This action might not be possible to undo. Are you sure you want to continue?
All rights reserved
Ó 2010 John Wiley & Sons A/S
Response of chronic and aggressive periodontitis to treatment
D A V I D E. D E A S & B R I A N L. M E A L E Y
In the late 1980s one of our residency mentors envisioned a day when a combination of clinical indices, microbiologic sampling and antibody proﬁles would both indentify and direct the treatment of speciﬁc periodontal diseases. Even though our knowledge base has expanded signiﬁcantly in the ensuing years, this has clearly not yet happened. The classiﬁcation scheme introduced in 1999 listed chronic periodontitis and aggressive periodontitis as two of the major forms of periodontal disease (1); but separating diseased patients into these two groups based on this classiﬁcation can be a subjective task. On initial presentation the two diseases share a number of clinical, microbiological and host response features (37, 56). Even though genetic testing and cytokine monitoring have opened new diagnostic vistas, it is still not always easy to identify one disease from the other or to use these tests to predict treatment outcome (28). It can also be argued that because aggressive periodontitis, although not rare, is a fairly uncommon condition, little is known about its optimal management. Protocols for treating chronic periodontitis are fairly well established. Protocols for treating aggressive periodontitis are largely empirical and have been subjected to few well-controlled comparative studies (72). In this section, we will focus on the response of aggressive periodontitis to treatment, using as comparison the response to treatment of chronic periodontitis, about which much more is known. To avoid confusion, the most current terminology for both disease categories and pathogenic bacteria will be used, even though different terms were often used in the speciﬁc articles cited.
The opinions expressed in this article are those of the authors and are not to be construed as ofﬁcial or as representing the views of the United States Air Force or the Department of Defense.
Diagnosis and prognosis
Establishing a diagnosis based on disease type, extent, location and severity is an essential ﬁrst step in treatment, and the steps do not differ markedly regardless of whether the patient has chronic periodontitis or aggressive periodontitis. Although little has been written about prognostic factors in aggressive disease (28), persistent deep pockets, loss of attachment, mobility, furcation invasion, suppuration, plaque, calculus and other factors such as root grooves, cervical enamel projections, root fractures and poor restorations can help clinicians to predict the outcome of both diseases. The extent of attachment loss in a patient with aggressive periodontitis may negatively inﬂuence the prognosis, but this may be somewhat counterbalanced by a desire to go to additional lengths not to extract teeth in younger patients. These tooth-level factors are used in the formulation of prognosis in conjunction with a number of subject-level factors, including smoking, genetic predisposition, age, gender, race and contributing medical conditions. This is appropriate regardless of whether the potential outcome variable is tooth loss or a surrogate variable such as probing depth or attachment loss (64). The relative value of these subject-level factors becomes more important if one considers that tooth-level indicators, such as bleeding on probing, have in some studies shown a greater association with future attachment loss at a subject level rather than at a site level (32). Smoking, in particular, has been shown to be an important subject-level prognostic factor in aggressive periodontitis. In two separate studies of nonsurgical therapy, smokers with aggressive periodontal disease responded signiﬁcantly less well to treatment than nonsmokers. Combining the results of these two
the therapist who cannot only inform their patients of the dangers of smoking. The effects of surgical debridement as part of the treatment of chronic periodontitis are also well documented (4. (25). Every periodontist has had treatment success in patients with an initially poor overall prognosis. 20. Overall.1–0. 26.2–0. More difﬁcult to assess independently are the added effects of regenerative techniques in treating chronic periodontitis. 29. Bone grafting with a variety of materials has been estimated to decrease probing depths and lead to gains in clinical attachment of 0.8 times more likely to have ‡30% of sites not responding to treatment. along with an increase in the number of gram-positive cocci.Response of chronic and aggressive periodontitis to treatment studies. management of modiﬁable risk factors and maintenance. oftentimes a complex restorative phase and always a strict maintenance regimen.2 mm additional attachment level gain over scaling and root planing alone. there is general consensus that the use of antibiotics in chronic periodontitis should be reserved for those patients and sites that do not respond to conventional treatment (5. Although it is impossible to determine a common thread between these cases.4 mm decrease in probing depth. clinicians should expect a mean reduction in probing depth of approximately 1 mm and a gain of clinical attachment level of approximately 0. Regardless.5–1 mm beyond that of surgical debridement alone (53).6 mm decrease in probing depth and 0. A comprehensive meta-analysis of nonsurgical treatment reported that following scaling and root planing at sites with probing depths of 4–6 mm. it is likely that risk factors have similar long-term inﬂuences on both chronic periodontitis and aggressive periodontitis. although local and systemic antibiotics may slightly improve clinical parameters over nonsurgical therapy alone. Response to therapy – chronic periodontitis The clinical response and the microbiological response to nonsurgical therapy in the treatment of chronic periodontitis have been well documented. The added effect of adjunctive antibiotic therapy has been found to be modest. the potential exists for greater gains in probing depth. nonsurgical and ⁄ or surgical therapy. 69). 