Therapeutic management of a case of generalised aggressive periodontitis in an 8-year old child: 18-month results.
Periodontal disease in children presents in various forms, ranging from conditions limited to mild gingival inflammation up to severe periodontal tissue destruction that can, in some cases, cause early tooth exfoliation. Epidemiological studies in children have indicated that the prevalence of gingivitis is similar to that of the adults and ranges from 40-60%, while periodontitis is relatively uncommon and ranges from 0.15% [Califano, 2003]. In the past decades, a variety of terms have been proposed to describe periodontal destruction in young patients [Armitage and Cullinan, 2010]. Lately, the term aggressive periodontitis was used to replace a group of dissimilar destructive periodontal diseases collectively termed "Early-onset Periodontitis" [Armitage, 1999]. The onset of the disease is often circumpubertal and its main features include a history of rapid and severe bone loss as well as familial aggregation in individuals who are systemically healthy [Clerehugh and Tugnait, 2001; Califano, 2003].
The main aetiological factors do not differ from those associated with chronic periodontitis, such as virulent periodontal pathogenic microbiota and/or impaired host defence mechanisms [Clerehugh and Tugnait, 2001; Oh et al., 2002; Portaro et al., 2008]. Aggressive periodontitis can be either localised or generalised, depending on the percentage of sites affected (< 30% localised and > 30% generalised) [Modeer and Wondimu, 2000; Wiebe and Putnins 2000]. Generalised aggressive periodontitis (GAP) may affect both primary and permanent dentitions and causes rapid alveolar bone destruction and attachment loss in multiple teeth, not only limited to first molars and incisors. Controversy exists concerning the presence of plaque and calculus. More specifically older reports find very little if any supragingival plaque, while recent ones demonstrate a positive correlation between subgingival calculus, gingival inflammation and periodontal destruction [Wara-aswapati et al., 1999; Clerehugh and Tugnait, 2001]. GAP has been associated with recurrent infections, e.g upper respiratory tract and otitis media as well as sinusitis, pneumonia and dermatitis [Watanabe, 1991; Dibart et al., 1998; Aren et al., 2003].
In the literature there are few case reports published on GAP in children [Watanabe, 1991; Firatli et al., 1996; Kamma et al., 1998; Bodur et al., 2001; Aren et al., 2003; Vandana and Venkata Ramesh Redy, 2003; Portaro et al., 2008] most of which are associated with underlying systemic disease. The aim of this paper is to a) describe the clinical, radiographic and microbiological findings of a systemically healthy 8-year old child with GAP and b) discuss the patient's response to treatment up to 18-months follow-up.
An 8-year old caucasian male was referred by a private orthodontist to the post-graduate clinic of paediatric dentistry in the university of Athens, due to increased mobility of the primary dentition. His medical history was non-contributory, although the mother reported episodes of recurrent ear infections while the patient was younger (up to the age of 5 years). Both parents and his younger sister (6 years old) were systemically healthy and reported no history of periodontitis. The reported dental history revealed that the patient was a sporadic attendee to the dentist and he had already received restorative treatment of several primary teeth. He brushed his teeth once a day and he did not use floss.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
Clinical examination. Clinical oral examination (Fig. 1) revealed moderate oral hygiene with a PI (simplified plaque index)[O'Leary et al., 1972] score of 35% and increased gingival inflammation, with a GI (simplified gingival index) [Lindhe, 1981] score of 89%. Temporary restorations were found in primary molars (teeth 54 and 55). Detailed periodontal examination revealed bleeding on probing at 60% of the sites, as well as sites with probing pocket depths (PPD) up to 6 mm in all four permanent molars and up to 9 mm in primary canines (Table 1). Second-degree mobility was noticed in the maxillary and mandibular primary canines. Orthodontic assessment showed crowding in both maxillary and mandibular arches and anterior cross-bite in central as well as lateral permanent incisors.
