gingiva and periodontal problems in children
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This document provides an overview of gingival and periodontal diseases in children. It begins with an introduction stating that many periodontal diseases originate during childhood, so early detection and treatment are important. It then covers topics such as the normal periodontium in children, classifications of gingival diseases including gingivitis, acute gingival diseases like herpetic gingivostomatitis, and gingival enlargement. It also discusses periodontitis, specifically aggressive periodontitis which can occur in adolescents, as well as systemic diseases associated with periodontal problems. The conclusion emphasizes that early detection and treatment of periodontal issues in children can prevent more advanced diseases and also identify underlying systemic conditions.
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gingiva and periodontal problems in children
- 1. Gingival and Periodontal Diseases in children Presentation By: Garima singh
- 2. Contents: • Introduction • Gingiva • Gingival diseases • Gingivitis • Acute gingival diseases • Gingival enlargement • Eruption gingivitis • Gingival abscess • Ascorbic acid deficiency gingivitis • periodontitis • Systemic diseases and Conditions with associated periodontal problems • Conclusion 2
- 3. Introduction • Periodontal diseases peak their destructive stages in the middle age , but many of them have their inception during childhood. • The early detection and early treatment are important from a preventive aspect since, the prevention of most periodontal diseases are relatively simple and very effective, providing lifetime benefits. 3
- 5. • The clinical and radiographic images of gingiva and periodontium in children and adolescent differ from those seen in adults, owing to the significant changes taking place during growth and development. • The periodontium during childhood and puberty is in constant state of change owing to the exfoliation and eruption of teeth. • This makes a general description of the normal periodontium difficult because it varies with age of the patient. (Baer and Benjamin, 1974) 5
- 6. 6 Features Children Adults Gingival colour More reddish Coral pink contour Free gingival margin- rounded Gingival margin- knife edge Consistency Flabby due to less CT density and lack of organized collagen fiber bundles Firm and resilient Surface texture Stippling absent in infancy. `Mostly seen by age of 6 yrs Stippling present
- 7. 7 feaatures Children Adults Interdental area Saddle shaped gingiva Papillary gingiva Gingival sulcus Newly erupted teeth sulcus depth is greater than deciduous predecessor 1-2mm Attached gingiva Width increases with age and concomitant decrease in sulcus depth Greater in adults
- 9. Classification: GINGIVAL CONDITIONS Acute gingivitis • Herpetic gingivostomatitis • Necrotizing ulcerative gingivitis Chronic gingivitis • With local contributing factor (Plaque induced) • Without local contributing factor Gingivitis associated with systemic disease 9 Welbury R, Duggal MS, Hosey MT. Pediatric dentistry , ed 4, Oxford, 2012
- 10. PERIODONTAL CONDITIONS WITH LOSS OF CONNECTIVE TISSUE ATTACHMENT Early-onset periodontitis • Localized aggressive periodontitis • Generalized aggressive periodontitis Prepubertal periodontitis associated with systemic disease • Papillon-Lefevre syndrome • Ehlers-Danlos syndrome • Chediak-Higashi syndrome • Leucocyte adhesion deficiency syndrome • Neutropenias 10
- 12. Gingivitis • Dental plaque induced gingival inflammation is the most common form of gingivitis. • It is characterized by inflammation of gingival tissues without loss of attachment or bone. • Local factors contributing to gingivitis in children • Crowded teeth • Orthodontic appliances 12
- 13. • Gingivitis associated with poor oral hygiene is usually classified as • Initial lesion • Early lesion • Moderate lesion • Advanced lesion 13
- 14. 14 stage Initial stage Early stage Established stage Time (days) 2-4 4-7 14-21 Blood vessels Vascular dilatation Vascular proliferation Vascular proliferation, Blood stasis Junctional & Sulcular epi. Infiltration by PMNs Same as stage 1, Same but more advanced Predominant immune cells PMNs Lymphocytes Plasma cells Collagen Perivascular loss Increased loss Continuous loss Clinical findings Gingival fluid flow Erythema, Bleeding on probing Changes in color, texture, size Stages of gingivitis