24. In 4–6 mm pockets. attachment levels and bone ﬁll. Depending on the depth and morphology of osseous defects. surgical treatment gained an additional 0. Immediately after subgingival scaling there is a signiﬁcant decrease in the number of gram-negative organisms that include numerous periodontal pathogens. the treatment plan presentation should include a very frank discussion with the patient about the severity of the condition. Therefore. We know through such cases that even the most advanced or aggressive disease can be treated successfully. may have better results. 33. In general. but a loss of 0.2 mm gain of clinical attachment level over scaling and root planing alone (9. The bacterial response following treatment is also fairly consistent following scaling and root planing in chronic periodontitis. as well as higher levels of Prevotella intermedia and Tannerella forsythia after treatment (10. This leads to a point that we feel must be stressed. The therapist who is conﬁdent in ordering and interpreting certain blood tests is likely to have more inﬂuence with his patients than one who is not. As outlined in a systematic review by Heitz-Mayﬁeld et al. the odds of success and the requirement for near-perfect compliance with plaque control. the reduction in probing depth averages approximately 2 mm and the gain in clinical attachment level averages about 1 mm (29). with an additional 0. Similarly.6 mm mean probing depth reduction and 0. but statistically signiﬁcant. smokers with aggressive periodontitis were 3. but can also assist them with smoking cessation. Both must understand from the outset that without good cooperation from the patient and assertive management by the clinician the treatment has little chance of long-term success. A 155 . in pockets deeper than 6 mm surgical treatment resulted in an additional 0. Depending on the regimen. adding antibiotics to the treatment may further suppress the pathogenic microbiota and delay the return to baseline (5). 28).5 mm. This new microbiota remains established for approximately 4–8 weeks before returning to baseline by 12–24 weeks (5). although one could argue that with younger patient age and greater initial attachment loss they may dictate a poorer long-term prognosis in aggressive disease (64). 24.4 mm in attachment level beyond scaling and root planing (25). modulating and correcting these risk factors are critical in the treatment of both chronic periodontitis and aggressive periodontitis. These cases may involve strategic extractions. The patient with aggressive disease has given the clinician a difﬁcult task with an uncertain outcome. 18. it is likely that most of them had at their core a highly motivated patient. Just as essential for success is a clinician who is comfortable in helping patients to control risk factors (39). 19. 29). In deeper sites (probing depth ‡7 mm). 53).
A similar treatment approach carried out by Kornman & Robertson (38). There are few reports of nonsurgical therapy alone as a treatment of localized aggressive periodontitis. Upon re-evaluation. the number of spirochetes. but did not eliminate. those treated surgically. selective occlusal grinding. In contrast to these ﬁndings are those reported by Gunsolley et al.7 and 2. surface translocating bacteria or A. the combination of oral hygiene instructions.Deas & Mealey comprehensive meta-analysis of regeneration studies by Laurell et al. Two discoveries led to an emphasis on mechanical debridement supplemented with chemotherapeutic agents in the treatment of localized aggressive periodontitis. Only the two groups that received Ôlocal treatmentÕ (consisting of curettage. It is also interesting to consider the way in which the two types of aggressive disease respond to no treatment. in conjunction with open ﬂap debridement of the periodontal defects. Also at this point we must distinguish the treatment response between localized aggressive periodontitis and generalized aggressive periodontitis. actinomycetemcomitans. rather on than disease type. in a group of eight patients with localized aggressive periodontitis. reduced. patients were advised to have follow-up treatment. They found that scaling and root planing alone resulted in essentially no improvements in either pocket depths or in the percentage of culturable microbiota composed of black-pigmented Bacteroides species. Gunsolley et al.1 mm respectively. (23) examined 327 patients with either localized aggressive periodontitis or generalized aggressive periodontitis as part of a study of families with early onset disease. evaluated scaling and root planing alone as the ﬁrst stage in a treatment protocol where success was based on improvement in clinical and microbiologic parameters. Response to therapy – aggressive periodontitis The response to periodontal treatment in aggressive periodontitis is much less well understood. Another early report described aggressive occlusal or incisal grinding to allow the affected teeth to move occlusally. Slots & Rosling (61) evaluated nonsurgical treatment. Aggregatibacter actinomycetemcomitans and Capnocytophaga species and resulted in a small improvement in post-treatment probing depths. As most studies evaluating surgical outcomes of regeneration techniques selected groups on the basis of defects. an important pathogen associated with localized aggressive periodontitis. Following baseline examination of clinical indices. but it could not be determined which portion of the treatment regimen was responsible for the clinical improvement (14). beyond surgical debridement alone. One early study monitored ﬁve treatment groups of ÔperiodontosisÕ patients over a 3-year treatment and follow-up period. At a 15-year follow-up. actinomycetemcomitans. as one arm of a staged combination therapy. mentioned above. on the clinical and microbiological parameters of 20 deep pockets and 10 normal sites in six patients with localized aggressive periodontitis. These authors reported that patients with localized aggressive periodontitis who received treatment showed a gain in periodontal attachment over the 15-year period and that there was no difference in the response of those who received scaling and root planing alone vs. Three cases were shown to document the success of this approach. 