|
 
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| REVIEW ARTICLE |
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| Year : 2016 | Volume
: 5
| Issue : 2 | Page : 78-83 |
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Diagnosis and management of periodontal disease in children and adolescents: A brief review
Vineet Kini1, Raju Umaji Patil2, Tushar Pathak1, Amit Prakash3, Bharat Gupta1
1 Department of Periodontics, MGM Dental College and Hospital, Navi Mumbai, Maharashtra, India
2 Department of Pedodontics and Preventive Dentistry, STES Sinhgad Dental College and Hospital, Pune, Maharashtra, India
3 Department of Orthodontics, Peoples College of Dental Sciences, Bhopal, Madhya Pradesh, India
| Date of Web Publication | 25-Oct-2016 |
Correspondence Address:
Raju Umaji Patil
Department of Pedodontics and Preventive Dentistry, STES Sinhgad Dental College and Hospital, S. No. 44/1, Vadgaon Budruk, Off Sinhgad Road, Pune - 411 041, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2277-4696.192978
Periodontal disease when occurring in children leads to premature tooth loss, affecting the quality of life. Thus, screening pediatric and adolescent patients early, for periodontal disease is deemed imperative to its early management for improved prognosis. Chronic periodontitis (CP) has slow rate of progression, whereas aggressive periodontitis (AP) affecting children and young adults has rapid rate of progression. The management of AP in particular is affected by bacterial virulence of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis in plaque leading to rapid attachment and bone loss around the affected teeth. Nonsurgical treatment, use of appropriate antimicrobial therapy, and surgical correction of defects is required to mitigate disease followed by a comprehensive supportive periodontal therapy. This review visits the current understanding of periodontal disease, its management in pediatric and adolescent patients. Keywords: Adolescent, aggressive periodontitis, children, chronic periodontitis, periodontitis
How to cite this article:
Kini V, Patil RU, Pathak T, Prakash A, Gupta B. Diagnosis and management of periodontal disease in children and adolescents: A brief review. J Dent Allied Sci 2016;5:78-83 |
How to cite this URL:
Kini V, Patil RU, Pathak T, Prakash A, Gupta B. Diagnosis and management of periodontal disease in children and adolescents: A brief review. J Dent Allied Sci [serial online] 2016 [cited 2023 Jun 6];5:78-83. Available from: https://www.jdas.in/text.asp?2016/5/2/78/192978 |
| Introduction | |  |
The most prevalent periodontal diseases are plaque-associated gingivitis and periodontitis. Plaque-associated gingivitis being inflammation of the marginal gingiva, whereas in periodontitis, there is loss of tooth-attached fibers and alveolar bone in the affected teeth.[1] American Academy of Periodontology (AAP) classification of periodontal disease (1989) based on the World Workshop in Clinical Periodontics (1989), have recognized the Early Onset Periodontitis complex. Early onset periodontitis was divided into prepubertal periodontitis, juvenile periodontitis, and rapidly progressive periodontitis based mainly on early age of onset of the disease and rapid rate of progression of attachment loss.[2] Adult onset periodontitis has slow rate of progression with the onset of disease in adulthood.[2] The International Workshop for a Classification of Periodontal Diseases and Conditions (1999) changed the classification and categorized plaque-induced periodontal disease into aggressive periodontitis (AP) for early-onset periodontitis, and chronic periodontitis (CP) for adult onset periodontitis.[3],[4] This classification currently followed by The AAP (1999) is based on an infection/host response paradigm in which the age of onset not being a consideration but the rate of progression serving as a criteria for diagnosis. CP with slow rate of progression and no site specificity, with attachment and bone loss consistent with local irritating factors (plaque and calculus) usually occurs in adults but can affect children as well, whereas AP occurs mostly in children and young adults with rapid attachment loss and bone destruction inconsistent with the amount of dental calculus and plaque with increased proportions of A. actinomycetemcomitans and P. gingivalis.
