 3 weeks or more. Adults also may develop acute gingivostomatitis, but it is less severe and is associated more often with a posterior pharyngitis. 10. Treatment: The availability of effective chemotherapy underscores that the prompt recognition of the infection early initiation of therapy are of utmost importance in the management of the disease. The goals of treatment are to make the patient comfortable and to prevent secondary infections or worsening systemic illness. It includes: 11. Pharmacotherapy Antiviral treatment . Symptomatic treatment 12. Antiviral treatment : Overall, medical treatment of HSV revolves around specific antiviral treatment. Patients should be advised about the potential for autoinoculation if they touch the herpetic lesion and then touch a mucous membrane or an eye. Controlling autoinoculation can be a challenge if the patient is a young child. 13. Symptomatic treatment In situations in which constitutional effects such as fever occur, symptomatic treatment can be used. Analgesics, such as acetaminophen, may make the patient more comfortable. Aspirin should be avoided in pediatric patients because of the possibility of Reye syndrome. Topical anesthetics and coating agents may make the patient more comfortable and may aid in the consumption of food; however, they do not speed healing. Appropriate wound care is needed, and treatment for secondary bacterial skin infections may be required 14. Supporting treatment : Soft diet Be kept well hydrated: The patient should maintain fluid intake and a balanced diet with the use of liquid food replacement if necessary Bed rest 15. Warnings to parent: No school, day care etc. Children are highly contagious Sterilize eating and drinking utensils Disease is self-limiting; 10-14 days in duration 16. Acute necrotizing ulcerative gingivitis(ANUG) Aetiology: Broad anaerobic infection Causative organism: Fusiform bacteria , Spirochaete Other Gram-negative anaerobic organism Clinical features: Necrosis and ulceration Interdental papillae marginal gingival Covered by yellowish-grey pseudomembranous slough, Acute stage enters a chronic phase after 5-7days. Recurrence of the acute condition is inevitable Pre-existing gingivitis Distinctive halitosis 17. Treatment Intense oral hygiene Oxidant: hydrogen peroxide Mechanical debridement Metronidazole 18. Chronic gingivitis Chronic gingivitis is a common condition.Untreated, gingivitis may progress to gum disease or periodontal disease. Gingivitis is painless in the early stages, but may lead to bleeding gums and other oral problems. Bleeding gums are only one sign of gingivitis. Gums become red and swollen, teeth may become loose or may eventually fall out. 19. Prevalence: increases steadily between the ages of 5 and 9 years, peaks at 11 years and decrease slightly with age to 15 years. Etiology: Closely associated with the amount of plaque, debris and calculus present. Eruptive gingivitis Filth gingivtis Crowding gingivtis Puberty gingivitis Catarrh gingivitis 20. scurvy People at risk of scurvy include: People with chronic malnutrition or those that eat less than 2 servings of fruits/vegetables per day Alcoholics Elderly Men who live alone (bachelor or widower scurvy) Children People on peculiar diets or food fads People with other medical conditions that may prevent the intake and/or absorption of vitamin C Dialysis patients Malabsorption disorders Severe dyspepsia. [2]+[1] 21. Signs & symptoms Symptoms of scurvy generally develop after at least 3 months of severe or total vitamin C deficiency, they includes: Weakness & fatigue Bruising easily & bleeding from weakening blood vessel, connective tissue & bones due to collagen loss. Hair, teeth loss & gingivitis . Infants may be irritable, have pain when they move, and lose their appetite. Infants do not gain weight as they normally do. In infants and children, bone growth is impaired, and bleeding and anemia may occur. 22. Oral manifestations gums may swell and become red, soft and spongy. Any slight friction may cause the gums to bleed. Often this results in poor oral hygiene and dental diseases The gum findings are most striking in the interdental and marginal gingiva, which become red, smooth, swollen, and shiny. Later thegums appear purplish, sometimes even black and necrotic5, 23. Papillon Lefevre Syndrome -Papillon-Lefevre Syndrome (Palmoplantar Keratoderma with Periodontosis) -Inherited as an autosomal recessive trait -Mutation of the gene that produces the enzyme Cathespin C. -Greater frequency in consanguineous offspring 24. Clinical features -Children are born looking completely normal. They may have