88 of these patients were re-examined: 47 of them had received treatment and 41 had not. 156 . The second was the ﬁnding that A. (23). This is partly because the two types of periodontitis respond somewhat differently to treatment and partly because the literature usually reports on one group or the other. in part because the low prevalence of this disease makes it difﬁcult to recruit sufﬁcient numbers of patients for controlled clinical trials of different treatment modalities (72). surgery and oral hygiene instructions) as part of their therapy showed improved clinical status (63). The ﬁrst was when the predominant culturable microbiota of localized aggressive periodontitis was identiﬁed and found to be susceptible to tetracycline (49). it is possible that the treatment groups in these studies may also have included at least some patients with aggressive periodontitis. untreated sites in patients with generalized aggressive periodontitis showed increasing amounts of attachment loss and tooth loss. along with subgingival scaling and root planing. The authors reported that while untreated sites in patients with localized aggressive periodontitis tended to stabilize over time. (40) found that guided tissue regeneration generally improved attachment levels and bone ﬁll by 2. Localized aggressive periodontitis Much of what we know about the response to treatment of localized aggressive periodontitis was discovered when this condition was known by other terminology.
reported oftentimes dramatic improvements in both clinical and microbiological assessments. actinomycetemcomitans and Capnocytophaga species were reduced to almost undetectable levels. actinomycetemcomitans. actinomycetemcomitans from subgingival pockets. radiographic analysis of crestal alveolar bone mass and elimination of A. doxycycline and minocycline (71). Of particular interest in treating localized aggressive periodontitis was the discovery of resistance of A. After 5 years of maintenance. but was found in 9 ⁄ 26 sites in the tetracycline group. Autogenous grafts of both osseous coagulum and frozen autogenous hip marrow have been utilized. Mabry et al. The rationale for surgery at localized aggressive periodontitis sites is based both on the difﬁculty of root instrumentation in deep pockets as well as a perceived need to remove tissue invaded by A. Slots & Rosling (61). as well as osseous coagulum grafts covered with soft tissue autografts (12. The authors noted that after tetracycline treatment the number of spirochetes. The authors found that the average defect ﬁll was 80%. and evidence of radiographic bone ﬁll. thus placing it beyond the inﬂuence of subgingival scaling (7). 70). in the ﬁnal step of their staged treatment study mentioned above. Lindhe & Liljenberg (42) treated 16 cases of localized aggressive periodontitis with a combination of tetracycline and modiﬁed Widman ﬂap surgery. Similarly. (43) split 16 patients with localized aggressive 157 . Mandell et al. Following a strict 1-year maintenance regimen. It was noted. the other ﬁve subjects required periodontal surgery.Response of chronic and aggressive periodontitis to treatment could penetrate the pocket epithelium. (65) compared the response of an experimental group of 10 patients with localized aggressive periodontitis treated with scaling and root planing plus a metronidazole ⁄ amoxicillin regimen vs. 62). A variety of surgical techniques have been successfully utilized to treat localized aggressive periodontitis. Saxen & Asikainen (55) divided 27 patients with localized aggressive periodontitis into three groups receiving either subgingival debridement alone or subgingival debridement in combination with 1 g of tetracycline or 600 mg of metronidazole per day. Other authors have reported success of regenerative techniques in the treatment of patients with localized aggressive periodontitis. usually in combination with systemic antibiotics. 30). (44) used tetracycline ﬁbers to treat 12 sites in four patients with localized aggressive periodontitis. This failure to respond to treatment was linked to a growing level of bacterial resistance to tetracycline and other antibiotics such as amoxicillin. Success with other combinations of surgical debridement and antibiotic therapy has also been reported (3. actinomycetemcomitans. that up to 25% of patients treated in this manner experienced continued disease progression (41). administered 1 g of tetracyclineHCl per day for 14 days following subgingival debridement. Yukna & Sepe (73) treated osseous defects in 12 patients with localized aggressive periodontitis using freeze-dried bone allograft in a 4:1 mixture with tetracycline powder. actinomycetemcomitans and black-pigmented Bacteroides species. and bone ﬁll of greater than 50% was achieved in 98% of the defects. These problems with tetracycline treatment led to the investigation of other systemic antibiotics com´ bined with scaling and root planing.3 mm gain in attachment level. the focus of treatment studies shifted to combinations of conventional therapy with systemic antibiotics. a similar sized control group receiving scaling and root planing alone. 51 of the original 62 defects were surgically re-entered. actinomycetemcomitans to tetracycline (55. Tinoco et al. Kornman & Robertson (38) reported that modiﬁed Widman ﬂap surgery and a tetracycline regimen were effective at treating sites with initially high levels of A. 27. These and other studies using the 1 g per day tetracycline regimen. and that this corresponded to a 0. however. They concluded that the combination of root surface debridement and tetracycline was successful in treating most localized aggressive periodontitis sites. actinomycetemcomitans was reduced below the detection threshold in all test sites in metronidazole-treated patients. A. both with (60) and without (51) scaling and root planing. Not much has been published about the treatment of localized aggressive periodontitis with locally delivered antibiotics in conjunction with scaling and root planing. In response to these ﬁndings. attachment level measurements. It is possible that this failure was caused by the inability of tetracycline to adequately penetrate the pocket epithelium. Kornman & Robertson (38) reported that the combination of scaling and root planing plus tetracycline signiﬁcantly improved the clinical indices in three of their eight patients. 15. obviating the need for surgical treatment in these patients. they found signiﬁcant improvements in probing depths and attachment levels. actinomycetemcomitans from other potential reservoirs in the mouth (70). the antibiotic group had better improvement than controls in terms of probing depth. One year following treatment. A. This treatment failed to either stop the progression of attachment loss at these sites or eliminate A. or possibly as a result of the repopulation of A.