In AP, there is marked molar incisor site specificity, history of familial aggregation, phagocyte abnormalities, hyper responsive macrophage phenotype including increased levels of prostaglandin E2 and interleukin (IL)-1β. Progression of attachment loss and bone loss may be self-arresting.[2],[3],[4]
Knowledge about the contributing risk factors toward CP and AP is therefore essential for effective management and maintenance.[5] This literature review is a brief insight into current diagnostic methods and management of Periodontitis in children and adolescents particularly AP which causes premature loss of both deciduous and permanent dentition causing early partial edentulousness affecting the quality of life.
| Epidemiology | | |
Cross sectional studies with partial mouth examination protocols with developmental changes in the mixed dentition render rate of progression estimation and data interpretation difficult.[6],[7] Existent data shows CP to have adult onset with no marked gender or familial predilection, whereas AP having circumpubertal onset from puberty to about 25 years of age, female preponderance and having familial predilection with prevalence rate higher in parents and siblings.[8],[9],[10],[11]
| Clinical Features | | |
CP with slow rate of progression and no site specificity with attachment and bone loss consistent with local irritating factors of plaque demonstrates predominantly horizontal pattern of bone loss with extent determined by percentage of site involvement. AP occurs in localized and generalized forms. Localized AP (LAP) has a circumpubertal onset with interproximal attachment loss in at least two permanent teeth, out of which one being a permanent first molar with two or fewer permanent teeth other than the first molars or incisors involved [12] [Figure 1],[Figure 2],[Figure 3]. Generalized AP (GAP) usually affects people under 30 years of age, with episodic attachment loss and bone destruction, affecting at least three permanent teeth other than the first molars and incisors.[13] Progressive attachment loss in adolescents occurs with breakdown occurring most frequently at mesial surfaces of first molars with very little plaque and calculus present.[14] Incidental attachment loss caused because of recessions due to faulty tooth brushing, overhanging restorations, and primary endodontic lesions can confound diagnosis.[7] | Figure 1: Clinical picture of localized aggressive periodontitis in maxillary anterior teeth
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 | Figure 2: Clinical picture showing pronounced inflammation with minimal amount of deposits on the teeth
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 | Figure 3: Clinical picture of localized aggressive periodontitis in mandibular anterior teeth
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| Predisposing Factors | | |
Familial aggregation
CP is not known to display any familial aggregation, whereas genetic predisposition to AP from segregation analyses of families with affected individuals in two or more generations are consistent with both autosomal-dominant and autosomal-recessive inheritance, as well as X-linked dominant inheritance.[15] The increased prevalence among females and transmission of the disorders through generations, support the hypothesis of X-linked dominant inheritance.[16],[17] Gene polymorphisms as possible markers, in IL-1, IL-4, IL-10, tumor necrosis factor-alpha (TNF-α), Fc gamma receptor, human leukocyte antigen, Vitamin D receptor, and N-formylpeptide suggest a genetic heterogeneity of AP.[15],[17]
| Microbiology | | |
Dental plaque in LAP has predominantly A. actinomycetemcomitans displaying virulence characteristics of leukotoxin, lymphocyte suppression factor, fibroblast and keratinocyte inhibitor, collagenase, and lipopolysaccharides. The other bacteria in plaque associated with AP include P. gingivalis, Prevotella intermedia, Capnocytophaga sp., Fusobacterium nucleatum, Eikenella corrodens, Tannerella forsythia, Eubacterium, Spirochetes, and black pigmented aerobic rods.[18],[19]P. gingivalis also has host specific proteases, gingipains that add to its virulence. In CP and GAP, the plaque bacteria present more diversity but mainly comprises P. gingivalis, P. intermedia, T. forsythia, Eubacterium sp., and F. nucleatum. In addition, GAP demonstrates equal number of A. actinomycetemcomitans, Campylobacter rectus, and Spirochetes.[19]
Immunological aspects of aggressive periodontitis
There is a significant elevation in the serum IgG levels to A.Surgical therapy is carried out to facilitate more ac actinomycetemcomitans and P. gingivalis, in subjects with LAP referred to as the robust serum antibody reaction. The diagnostic value of immunological parameters is more predictable in the cases of LAP as compared to GAP.[19] The serum level of antibody IgG2 reactive with A. actinomycetemcomitans in LAP was higher than in GAP and CP patients.[15],[19],[20],[21]
Influences of systemic diseases