- 16. Acute gingival diseases • Primary herpetic gingivostomatitis • Recurrent aphthous ulcer • Acute necrotizing ulcerative gingivitis (vincent infection) • Acute candidiasis (thrush, candidosis) 16
- 17. Primary herpetic gingivostomatitis • Caused by Herpes simplex virus type 1 • Age-Children younger than 6 yrs, but also may be seen in adolescents and adults. • Primary infection is asymptomatic • Location- lesions mainly involve hard palate, attached gingiva and oral mucosa. • Manifestations include blister outside the lip so disease commonly called recurrent herpes labialis. 17
- 18. • Characteristic oral finding: • Diffuse erythmatous involvement of gingiva. • Initial stage in characterized by discrete spherical gray vesicles. • Lip- excoriation involving lip become hemorrhagic • Course is self limited to 7-10 days. 18
- 19. • Oral symptoms: • Generalized soreness • Ruptured vesicles – focal site of pain • Infants show irritability and refusal to eat • Pain upon swallowing • Extra oral symptoms: • Cervical lymphadenopathy • Fever ( 101- 105℃) • Generalized malaise, irritability 19
- 20. Treatment • Symptomatic & supportive. • Application of mild anesthetic such as dyclonine hydrochloride(0.5%) • Bed rest , soft diet are recommended during the febrile stage & the child should be kept well hydrated. • Pyrexia - paracetamol suspension and secondary infection of ulcers may be prevented using chlorhexidine. • In severe case, systemic acyclovir(200 mg daily for 5 days). 20
- 21. Recurrent aphthous ulcer • Characterized by painful ulceration on the oral mucosa • Occurs between school age and adults • Recurrent ulceration with painful discrete and confluent lesions. • Lesions are round to oval crateriform base, raised and reddened margins. 21
- 22. • Etiology: • Immunological abnormality: mucosal destruction T-mediated immunological reaction. • Microbial organism: ∝-hemolytic strept. And S. sanguis. • Systemic factors: like nutritional deficiency 22
- 23. • Clinical features: • Occur between second and third decade of life. • Buccal and labial mucosa tongue and gingiva are commonly involved. • Symptoms- lesions are typically very painful. • Signs- begins as single or multiple superficial erosion covered by grey membrane, surrounded by localized area of erythema. 23
- 24. Treatment • Symptomatic treatment • Topical corticosteroid triamcinolone 3-4 times daily by rinse and expectorate method. • Nutritional diet. • Maintenance of oral hygiene. 24
- 25. Acute necrotizing ulcerative gingivitis • Characterized by sloughing of gingival tissue • Uncommon in children • Predisposing factors: • Local: poor oral hygiene, pre-existing gingivitis and smoking • Systemic: Emotional stress • Nutritional deficiency –Vit B and C 25
- 26. • Clinical features • Characteristic lesions are punched out, crater like depression at the crest of interdental papillae • Surface of gingival craters is covered by pseudomembranous slough. • Linear erythma. 26 . Atout RN, Todescan S. Managing patients with necrotizing ulcerative gingivitis. J Can Dent Assoc. 2013;79:d46.
- 27. • Extra oral and systemic symptoms: • Local lymphadenopathy • Elevation in temperature • Increased pulse rate, leukocytosis, loss of appetite, and general lassitude • Systemic reactions are more severe in children, insomnia, constipation, GIT disorders, headache etc. 27
- 28. • Treatment: • Perform debridement under local anesthesia. • Remove pseudomembrane. • Patient counselling should include specific oral hygiene instructions, instruction on proper nutrition, • For any signs of systemic involvement, the recommended antibiotics are: o Amoxicillin, 250 mg 3 x daily for 7 days and/or o Metronidazole, 250 mg 3 x daily for 7 days 28
- 29. Acute candidiasis (thrush, candidosis) • Acute candidiasis: 1. Pseudomembranous 2. erythmatous • Causative organism- C. albicans ( yeast like fungus. • Pathogenesis- 29
- 30. • Clinical features: • Pearly white or bluish white plaque present on oral mucosa which may extend to circumoral tissues. • Painless and noticed on careful evaluation. They may be removed with little difficulty. • Patient may complain of burning sensation. 30
- 31. • Treatment: • Infants and very young children • Nystatin 1ml (100,000U) dropped in to mouth for local action four times a day. • Clotrimazole suspension (10mg/ml) 1 to 2 ml applied over affected areas four times daily • Systemic fluconazole suspension (10mg/ml) 6mg/kg body weight 31