After a strict maintenance regimen over a 12-month period. with or without chlorhexidine irrigation. 48). They also reported that 32% of patients did not respond to this treatment.11 mm and a mean attachment level gain of 1. While both techniques demonstrated success at 1 year. patients received nonsurgical root surface debridement in four visits together with oral hygiene instructions. putative periodontal pathogens were reduced to undetectable levels from defects in both groups. and close collaboration is necessary between all members of a treatment team. the hygienist and the patientÕs physician (48). The authors reported that while grafted defects did better than debrided defects in both groups. A separate study compared the success of guidedtissue regeneration treatment with expanded polytetraﬂuoroethylene membranes in two groups of 10 patients with either early onset periodontitis (mostly localized aggressive periodontitis by description) or chronic periodontitis. expanded polytetraﬂuoroethylene membrane + root conditioning + composite graft) followed by post-operative systemic doxycycline. the authors of this study reported that while all sites gained attachment and defect ﬁll. the restorative dentist. that each of the above studies contained few subjects and defects. in the treatment of patients with generalized aggressive 158 . The bottom line is that the patient with generalized aggressive periodontitis requires careful monitoring. Hughes et al. Half of the defects in each group were treated with surgical debridement alone. making between-group comparisons difﬁcult. the combination of graft plus systemic tetracycline was the superior treatment overall. including the periodontist. Upon re-evaluation at 10 weeks. it was also noted that the membrane sites had the greatest variability in results. at initially deep sites. (59) compared guided-tissue regeneration using expanded polytetraﬂuoroethylene membranes with osseous resection in a group of six patients that included two individuals with localized aggressive periodontitis. there are at least a few studies on this condition that have investigated the effects of scaling and root planing alone. As mentioned earlier. generalized aggressive periodontitis is perhaps more likely to be confused with periodontitis as a manifestation of systemic disease and does not classically reach a Ôburned outÕ stage where it responds well to conventional periodontal therapy (23. treatment studies have only been able to include small numbers of subjects. This may be further complicated by the fact that it can be extremely difﬁcult to separate patients with generalized aggressive periodontitis from patients with severe or refractory forms of chronic periodontitis. PA) during the ﬁrst week post-operatively. the guided-tissue regeneration sites demonstrated signiﬁcantly better improvements in probing depth and attachment gain. while the other half received debridement and freeze-dried bone allografts mixed with tetracycline. Guided-tissue regeneration has also been successful in treating localized aggressive periodontitis. Fritz et al. A more recent study evaluated ultrasonic debridement. It is important to note. Although antibiotic therapy is widely used in the treatment of generalized aggressive periodontitis. Both groups received AugmentinÒ (SmithKline Beecham. Generalized aggressive periodontitis Our knowledge of the response of generalized aggressive periodontitis to treatment is hampered by several factors. Interpore International. (28) conducted a prospective intervention study of 79 patients with generalized aggressive periodontitis. expanded polytetraﬂuoroethylene membrane alone. Additionally. the authors reported a mean reduction in probing depth of 2. because the prevalence of aggressive periodontitis is low.77 mm. and that smoking was the biggest factor associated with nonresponse. King of Prussia. regenerative techniques work well for the treatment of localized aggressive disease. Following the collection of baseline data. who treated defects in seven patients with localized aggressive periodontitis using four different surgical treatment modalities (debridement. no signiﬁcant differences were noted between any of the surgical techniques. In contrast to the above studies suggesting superior results with regenerative procedures.Deas & Mealey periodontitis into two treatment groups depending on whether or not they received systemic tetracycline. Irvine. and all defects responded equally well from the standpoint of probing depth reduction and attachment level gains (74). Sirirat et al. demineralized freeze-dried bone. which leads to an inability to adequately compare multiple treatment groups. however. This is illustrated in a study by DiBattista et al. expanded polytetraﬂuoroethylene membrane + root conditioning. CA). or alloplastic graft (InterporeÒ. (13). (16) showed that intrabony defects in patients with localized aggressive periodontitis treated with expanded polytetraﬂuoroethylene membranes had slightly greater attachment gains than sites treated with ﬂap debridement. The results of the above studies suggest that where allowed by defect morphology.