CP and AP are plaque induced host mediated diseases in an otherwise systemically healthy host. Systemic conditions may confound diagnosis as they increase susceptibility to severe periodontal bone as a result of compromised host response.[22] Qualitative neutrophil defects particularly Chédiak-Higashi and leukocyte adhesion deficiency syndrome as well as neutropenia have been associated with cases of advanced periodontal bone loss in children and adolescents accompanied by early severe periodontal bone loss of deciduous dentition causing exfoliation before the eruption of permanent teeth.[23],[24],[25],[26] The Papillon Lefèvre syndrome disease characterized by transgradient palmoplantar keratosis and Haim–Munk syndrome with added arachnodactyly, acroosteolysis, and onychogryphosis cause premature loss of both the deciduous and permanent dentitions.[22],[27] Down's syndrome may demonstrate atypical severe periodontal bone loss early in life affecting both deciduous and permanent dentitions attributed to inappropriate enzyme regulation, T-cell immunodeficiency, neutrophil functional defects, and defects in collagen biosynthesis.[22] Children and adolescents with insulin-dependent diabetes mellitus tend to be more susceptible to gingivitis and periodontal disease owing to impaired neutrophil function, susceptibility to infection, and delayed wound healing.[22] Congenital hypophosphatasia characterized by deficiency of serum alkaline phosphatase, defective bone and tooth mineralization, and cementum hypoplasia presents with premature exfoliation of the primary dentition.[28] Periodontitis is a host-mediated response to plaque microbes such as A. actinomycetemcomitans and P. gingivalis, which leads to the attachment loss and bone destruction influencing systemic antibodies, especially IgG2 and IgA.[29] Periodontitis-associated serum prostaglandins, cytokines, and TNF-α are pro-inflammatory.[30] Family linkage studies suggest that the cylcooxygenase-1 enzyme system may be associated with the susceptibility to AP.[31] Host defense defects that may increase the susceptibility to AP are neutrophil chemotactic defects.[32] Decreased neutrophil chemotaxis in LAP has been linked to reduced receptors such as N-formyl-methyl-leucyl-phenylalanine, C5a, leukotriene B4, and IL-8.[33],[34]
Radiographic investigation should be performed when it is clinically justifiable in affecting patient prognosis and management. Although panoramic radiography [Figure 4] gives information on unerupted permanent and missing teeth, the alveolar bone levels are best assessed by intraoral periapical and bitewing radiography.[35] LAP presents reverse architecture of alveolar bone with mirror image appearance of vertical arc shaped patterns of bone loss at first molars and one or more incisors on both sides of the dental arch.[36] However, bone sounding is more accurate as radiographic images tend to underestimate bone loss as compared with clinical measurements.[37] | Figure 4: Panoramic radiograph showing angular bone loss around first molars in case of localized Aggressive Periodontitis
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| Management of Periodontal Disease in Pediatric and Adolescent Patients | | |
Plaque control
Plaque control program should be planned based on the chronological age and manual dexterity of the child and performed by caregiver if necessary.[35] Scrub technique of tooth-brushing technique has been found to be effective in children but the modified Bass technique and can be taught to adolescents with dexterity.[35],[38],[39] Periodontal lesions predominantly being interdental, older individuals can be advised use of interdental cleaning aids.[40] Triclosan with copolymer and fluoride containing dentifrices have shown to significantly reduce attachment loss in adolescents aged 11–13 years.[41] Keyes's technique involving a paste of baking soda, salt, and hydrogen peroxide as a dentifrice and irrigation with a saturated salt solution performed with a regimen of tetracycline hydrochloride administered orally has been prescribed to patients having AP showing good results.[42] Triclosan with copolymer and stannous fluoride containing dentifrices have shown reduction in gingivitis but were not accompanied by a decrease in plaque scores.[43],[44]
Nonsurgical periodontal therapy
Microbial plaque load being significantly reduced after scaling and root planing bring down the level of inflammatory cytokines thereby reducing inflammation, bleeding on probing, and probing depths in CP and AP.[45],[46] In AP, however motile organisms such as A. actinomycetemcomitans invade soft tissues of the periodontium causing recolonization leading to a poor clinical response to therapy.[47] One stage full mouth disinfection protocol including scaling and root planing, tongue brushing with 1% chlorhexidine for 1 min, mouth rinsing with 0.2% chlorhexidine for 2 min, and irrigation of periodontal pockets with 1% chlorhexidine, within 2 appointments in a 24 h time span followed by daily rinsing with chlorhexidine was found to result in better response in clinical outcomes in cases of AP.[48]
Systemic antimicrobial therapy