Radiographic examination. Comparison of the two panoramic radiographs (Fig. 2) taken within a one year interval, revealed rapid progression of vertical and horizontal bone loss mainly around primary molars and canines (indicated with circles in the second panoramic radiograph). Periapical radiographs (Fig. 3) showed advanced bone loss in primary molars and canines, with the alveolar bone covering at most half of the root length. More specifically, the alveolar bone was covering less than 1/3 of the length of the mesial root of 54 and 64, almost half of the length of the mesial and less than 1/3 of the distal root of 74 and 84 respectively. Similar findings were registered for the mesial roots of 75 and 85. Regarding the primary canines, alveolar bone was covering 1/3 of both mesial and distal roots of 53 and 63 and 1/2 of the roots of 73 and 83, respectively. Maxillary and mandibular permanent teeth were not severely affected, with the bone loss being less than 1/3 of the root. Several carious lesions (teeth 74, 75, 84 and 85) and periapical pathology in primary molars (54 and 55) were also found.
[FIGURE 3 OMITTED]
Microbiological tests. Teeth were isolated and the supragingival plaque was removed. Pooled subgingival plaque samples were taken from primary canines and molars as well as permanent molars, by inserting sterile paper points into the deepest pockets of these teeth and allowing them to remain for 10 sec. The samples were placed into RTF and transferred to the laboratory. Aliquots of 0.1 ml of serial dilutions were plated in duplicate onto a) enriched trypticase soy agar (ETSA) supplemented with 4% defibrinated blood to determine the predominant cultivable microbiota [Syed et al., 1980]; b) KVLB-2 agar (kanamycin 75[micro]g/ml-vancomycin 2[micro]g/ ml blood) for the isolation of pigmented and non-pigmented Prevotella spp, Porphyromonas spp and Bacteroides spp; c) TSBV (trypticase-soy-agar) supplemented with 5% serum 75 [micro]g/ml bacitracin and 5 [micro]g/ml vancomycin to quantify Aggregatibacter actinomycetemcomitans [Slots, 1982]. After incubation, the identification of the bacteria was performed based on colony morphology, Gram staining and biochemical tests [Krieg and Holt, 1984]. The frequency of detection for a given species was calculated on the basis of the total isolated subgingival microbiota. The microbiological results showed that in permanent molars, increased percentages of A. actinomycetemcomitans and Porphyromonas gingivalis were isolated from the total subgingival microbiota. The findings were similar in primary molars and canines with the percentages of A. actinomycetemcomitans and P. gingivalis varying from 19-25% (Table 2).
Differential and final diagnosis. Based on the medical history, as well as the clinical and radiographic findings reported previously, differential diagnosis was made between GAP, periodontal manifestations of systemic (e.g. eosinophilic granuloma) and haematological disease (e.g. cyclic neutropenia, leukaemia) or genetic disorder (e.g. leukocyte adhesion deficiency syndrome, Papillon-Lefevre syndrome). The patient was referred for a more detailed medical examination for the exclusion of any underlying systemic disease. The laboratory values of the blood counts and serum biochemical tests were within normal limits for the patient's age (Table 3). A final diagnosis of GAP was made.
[[FIGURE 4 OMITTED]
The treatment plan consisted of an individualised oral health preventive program followed by periodontal therapy and restorative dental treatment. The oral health preventive program included oral hygiene instructions and more specifically toothbrushing twice daily with a fluoridated toothpaste, use of dental floss for interdental cleaning, and use of disclosing tablets to increase the effectiveness of plaque removal. Dietary instructions (decrease of sweets intake up to once per day) were also given. In office fluoride application was carried out every 3-4 months. The periodontal therapy included full mouth scaling and root planing under local analgesia in two visits within a one week interval. Antibiotics were also administered at the end of the second visit (amoxycillin 50mg/kg and metronidazole 30mg/kg tds) for 2 weeks [Lopez, 1992] along with the prescription of 0.2% chlorohexidine mouthrinse for 10 days. Two weeks after the completion of the initial phase of periodontal therapy, dental treatment was carried out. Extraction of primary teeth with periapical lesions was performed followed by restoration of carious primary teeth with composite resin.
A follow-up program was applied involving monthly recall appointments for the first six months, and every three months thereafter. At each follow-up visit, plaque accumulation and gingival bleeding were assessed as well as oral hygiene and dietary advice were reinforced. Supra- and sub-gingival debridement was also performed where it was necessary. Radiographic examination and plaque sampling for microbiological assessment was performed every 6 months.