A study by Guerrero et al. Six weeks after scaling and root planing. and clinical experience suggests that the magnitude of change in some sites may be greater when antibiotics are used. In a recent study. (57). It is possible that the 3-week re-evaluation used in this study was too soon to see a clinical beneﬁt.8 mm beyond those who were noncompliant or only partially compliant. Two months after scaling they found that the deepest sites in each quadrant experienced an approximate 1 mm reduction in probing depth and a 0. (36). The results demonstrated that clinical parameters improved at 2 and 6 months for both groups. In one study of 30 patients with generalized aggressive periodontitis. with a reduction of 0. By 6 months. It is important to remember. For example.Response of chronic and aggressive periodontitis to treatment periodontitis. At 6 months from baseline. Additional information on scaling in patients with generalized aggressive periodontitis can be gleaned from studies where scaling and root planing without antibiotics was used as either the ﬁrst arm of a clinical trial or as a control treatment. making it a more viable treatment option. By 6 weeks. although the proportions of sites with probing depths >6 mm were signiﬁcantly reduced in the two groups treated with metronidazole. An overall examination of these three controlled studies of adjunctive antibiotic treatment suggests a minimal additional beneﬁt of antibiotic use. doxycycline. the probing depth at four selected deep sites had been reduced by approximately 1 mm (according to median data). When combined with an enhanced scaling and root planing protocol. (52) provided scaling and root planing for 30 patients with generalized aggressive periodontitis as the ﬁrst part of a study comparing antibiotic treatments. The results suggested that both groups improved compared to treatment with scaling alone. All treatment was provided within 24 h and patients in both groups used chlorhexidine rinses for 2 weeks following treatment. This is consistent with the data obtained from the ﬁrst arm of a study comparing antibiotic regimens in the treatment of generalized aggressive periodontitis (72). Sigusch et al. A similar controlled study. It is also impossible to know the level of patient compliance in taking the antibiotics in these studies. who found that administering metronidazole ⁄ amoxicillin immediately after scaling and root planing was more effective in resolving deep sites in patients with generalized aggressive periodontitis than the same drug regimen given 3 months later. The timing of the antibiotic treatment in this study may be questioned in light of a more recent report by Kaner et al. A more recent study reported that tetracycline ﬁbers. metronidazole or clindamycin with a control group receiving no antibiotic treatment. (72). In sites initially 4–6 mm deep. (57) divided 48 patients with generalized aggressive periodontitis into four groups to compare systemically administered doxycycline.5 mm in attachment gain compared with controls.4 mm reduction in probing depth and a 1 mm gain in attachment level when compared with the control group.5% of sites in patients of the antibiotic group compared with 3.3% of sites in controls. in patients with generalized 159 . the authors found that both metronidazole and clindamycin signiﬁcantly improved the clinical response beyond that of the doxycycline or control groups. The adjunctive use of systemic antibiotics to treat generalized aggressive periodontitis is logical in theory but has been the subject of few controlled clinical trials.5 mm gain in attachment levels. the antibiotic group experienced an additional 1. disease progression was noted at 1. regardless of the irrigant used in the treatment (21). the clinical differences between the four groups were minor. metronidazole. who saw no improvements in probing depths or attachment levels following scaling and root planing in their group of 48 patients with generalized aggressive periodontitis. (22) compared the results of scaling and root planing alone to the results found following scaling and root planing plus treatment with systemic metronidazole and amoxicillin in a group of 41 patients with generalized aggressive periodontitis. with no statistically signiﬁcant differences observed between groups (52). the difference was more modest.9 mm and attachment level gains of 0. (22) examined 18 patients with generalized aggressive periodontitis taking metronidazole ⁄ amoxicillin in conjunction with nonsurgical therapy. Local-delivery antibiotic treatment has also been evaluated in the treatment of generalized aggressive periodontitis. In sites originally ‡7 mm. was conducted by Xajigeorgiou et al. Purucker et al. 43 patients with generalized aggressive periodontitis were divided into four groups to receive metronidazole ⁄ amoxicillin. in conjunction with scaling and root planing. evaluating the relative effectiveness of antibiotic regimens. In contrast are the ﬁndings of Sigusch et al.4 mm in probing depth and 0. Guerrero et al. however. They found that subjects who were fully compliant in taking their medications had probing depth reductions of 0. half of the subjects received monolithic tetracycline ﬁbers at affected sites while the other half received systemic AugmentinÒ. or placebo for 7–14 days. depending on the drug. that these reports contain averaged data.
