Periodontal diseases in children


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Periodontal diseases in children

  1. 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. 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. 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. 4. Gingival conditions  Acute gingivitis  Chronic gingivitis  Gingival overgrowth  Factitious gingivitis  Mucogingival problems
  5. 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. 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. 7. Clinical features: Age:  6 months to 3 years Incubation period  1 week Prodrome:  Febrile illness  Headache, malaise, oral pain  Cervical lymphadenopathy
  8. 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. 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. 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. 11. Pharmacotherapy  Antiviral treatment .  Symptomatic treatment
  12. 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. 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. 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. 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. 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. 17. Treatment  Intense oral hygiene  Oxidant: hydrogen peroxide  Mechanical debridement  Metronidazole
  18. 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. 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. 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. 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. 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. 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. 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. 25. Clinical Features
  26. 26. Papillon-Lefevre Syndrome
  27. 27. Radiographic Features teeth seem to be “floating on air” -severe bone loss
  28. 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. 29. Filth gingivtis  Clinical feature:  Age: 3Y~5Y  Site:Buccal, Papi  Symptom:redness, bleeding  Treatment:  1)Local cleaning, antiinflection  2)Oral hygiene
  30. 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. 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. 32. Crowding gingivitis  Symptom:  Redness and thickness  Treatment:  Oral hygiene  Orthodontic treatment
  33. 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. 34. Riga–Fede disease  Riga–Fede 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. 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. 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. 37. Periodontal complications of orthodontic treatment  Gingivitis  Gingival overgrowth  Attachment and bone loss  Gingival recession  Trauma
  38. 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. 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. 40. CONCLUSION  Oral hygiene is general index of health… visit your dentist regularly…  prevention is better than cure 
  41. 41. THANK YOU Submitted by Aghil Madathil CRRI JKKNDC