Gradual improvement of oral hygiene (PI, initial examination: 35% vs 18 months: 10%), decrease of gingival inflammation (GI, 89% vs 20%) and reduction in the number of sites with bleeding on probing were found (60% vs 12%) (Table 1). Radiographic findings revealed reduction of bone loss, with alveolar bone covering more than 2/3 of the root length of the previously affected teeth (Fig. 4). Permanent incisors and premolars erupted with indications of a healthy periodontium.
Microbiological findings indicated a significant decrease in the detectable percentages of most periopathogenic microbes especially in permanent teeth during the first six months when the patient was kept in the monthly-recall program (Table 2). At 12- and 18-month visits, P. gingivalis and A. actinomycetemcomitans were isolated from the affected sites, although at lower levels than those detected at initial examination. Prevotella intermedia, which was only detected in primary teeth at initial examination, was isolated at recall visits, but at very low levels, mainly from the canines (Table 2). Fusobacterium nucleatum was isolated at low levels from almost all sites at initial examination and remained so, at all visits.
The current case report describes an 8-year-old boy that presented increased mobility in his primary dentition. Based on the clinical and radiographic findings showing tooth mobility and attachment loss at more than 30% of sites in the mouth [Wiebe and Putnins, 2000], the patient was diagnosed as having generalised aggressive periodontitis (GAP). Medical history and further medical examination did not reveal a systemic disease or other health problems while the family history showed no immediate relatives with periodontal disease.
Despite having severe periodontitis, the child was apparently healthy and showed no unusual infections. However, abnormalities in neutrophil function could not be ruled out, since the required diagnostic methodology was not available. Based on the literature, reports have shown that aggressive periodontitis can occur in the absence of detectable neutrophil defects [Lopez, 1992; Bodur et al., 2001], while others reported a decrease in neutrophil chemotaxis [Celenligil et al., 1987; Firatli et al., 1996]. Hence, there is no consistent association of functional defects with aggressive periodontitis in the primary or permanent dentition.
Destructive periodontal disease is associated with specific bacterial pathogens, such as A. actinomycetemcomitans and P. gingivalis, which are thought to play an important role in the pathogenesis of the disease [Clerehugh and Tugnait, 2001; Portaro et al., 2008]. The microbiological examination of the subgingival plaque of the patient showed that P. gingivalis was found in both primary and permanent teeth, comprising the highest proportion of the periodontopathic microbiota, followed by A. actinomycetemcomitans. Studies have shown that highly virulent strains of A. actinomycetemcomitans in combination with Bacteroides-like species such as P. gingivalis and P. intermedia have been implicated in the aetiology of GAP [Haraszthy et al., 2000; Califano, 2003]. A. actinomycetemcomitans is suggested to be more easily transmitted to humans with immature oral subgingival biofilm, which is the case during eruption and exfoliation of teeth. Consequently first molars and incisors are the first teeth affected in GAP [Bodur et al., 2001].
Therapeutic strategies in the treatment of periodontal disease are directed towards the reduction of supra- and subgingival microorganisms. A combination of mechanical (non-surgical or surgical) debridement with a systemic antibiotic regime has been suggested in several studies for the treatment of GAP [Bodur et al., 2001; Valenza et al., 2009; Aimetti et al., 2012]. A similar approach was employed in the present case using non-surgical debridement and administration of metronidazole and amoxycillin.
Extraction of severely affected primary teeth has also been suggested in the literature in order to reduce the risk of infection spread to the erupting permanent teeth [Modeer and Wondimu, 2000; Bodur et al., 2001; Vandana and Venkata Ramesh Redy, 2003; Portaro et al. 2008]. In our case, we followed a more conservative approach, extracting only primary teeth with periapical lesions. Our treatment aim was to maintain a functional and aesthetic dentition, based on periodontal therapy and close monitoring. On the other hand, the present approach has the drawback of relying on patient compliance to achieve a positive treatment result, which is a tough challenge for a patient at this age. Parental involvement and tight periodontal maintenance is, therefore, essential for a successful therapeutic outcome, when such an approach is employed.