6 mm and 3. 36. 160 . Both groups received systemic metronidazole and amoxicillin as well as chlorhexidine rinses. (47) divided 30 patients with generalized aggressive periodontitis into two groups to evaluate traditional quadrant-wise scaling using a full-mouth debridement approach where all scaling was completed within 24 h. The test group subjects received an additional round of root planing where the instrumentation frequency of curet strokes per root surface was based on the probing depth. (23). Of the 100 sites followed to 60 months. While many of the details of these patients. There are several perfectly logical reasons for this: severe attachment loss on presentation. there were no signiﬁcant differences between groups at either 2 or 6 months. While a cautious approach to surgery in patients with generalized aggressive periodontitis is prudent. possible links with covert or undetected systemic disease. the authors reported mean probing depth reductions and attachment level gains of 3. While the use of antibiotics in periodontal treatment will probably always be controversial. 26). the authors reported signiﬁcantly improved probing depth reduction and attachment level gain using the enhanced technique. (46) used radiographs and clinical indices to follow a group of 16 healthy. determined that patients with aggressive periodontitis appear to beneﬁt from the adjunctive use of systemic antibiotics during treatment. it was clear to the authors that they had received little beneﬁt from therapy. After 5 years. Patients received systemic metronidazole ⁄ amoxicillin during both scaling and root planing and surgical phases of treatment. 69). While clinical parameters improved in both groups. although the variation at individual sites was large. 28 had received treatment. Both of these reports. and furcation defects were excluded. The authors further reported a radiographic defect ﬁll of 47. dosage and duration providing the greatest effect was unknown at this time (24. and only 7. Buchmann et al. very little has been published about the surgical treatment of generalized aggressive periodontitis.3 mm at the sites receiving bioactive glass. Of the 48 patients with generalized early onset peri- odontitis. or a reluctance to perform surgery in patients with poor prognoses. 12. and 20 were treated with bioactive glass. One ﬁnal element of nonsurgical therapy in the treatment of aggressive periodontitis is the use of enhanced root planing techniques. Individual sites had attachment level gains of as much as 7 mm. 24. 86 with initial probing depths of ‡6 mm were subjected to modiﬁed Widman ﬂap procedures with no osseous surgery.1% of sites did not respond to initial treatment. It is important to note that smoking and systemic disease were exclusion criteria in this study. A more recent study by Mengel et al. Sigusch et al.0 mm at the membrane-treated sites. (6) followed 13 patients with generalized aggressive periodontitis for 5 years through active and maintenance therapy. re-examined after 15 years by Gunsolley et al. Moreira et al. reports from both the American Academy of Periodontology and the European Federation of Periodontology contain valuable guidelines for their use.Deas & Mealey aggressive periodontitis was more effective than scaling and root planing alone (54). both also emphasized that knowledge of the optimal drug. the inability to control risk factors. however. These studies suggest that local-delivery antibiotic treatment may be of beneﬁt in situations where systemic antibiotics are contraindicated. and mean probing depth reductions and attachment level gains of 3. Very little has been written about the use of enamel matrix derivative in aggressive periodontitis (35. as well as at 3. For each patient. (58) compared traditional scaling and root planing with an enhanced root planing technique in a group of 42 patients with generalized aggressive periodontitis who were also treated with systemic metronidazole. Approximately 25% of the sites in both groups had probing depths of ‡5 mm after 5 years. following exhaustive literature searches. At 6 and 24 months. Three months following treatment. nonsmoking patients with generalized aggressive periodontitis through active therapy and maintenance for 5 years. 6.5 and 3. and in some cases that treatment included surgery. The sites monitored included only those with one to three wall intrabony defects of ‡4 mm. regarding risk factors and follow-up care. Beyond isolated case reports. a history of poor surgical outcomes with previous patients with generalized aggressive periodontitis. there is at least some evidence that it can be successful under certain circumstances. there was a mean 2.5% in membrane-treated defects and 65% ﬁll in bioactive glass-treated sites. they monitored attachment level measurements on two teeth with >50% bone loss per quadrant at baseline. are unknown.23 mm gain of clinical attachment at all sites that remained stable over the maintenance period. Twenty-two of the defects were treated with bioabsorbable membrane alone. it is possible that this may be because of an overall reluctance of clinicians to perform surgery on patients with generalized aggressive periodontitis. 48 and 60 months after treatment.