Antimicrobials selected by sensitivity testing have no added clinical benefit over empirical selection.[49] According to the AAP, patients likely to benefit from antibiotics are those for whom conventional mechanical treatment has proven ineffective, those with AP, and certain medical conditions.[50]A. actinomycetemcomitans can recolonize periodontal pockets after scaling and root planing, therefore use of systemic antimicrobials are indicated.[51] Antibiotics are commonly administered for a period between 7 and 14 days for severe CP and AP depending on the regimen. The dosage should be adjusted as per the child weight and age. As per adult doses and individuals weighing 40 kg and more, tetracycline in 250 mg qid and doxycycline in 100 mg od have the ability to concentrate in the gingival crevicular fluid and inhibit the growth of A. actinomycetemcomitans, exhibit anticollagenase effect, which can inhibit tissue destruction and aid in bone regeneration.[52],[53] Tetracyclines cause tooth discoloration in calcifying teeth and photosensitivity and depress skeletal growth in children therefore are not recommended in children of <8 years of age. As per adult doses and individuals weighing 40 kg and more, metronidazole and amoxicillin 250–500 mg each, given tid for 8 days is appropriate for most cases of severe periodontitis.[54] Metronidazole and ciprofloxacin 500 mg each, given bid for 8 days is effective against some enteric Gram-negative rods not affected by the metronidazole-amoxicillin regimen.[54] Clindamycin has very little impact on A. actinomycetemcomitans.[55] As per adult doses and individuals weighing 40 kg and more, amoxicillin 500 mg and potassium clavulanate 125 mg bid have shown good results in AP owing to potassium clavulanate being an inhibitor of beta-lactamase and thus overcoming the bacterial resistance to amoxicillin.[53],[54]
Sub-antimicrobial dose doxycycline by oral administration of 20 mg doxycycline twice daily over 6–9 months controls the activation of matrix metalloproteinase, especially collagenase from resident cells of the periodontium primarily neutrophils. This with scaling and root planing resulted in clinical improvement in patients with CP.[56] Its efficacy in AP needs more research.
In case of local drug delivery of antimicrobials, CP cases have been found to have responded with good success, it has been found that the cases of AP respond better to systemic delivery of antimicrobials.[57],[58]
Surgical therapy
Surgical therapy is carried out to facilitate more accessibility and instrumentation of affected sites to remove tissue invaded by A. actinomycetemcomitans. At the same time, osseous defects resulting from the disease process can be subjected to regenerative procedures to improve osseous support and enhance the prognosis of the teeth. Open flap debridement with systemic antimicrobial therapy in LAP has found to significantly reduce probing depths and improve attachment levels in affected teeth.[59],[60] Osseous grafting with debridement when performed with systemic antimicrobials in cases of LAP provided better results in osseous defect resolution as compared to when graft with debridement was used or when debridement alone was performed.[61],[62]
With defect morphology being favorable, Guided Tissue Regeneration has shown good results in the treatment of LAP as compared to when osseous grafting is performed.[63],[64],[65] Surgical outcomes to cases of GAP have been attributed variable to poor prognosis, poor compliance, and undetected systemic risk factors. Results can be more favorable if the risk factors be identified and addressed with special effort towards cessation of smoking.[66]
Maintenance
Patients with prior history of AP have to be considered at high risk for recurrent disease after therapy due to residual probing depths and increased inflammatory response to plaque, therefore require frequent review.[66] During each visit, a periodontal examination needs to be carried out to monitor the stability of attachment levels and check for inflammation. Qualitative chair side diagnostic aids for predicting the risk for future attachment loss for severe cases of CP and AP incorporates the use of chair-side assays such as ELISA for detecting presence of A. Actinomycetemcomitans, P. gingivalis and P. intermedia in plaque samples, and Benzoyl-DL-arginine-napthylamide assay for trypsin such as proteolytic enzymes in plaque samples containing P. gingivalis, T. forsythia, and Treponema denticola. Radiographic evaluation can be carried out in high risk teeth with deplaquing and occlusion adjustments performed when indicated.
| Conclusion | | |
In pediatric dentistry, knowledge of different conditions, referral, and interdisciplinary approach is mandatory.[67] CP has a slow progression rate and has a better prognosis and responds to therapy better as compared to AP. In view of multifactorial etiology and predisposing factors that lead the susceptible host to develop AP, special care needs to be taken that all facets influencing diagnosis and therapeutic outcomes be addressed. AP affects young individuals with early loss of teeth which influences quality of life. Early diagnosis with meticulous therapeutic intervention and monitoring of the child and adolescent is therefore advised with thorough periodontal examination and early intervention.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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