- 32. Gingival enlargement • Inflammatory enlargement • Chronic inflammatory enlargement • Acute inflammatory enlargement • Drug induced gingival enlargement • Vitamin C deficiency associated gingival enlargement 32
- 33. Chronic inflammatory gingival enlargement • Long standing gingivitis in young patient sometimes results in chronic inflammatory gingival enlargement, which may be localized or generalized. • Etiology: • Prolonged exposure to plaque • Factors that favour plaque accumulation and retention. • Chronically dried gingiva in mouth breathing 33
- 34. • Clinical features: • Characterized by slight ballooning of interdental papilla and marginal gingiva. • In early stage , it produces a life preserver-shaped bulge around the involved teeth. • Treatment: • Removal of local irritants • Oral hygiene maintenance 34
- 35. Acute inflammatory enlargement • Gingival abscess • Is a localized, painful rapidly expanding lesion that is usually of sudden onset • Etiology: • Irritation from foreign substance • Tooth brush bristle • Piece of apple core • Lobster shell fragment –embedded in to gingiva 35
- 36. • Clinical feature: • Localized, painful, rapidly expanding lesion • Limited to the marginal gingiva or interdental papillae • Early stage: red swelling with smooth shiny surface • With in 24 hours to 48 hours- lesion will be fluctuant. • Management: Incision and drainage 36
- 37. Drug-induced gingival enlargement • Drug-induced gingival enlargement: • Anticonvulsant • Immunosuppressant cyclosporine • Calcium channel blocker • Clinical and microscopic features of enlargement caused by different drugs are similar. 37
- 38. • Clinical features: • The growth starts as a painless, beadlike enlargement of the interdental papilla and extends to the facial and lingual margins. • As the condiiton progress, marginal and papillary enlargment units and may develop into a massive tissue fold. • May interfere with occlusion. 38
- 39. Treatment modalities Mild – < 1/3 of clinical crown oral hygiene maintenance and frequent dental care Moderate- 1/3 to 2/3 of clinical crown oral hygiene Antiplaque mouthrinse 4 consecutive weekly office visits for prophylaxis, 5th week- evaluate the gingiva If no improvement – surgical correction Severe – > 2/3 of clinical crown If does not respond above treatment. Surgical correction is done -meticulous oral hygiene is essential . Surgical procedure:- gingivectomy, laser, or electrosurgery. 39
- 40. Ascorbic Acid Deficiency Gingivitis • Associated with vit C deficiency • Involves marginal and papillary gingiva in the absence of local predisposing factors • Complains of severe pain and spontaneous hemorrhage • Treatment: Complete dental care, improved dental hygiene, and supplementation with vit C – improves gingival conditions 40
- 41. Eruption Gingivitis • Gingivitis associated with tooth eruption. • Tooth eruption usually does not cause gingivitis, however inflammation associated with plaque accumulation around erupting tooth. • perhaps secondary to discomfort caused by brushing these friable areas, may contribute to gingivitis. • Treatment: Complete dental care, improve oral hygiene. 41
- 42. Periodontitis 42
- 43. • It is inflammatory disease of gingiva and deeper tissues of periodontium. • Characterized by pocket formation and destruction of supporting alveolar bone. • Periodontal probing for attachment loss and bitewing radiograph are often used to clinically confirm the diagnosis. 43
- 44. • According to Delaney, in preschool children with periodontitis, recession, gingival erythema, and oedema are not usually found unless the child is neutropenic. • Bimstein and Colleagues demonstrated abnormal alveolar bone resorption in 7.6% of 4yr old children and 5.9% of 5yr old children with high caries. • In its classification of periodontitis, the American Academy of Periodontology categorized the early- onset form under Aggressive Periodontitis. Delaney JE. Periodontal and soft tissue abnormalities. Dent Clin North Am. 1995;39:837-850 Bimstein E, et al. Radiographic assessment of alveolar bonein children and adolescents. Pediatr Dent.1988;10:199 American Academy of Periodontology. Parameter on aggressive periodontitis. J Periodontol. 2000;71(suppl):867.44
- 45. Aggressive periodontitis • Albander and associates proposed the term early-onset periodontitis. • This term is replaced by aggressive periodontitis following the classification given by American Academy of Periodontology in 1999. 45 Page and colleagues believe that there are four different forms of periodontitis : prepubertal, juvenile, rapidly progressing and adult.