(6) followed the treatment of 13 patients with aggressive periodontitis (by description. Periodontal maintenance Regardless of whether the original diagnosis is chronic periodontitis or aggressive periodontitis. Lindhe & Liljenberg (42) used a combination of surgical debridement and systemic tetracycline to treat 16 patients with localized aggressive periodontitis and 12 older patients with chronic periodontitis. even when treated. (68) used enamel matrix derivative to treat selected defects in four patients with aggressive periodontitis and compared the results at 9 months with similar defects in a control group of four patients with chronic periodontitis. especially smoking. A recent retrospective study by Matuliene et al. Kamma et al. at all sites deeper than 4 mm showing bleeding on probing. generalized aggressive periodontitis) through modiﬁed Widman ﬂap surgery and systemically administered metronidazole and amoxicillin. persistent gingival inﬂammation results in a greater risk for tooth loss and attachment loss over time. A possible conclusion of the above studies is that if risk factors. of ‡2 mm. diseased sites in the patients with localized aggressive periodontitis responded as well to treatment as sites in the patients with chronic periodontitis. then every 3 months until the end of the study. If. the patient with aggressive periodontitis may have residual deep pockets. tended to experience continued tooth loss and attachment loss over time. then surgical therapy can be as beneﬁcial to the patient with generalized aggressive periodontitis as it is to any other patient. after therapy. in patients with aggressive periodontitis. Patients were seen monthly for maintenance care during the ﬁrst 6 months. The relatively high rate of sites breaking down over time. residual probing depths of 5–7 mm represented signiﬁcant risk factors for both attachment loss and tooth loss. The previously mentioned study by Buchmann et al. and the extent of tissue invasion by these bacteria did not decrease following treatment (31. Despite this increased risk for recurrence. There are several potential reasons for this. and no differences were found between the two groups. Following treatment. The authors reported that in general. 67). with an additional 2–4% of sites experiencing additional attachment level gain. the site effect of mechanical therapy plus systemic metronidazole and amoxicillin on potential pathogens was transient. patients with aggressive periodontitis before therapy have to be considered at high risk for recurrent disease after therapy. suggests a likely need for retreatment during the maintenance phase. After 5 years of maintenance care.Response of chronic and aggressive periodontitis to treatment In the larger of two case reports. there is evidence that attachment loss can be stabilized. (66) demonstrated that patients with aggressive periodontitis had a signiﬁcantly higher inﬂammatory response. the previously mentioned study by Gunsolley et al. Given the amount of pocket formation and attachment loss possible in aggressive disease. Although this is somewhat controversial. which included subgingival instrumentation. For example. than periodontally healthy patients. 8). the goal of maintenance care following active periodontal treatment is to maintain the level of periodontal health achieved during active therapy. however. can be eliminated. there is some evidence to support the concept that additional attachment loss is more likely to occur at sites with deeper residual pocket depths (2. Twenty of the 25 patients experienced additional attachment loss. although 4 of the 12 patients in the localized aggressive periodontitis group (a total of six sites) needed to be retreated for disease recurrence over the 5-year study period. Two recent reports demonstrated that despite a favorable initial clinical outcome. (34) followed a group of 25 patients with aggressive periodontitis through active therapy and maintenance care at 3–6-month intervals over a 5-year period. and if compliance with maintenance care is high. under local anesthesia. The authors reported signiﬁcant improvements in both probing depths and attachment levels. it is likely that after therapy. Another reason to fear additional attachment loss in aggressive disease is an increased inﬂammatory response. then the patient with aggressive periodontitis may be at increased risk. 161 . Given their initial susceptibility to disease. as some have suggested.4–5. as measured by gingival crevicular ﬂuid ﬂow. (45) re-examined 172 patients at time points from 3 to 27 years after active periodontal therapy. An experimental gingivitis study by Trombelli et al. the authors found that only 1. Vandana et al. They found that compared with probing depths of £3 mm. the patients were recalled at 3–6-month intervals for maintenance. (23) showed that patients with generalized early onset periodontitis. Residual deep sites may explain why the long-term treatment effect on bacterial pathogens may be limited in patients with aggressive periodontitis.3% of sites underwent disease progression during the recorded intervals. following treatment at a total of 134 sites.