redness on palms of hands and soles of feet. -Teeth erupt in normal sequence, position, and time. -At age 1, when primary teeth starting to erupt, the gum tissue is severely inflamed and generalized aggressive periodontitis accompany the teeth. -By age 4, the child has lost all of there primary dentition. -Gingival tissue in mouth goes back to healthy & normal. -Eruption of the permanent dentition begins at normal age and in normal sequence -Patient will loose their permanent teeth and be completely edentulous by age 14- 17 25. Clinical Features 26. Papillon-Lefevre Syndrome 27. Radiographic Features teeth seem to be floating on air -severe bone loss 28. Eruptive gingivitis Cause Trauma of gingiva Debris and food residue Clinical feature: Site: Primary teeth and the 1st permanent molar Treatment Oral hygiene 29. Filth gingivtis Clinical feature: Age: 3Y~5Y SiteBuccal, Papi Symptomredness, bleeding Treatment: 1Local cleaning, antiinflection 2Oral hygiene 30. Puberty gingivitis Cause: Increase of sex hormones in circulating levels *sex hormones : Oestrogen Increases the cellularity of tissues and provides suitable growth condition for species associated with established gingivitis Progesterone Increases the permeability of the gingival vasculature Clinical features Good oral hygiene, gum tends to bleed and hyperplasia Bad oral hygiene 31. Catarrh gingivitis Cause The infection of hemolytic streptococcus Clinical features Oral lesion soft and hematose gum, no vesicles or ulcers Systemic reaction fever headache myalgia, arthralgia Treatment Local: Rinse 32. Crowding gingivitis Symptom: Redness and thickness Treatment: Oral hygiene Orthodontic treatment 33. Factitious gingivitis Minor form Etiology: Rubbing or picking the gingiva using the fingernail, or from abrasive foods Management: correct the habit and remove the source of irritation Major form The injuries are more severe and widespread , can involve the deeper periodontal tissues. Other areas of the mouth such as the lips and tongue may be involved. Extraoral injuries may be found on the scalp, limbs or face. Management A Dressing and protection of oral wounds B No lying with dentists C Psychological or psychiatric consultation 34. RigaFede disease RigaFede disease is an oral condition found, ararely, in newborns that manifests as an ulceration on the ventral surface of the tongue or on the inner surface of the lower lip. It is caused bytrauma to the soft tissue from erupted baby teeth.[1] It can be described as a sublingual traumatic ulceration. Although it begins as an ulceration, it may progress to a large fibrous mass with repeated trauma 35. Drug-induced gingival overgrowth The clinical changes of drug-induced overgrowth are very similar irrespective of the drug involved. The first signs of changes are seen after 3-4months of drug administration. Progress: The interdental papilla become nodular before enlarging more diffusely to encroach upon the labial tissue Site:The anterior part is most severely and frequently involved Sypmtom: with a good standard of oral hygiene, overgrowth gingiva is pink,firm and stippled, When there is a pre-exiting gingivitis the enlarged tissues compromise an already poor standard of plaque control.the gingiva then exhibit the classical signs of gingivitis 36. Management A strict programme of oral hygiene instruction, scaling and polishing must be implemented. Severe cases of gingival overgrowth inevitably need to be surgically excised and then recontoured to procedure an architecture that allows adequate access for cleaning A follow-up programe is essential to ensure a high standard of plaque control and to detect any recurrence of the overgrowth. To modify or change the anticonvulsant therapy if phenytion-induced overgrowth is refractory Indefinite oral care if there is no alternative. 37. Periodontal complications of orthodontic treatment Gingivitis Gingival overgrowth Attachment and bone loss Gingival recession Trauma 38. Early-onset aggressive periodontal disease Generalized form Gingiva: fiery red,swollen,and haemorrhagic Tissue: hyperplastic with granular or nodularproliferation Gross deposits of plaque Progress: extremely rapidly, primary teeth loss:3-4 years Bone loss: may be restricted to one arch 39. Localized form A Progresses more slowly B Bone loss affects only incisor-molar teeth C Plaque levels are low Treatment A Intense oral hygiene at frequent intervals B Antibiotic C Extraction of the teeth 40. CONCLUSION Oral hygiene is general index of health visit your dentist regularly prevention is better than cure 41. THANK YOU Submitted by Aghil Madathil CRRI JKKNDC