- 46. COMMON FEATURES OF LAP AND GAP • Aggressive forms of periodontal disease have been defined based on the following primary features (Lang et al. 1999) Non-contributory medical history Rapid attachment loss and bone destruction Familial aggregation of cases 46
- 47. Localized Aggressive periodontitis(LAP): • Clinical features: • characterized by “localized loss of attachment and bone around permanent incisors and first permanent molars” 47
- 48. • Prevelence is 1% • It is linked to presence of Actinobacillus actinomycetemcomitans and successful treatment outcomes correlate well with eradication of bacteria. • Treatment : local measures in combination with systemic antibiotic therapy. 48
- 49. Generalized aggressive periodontitis (GAP): • It sometimes occurs in adolescents and teenagers. • Characterized by generalized interproximal attachment loss affecting at least three permanent teeth other than incisor and first molar. 49
- 50. 50 Radiographs showing the severe generalized nature of disease
- 51. 51 • A combined regimen of regular SRP with 2-week course of systemic tetracycline therapy (250 mg, four times daily) . • Aa is sensitive to tetracycline, which also has the ability to be concentrated up to 10 times in gingival crevicular fluid when compared with serum. Treatment:
- 52. 52 • A combination of metronidazole (250 mg) & amoxicillin (amoxycillin) (375 mg), three times a day for 8 days, in association with subgingival scaling, has also been found to be effective. • A more radical approach is to undertake flap surgery so that better access is achieved for root cleaning, and the superficial, infected connective tissues are excised. • An antimicrobial regimen can also be implemented in conjunction with a surgical approach.
- 53. Systemic diseases and conditions with associated periodontal problems • Diabetes • Down syndrome • Hypophosphatasia • Neutropenia • Leukemia 53
- 54. Conclusion • The early detection and treatment of periodontal problems in children and adoloscents are important for 1. Incipient periodontal diseases in children may develop into advanced periodontal diseases in children. 2. Severe periodontal destruction in children may be related to underlying systemic pathology. • Education and motivation of children regarding proper maintainence of periodontal health is the simplest and most effective way for prevention of periodontal diseases in the adult life. 54
- 55. References: • Dean, Mcdonald, Avery. Dentistry for the child and aolescented , ed 9, India, Elsevier, 2012. • Newman, Takei, Klokkevold, Carranza. Carranza’s clinical periodontology, ed 11, India, Elsevier, 2012 . • Pinkham, Casamassimo, Fields, Mctigue, Nowak. Pediatric Dentistry, ed 4, India, Saunders, 2005. • Delaney JE. Periodontal and soft tissue abnormalities. Dent Clin North Am. 1995;39:837-850 • American Academy of Periodontology. Parameter on aggressive periodontitis. J Periodontol.2000;71(suppl) :867. • Bimstein E, et al. Radiographic assessment of alveolar bonein children and adolescents. Pediatr Dent.1988;10:199 55
- 56. Thank you 56
Notes de l'éditeur
- In additoin, gingival anatomic problems, such as lack of attached gingiva , can arise during development and may necessitate early management.
- Contour –shape of teeth , their alignment in arch, location n size of area of proximal contact, facial & lingual gingival embrassure. Consistency- gingiva is firm and resilient , wih exception of free marginal gingiva,tightly bound to the underlying bon. collagenous nature of lamina propria and its contiguity with the mucoperiousteum of the alveolar bone determine the firmness of attached Stippling- Best view in dried gingiva, produced by rounded protubence n depressions in gingival surface. Papillary layer of connective tissue projects into elevation, and the elevated n depressed area are covered by strat. Squamous epi.
- Younger children have less plaque, and gingiva appear to be less reactive to the same amount of plaque. Uncommon in early primary dentition. Orthodontic applainces r associated with incresed plaque retention and incresed bleeding on probing.
- Gingivitis is quick reversible and can be treated with a good oral prophylactic treatment Gingivitis is generally less severe in children than in adults with similar plaque levels.