Clinical and radiographic parameters at the 18-month follow-up showed that the improvement in periodontal condition, attained immediately after active periodontal therapy, was maintained. In addition, erupting permanent teeth were not found to be periodontally affected microbiological findings showed that the periopathogens were significantly decreased at follow-up, however they reappeared at 12- and 18- months at low levels. A possible explanation is that, despite thorough scaling and root planing, the bacteria still remain in the tongue and other soft tissues and consequently could recolonise the pockets [Quirynen et al., 2001; Walker and Karpinia, 2002]. Although the reappearance of A. actinomycetemcomitans and P. gingivalis was at low levels, it reinforces the importance of close periodontal monitoring, in order to maintain a periodontitis-free permanent dentition.
Management of GAP in children with non-surgical root debridement along with systemic administration of antibiotics can be successful in achieving improvement and maintenance of periodontal health in the mixed dentition, despite retaining periodontally involved primary teeth. Long term, close follow-up of such patients is essential, both during the completion of the permanent dentition as well as throughout life, since they are likely to remain highly susceptible to periodontal disease.
Aimetti D, Romano F, Guzzi N, Carnevale G. Full-mouth disinfection and systemic antimicrobial therapy in Generalised aggressive periodontitis: a randomized, placebo-controlled trial. J Clin Periodontol. 2012; 39:284-294.
Aren G, Gurel N, Yalcin F, Firatli E. Clinical and immunological findings of two siblings in a family with Generalised aggressive periodontitis. J Dent Child 2003; 70:266-271.
Armitage G. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999; 4:1-6.
Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and aggressive periodontitis. Periodontology 2000 2010; 53:12-27.
Bodur A, Bodur H, Bal B, Balos K. Generalised aggressive periodontitis in a prepubertal patient: A case report. Quintessence Int 2001; 32:303-308.
Califano JV. Periodontal diseases of children and adolescents. J Periodontol 2003; 74:1696-1704.
Celenligil H, Kansu E, Eratalay K. Prepubertal periodontitis. A case report with an analysis of lymphocyte populations. J Clin Periodontol 1987; 14:85-88.
Clerehugh V, Tugnait A. Periodontal diseases in children and adolescents: I. Aetiology and diagnosis. Dent Update 2001; 28:222-232.
Dibart S, Chapple I, Skobe Z, Shusterman S, Nedleman HL. Microbiological findings in prepubertal periodontitis: A case report. J Periodontol 1998; 69:1172-1175.
Firatli E, Gurel N, Efeoglu A, Cebeci I. Generalised prepubertal periodontitis. A report of 4 cases with the immunological findings. J Clin Periodontol 1996; 23:1104-1111.
Haraszthy V, Hariharan G, Tinoco E, et al. Evidence for the role of highly leukotoxic Actinobacillus actinomycetem-comitans in the pathogenesis of localised and other forms of early-onset periodontitis. J Periodontol 2000; 71:912-922.
Kamma JJ, Lygidakis NA, Nakou M. Subgingival microflora and treatment in prepubertal periodontitis associated with chronic idiopathic neutropenia. J Clin Periodontol 1998; 25:759-765.
Krieg NR and Holt JG. Bergey's manual for systemic bacteriology. Baltimore: Williams & Wilkins, 1984.
Lindhe J. Treatment of localised juvenile periodontitis. In: Genco RJ, Mergenhagen SE, eds. Host-Parasite Interactions in Periodontal Disease. Washington, DC: ASM;1981 pp382-394.
Lopez NJ. Clinical, laboratory and immunological studies of a family with a high prevalence of Generalised prepubertal and juvenile periodontitis. J Peri odontol 1992; 63:457-468.
Modeer T, Wondimu B. Periodontal diseases in children and adolescents. Pediatr Dent 2000; 44:633-654.
Oh TJ, Eber R, Wang HL. Periodontal diseases in the child and adolescent. J Clin Periodontol 2002; 29:400-410.
O'Leary T, Drake RB, Nayer JE. The plaque control record. J Periodontol 1972; 43:38-40.
Portaro CP, Chopite YG, Cardenas AC. Generalised aggressive periodontitis in preschoolers: Report of a case in a 3-1/2 year old. J Clin Pediatr Dent 2008; 33:69-74.
Quirynen M, De Soete M, Dierick k, Van Steenberghe D. The intra-oral translocation of periopathogens jeopardizes the outcome of periodontal therapy. A review of the literature. J Clin Periodontol 2001; 28:499-507.
Slots J. Selective medium for isolation of Actinobacillus actinomycetemcomi tans. J Clin Microbiol 1982; 15:606-609.