- When gingivitis is establilshed, initial acute response is accompnied by chronic inflammation with lymphocytic and plasma cell accumulaiton, capilary formation, and collagen destruction. This too can be reversed by initial therepy but will require a longer period for gingival tissue to heal and restore lost collagen fibers.
- In some patients gingivitis proceeds to periodontitis , which is more difficult to treat. Therefore clinician must be vgilant to detect the early stage of gingivitis and carry out effective measures to prevent the progression of disease.
- moniliasis
- Remain letent untill reactivated, HSV-1 in trigeminal ganglion, HSV-2 in lumbosacral
- With varying degree of edema and gingival bleeding So that parting of lip during speech n swallowing become extreemly painful and difficult. Diagnosis:Rise in serum antibodies HSV-1,in cytologic study ballooning degenrtion of cells, multinucleated gaint cells, hisotpahtological finding- lipschutxz bodies. Lesion culture
- neutropenia of childhood is diagnosed between 6 and 24 months of age and is characterized by frequent and multiple pyogenic infections of the skin and mucous membranes.
- IgG IgM bind to the mucosal surface of pts suffering from
- Sussequently extending to the marginal gingiva anf rarely to attached gingiva and oral mucosa.
- Overgrowth of yeast on oral mucose leads to desquamation of epithilial cells and accumulation of bacteria, necrotic tissue. These debris combine to form pseudomb. Which adhere closely to mucosa.
- Characterstically – interdental papillae & marginal gingiva become enlarged , tissue is usually erythmatous , bleeds easily. t/t- it slowly resolves when adequat eplaque control is instituted, so gingivectomy is rarely required. Prolonged exposure to dental plaque and factors favour the accumulation and retention of it
- Exudative and prliferative features, deep red or bluish lesions are soft, friable with a smooth shiny surface, bleeds easily. Vascular engorgemnt, new capillary formation and associated degenrative changes. Firm , resilient, and pink- greater fibrotic components with an abundance of fibroblan and collagen.
- Localized painful rapidly expanding lesion tht has a sudden onset Limitied to marginal or interdental papilla Appers as red swelling with smooth shiny surface. Etiology; bacteria carried deep into the tissue when a forgein substance is forcefully embded into gingiva.
- Infiltraiton of PMN , purulent focus in conn. Tissue, edematous tissue and vascular enlargment.
- It is well-known consequence of administration of
- Covering to considerable amount of crown portion. h/f- hyperplasia of conn. Tissue and epi. Acanthosis of epi and elongated rete pages exiend deep into conn. Tissue, abundance of collagen bundles and fibroblant and formation of new BV.
- Conditions can becomeextreemsymptoms covering the crowns of teeth and interfering with the eruption or occlusion.
- scorbic acid is needed for accelerating hydroxylation and amidation reactions. In the synthesis of collagen, ascorbic acid is required as a cofactor for prolyl hydroxylase and lysyl hydroxylase. These two enzymes are responsible for the hydroxylation of the proline and lysine amino acids in collagen. Hydroxyproline and hydroxylysine are important for stabilizing collagen by cross-linking the propeptides in collagen. Defective collagen fibrillogenesis impairs wound healing. Collagen is an important part of bone, so bone formation is affected. Defective connective tissue leads to fragile capillaries, resulting in abnormal bleeding.
- AP is used as a generic term to describe a heterogenous grp of periodontal disease occuring in younger individual who are otherwise healthy. AP can be viewed as 2 categories of periodontits that may have overlapping etiologies and clinical presentations.
- It is also called localized juvenile periodontitis, is characterizd by the loss of attachment and bone around the permanent incisors and first permanent molars Attachment loss is rapid, 3 times the rate of chronic disease. 15- yr old black female pt who had atwin wid similar disease
- Metronidazole alone/ in combination with amoxicillin Some reattachment and resolutoin of periodontal defects can occur after antibiotic therapy, but localized surgical intervention is often necessary to manage the residual defects.
- It affect entire dentition and is not self-limiting. Not associated with high level of AAC tht occur in LAP but istead has a microbial profile closer to that of chronic disease. Clinical view showing minimal plaque and inflammation. A provisional wire and resin splint had been placed to stabilize the tooth. 22 Yr old black male patient with family history of early tooth loss
- Scaling anf root planing