Syed SA, Svanberg M, Svanberg G. The predominant cultivable dental plaque flora of beagle dogs with gingivitis. J Periodont Res 1980; 15:123-136.
Valenza G, Veihelmann S, Peplies J et al. Microbial changes in periodontitis successfully treated by mechanical plaque removal and systemic amoxicillin and metronidazole. Int J Med Microb 2009; 299:427-438.
Vandana KL, Venkata Ramesh Redy B. Prepubertal periodontitis: A report of 2 cases. J Dent Child 2003; 70:82-85.
Walker C, Karpinia K. Rationale for use of antibiotics in periodontitis. J Periodontol 2002; 73:1188-1196.
Wara-aswapati N, Howell TH, Needleman HL, Karimbux N. Periodontitis in the child and adolescent. J Dent Child 1999; 66:167-173.
Watanabe K. Generalised juvenile periodontitis in a thirteen-year-old child. J Dent Child 1991; 58:390-395.
Wiebe C, Putnins E. The periodontal disease classification system of the American Academy of Periodontology--an update. J Can Dent Assoc. 2000; 66:594-7.
K. Seremidi *, S. Gizani *, P. Madianos **
* Department of Paediatric Dentistry, ** Department of Periodontology,School of Dentistry, University of Athens, Greece
Postal address: Dr. K. Seremidi, 8 Anaxagora Street, 16675 Glyfada, Athens, Greece.
Table 1. Clinical results before treatment and during follow-up. PI GI BOP Pocket depth (mm) MPD MP Initial examination 35% 89% 60% 7.5 9 3-months recall 25% 65% 50% 6.2 8 6-months recall 20% 50% 40% 5.5 8 9-months recall 21% 40% 38% 4.8 7 12-months recall 15% 30% 29% 4.3 6 15-months recall 12% 25% 18% 4.0 5 18-months recall 10% 20% 12% 3.8 5 PI = plaque index, GI = gingival index, BOP = bleeding on probing, MPD = mean pocket depth, MP=maximum pocket detected Table 2. Frequency of detection of bacterial species in subgingival plaque samples at the initial examination (I.E) and recall visits. Tooth Permanent Molars Primary Microbes Molars I.E 6 mth 12 mth 18 mth I.E 6 mth p. g 24% / 12% 10% 21% / A. a 18% 6% 2,5% 7% 24% / P. i / / / / / / E. c / / / 9% 3% / F. n / 13% 9% / 9% 6% Tooth Primary Primary Canines Microbes Molars 12 mth 18 mth I.E 6 mth 12 mth 18 mth p. g 9% 10% 25% / 16% 13% A. a / 9% 19% / 4% 2% P. i / 6% 11% / 5% 8% E. c / / 3% / / / F. n 6% 7% 5% 6% 6% / Tooth Premolars Microbes 12 mth 18 mth p. g 12% 11% A. a / 3% P. i / 5% E. c 9% / F. n 12% / P. g = Porphyromonas gingivalis. A. a = Aggregatibacter actinomycetemcomitans. P. i = Prevotella intermedia. E. c = Escherichia coli. F. n = Fusobacterium nucleatum Table 3. Laboratory results Patient Normal range HGB 12.5 10.3-14.9 g/dL WBC 5600 4800-10800 /[mm.sup.3] PLT 248000 140000-400000 /[mm.sup.3] HCT 36.9 32-42 % RBC 4800000 4000000-5200000 /[mm.sup.3] MCV 76.9 73-87 m3 = fL Blood Glucose level 90% 70-110 mg (%) ALP 227 130-560 U/L IgG 1124 600-1300 mg/dL IgM 82 40-160 mg/dL IgA 125 41-297 mg/dL C3 129 90-180 mg/dL C4 26 10-40 mg/dL
|Printer friendly Cite/link Email Feedback|
|Author:||Seremidi, K.; Gizani, S.; Madianos, P.|
|Publication:||European Archives of Paediatric Dentistry|
|Article Type:||Case study|
|Date:||Oct 1, 2012|
|Previous Article:||Cross-sectional microhardness of bovine enamel subjected to three paediatric liquid oral medicines: an in vitro study.|
|Next Article:||Quality care for children under threat.|