Beyond that. defects in the early onset group experienced a mean probing depth reduction of 7. root canal therapy. surgical. In general. at a faster rate and to a greater extent than the patient with chronic periodontitis.g. reevaluation. stress. The authors attributed the success of treatment in part to an aggressive maintenance schedule of monthly professional cleanings and oral hygiene reinforcement. it is our opinion that the patient with generalized aggressive periodontitis. In addition. this cannot help but complicate the treatment-planning process. medications. monitoring other systemic factors. a thorough explanation of the disease process and its contributing factors is given to patients with both chronic and aggressive disease.Deas & Mealey Finally. Table 1. Although the cause-and-effect relationship is uncertain.g. orthodontic assessment) – extraction of hopeless teeth – scaling and root planing – local or systemic antibiotic treatment* Re-evaluation – re-assess prognosis of individual teeth and overall dentition • probing depths • attachment level measurements • bleeding on probing • furcation invasion • mobility • root sensitivity – oral hygiene – bacterial sampling of selected pockets* (if not completed during the initial phase) – additional laboratory tests (e.1 mm and an attachment level gain of 6. family history. strategic value of teeth for eventual restoration. 34). should be referred for a complete blood count and either a casual or a fasting blood glucose test. we would expect the patient with aggressive periodontitis to have experienced attachment loss at a younger age. but Initial phase – emergency treatment if needed – explanation of the disease process and contributing factors* – review of oral hygiene instructions – occlusal analysis and treatment of localized trauma from occlusion – bacterial sampling of selected pockets* – dental consultations (e. Because periodontitis as a manifestation of systemic diseases can present as aggressive periodontitis. the patient with chronic periodontitis may require little beyond an awareness of existing medical conditions and medications.1 mm. While the generally accepted phases of treatment – systemic. maintenance. it is critical that the practitioner performs a thorough medical history.g. The systemic phase for the patient with aggressive periodontitis is likely to be much more complex. for example. depression and malaise has also been recommended (48). It may also be a good idea to review the patientÕs social history to identify stress-related factors (17. If the expectation of the patient and the provider is to retain teeth. Zucchelli et al. In the systemic phase. a heightened requirement for identiﬁcation and modulation of risk factors is essential. such as weight loss. the amount of speciﬁc planning required at each step may be greater for the patient with aggressive disease (Table 1). especially. In the initial phase. 2-h postprandial glucose)* – medical consultation if indicated* – assessment of modulation of risk factors* – patient motivation 162 . fasting blood glucose)* – medical consultation if indicated – identiﬁcation ⁄ modulation of risk factors (e. Treatment planning sequence for patients with periodontitis Systemic phase – review of medical history. social history* – laboratory screening tests (complete blood count. At 1 year. and restorative – seem well suited for patients with both diseases. initial. diet)* – assess the need for a stress-reduction protocol during therapy Treatment planning The process of treatment planning for periodontitis patients is well established and an attempt will not be made to review each step. caries control. (74) used guided-tissue regeneration to treat single intrabony defects in 10 patients with localized early onset periodontitis and compared their results with the same treatment in patients with chronic periodontitis. smoking.
Although there is limited evidence to suggest that enhanced root planing techniques may offer an added treatment response to nonsurgical therapy (58). especially in patients with generalized aggressive periodontitis. where surgical debridement is an acceptable ﬁrst step if dictated by time or third-party payment constraints. another element of the initial phase that may have added emphasis in patients with aggressive periodontitis is consultation with other dental specialists to assess the strategic long-term restorative value of certain teeth before starting periodontal therapy. Monitoring compliance with oral hygiene procedures is critical in both groups. standard brushing ⁄ ﬂossing instructions are less likely to be sufﬁcient for patients with aggressive disease. both types of patients should be given a comprehensive review of oral hygiene techniques. If surgical treatment (including initial extraction of hopeless teeth) is undertaken in the patient with aggressive disease. The exception to this may be in certain cases of localized aggressive periodontitis. While the literature may be somewhat equivocal on the added value of antibiotics as an adjunct to initial therapy. we recommend a biopsy of associated granulation tissues to rule out certain pathological entities such as LangerhansÕ cell histiocytosis. is speculative at best. A 4–6-week re-evaluation interval seems as valid for a patient with aggressive periodontitis as for one with chronic periodontitis. even if somewhat placebo based. however. in our view should be given special emphasis in the patient with aggressive periodontitis. either singly or in combination. its superiority over other antibiotics. are always welcomed. attachment level measurements 6 months after completion of treatment. Given the likelihood of greater attachment loss at an earlier age. may proceed to maintenance or return to initial phase) – antibiotic treatment* – monitor healing of previously treated sites Maintenance phase – monthly for the ﬁrst 6 months following treatment. then it may be worthwhile. risk factor modulation – prophylaxis. however. we recommend (i) the initiation of antibiotic therapy 24 h before starting scaling and root planing. In our view. Improvements in either compliance or clinical indices. treatment of hypersensitivity – subgingival scaling of deep pockets – host modulation therapy if indicated* – local delivery antibiotic treatment of at-risk sites – full-mouth scaling and root planing (with or without adjunctive antibiotics if indicated by general breakdown)* – deﬁnitive occlusal adjustment if indicated – consider extraction of teeth with progressive disease to preserve alveolar bone* Restorative phase – assessment of prosthesis cleansability and function *Areas of special emphasis for patients with aggressive periodontitis. The re-evaluation should closely resemble the initial evaluation. The outcome of treatment in aggressive periodontitis is uncertain. many clinicians have noted that the magnitude of improvement at individual sites may be improved with antibiotic therapy (22). it is our view that this is a worthwhile step. the treatment of aggressive periodontitis should start with scaling and root planing in combination with systemic antibiotics. Even if the main beneﬁt of antibiotic therapy is to reduce the number of sites with probing depths >6 mm (72). If a full-mouth debridement approach demonstrates an added commitment or sense of importance to the treatment. with review of 163 . the practitioner should assess the family history of periodontal problems and consider evaluation of siblings and parents (11. Likewise. topical ﬂuoride treatment if indicated. then at each maintenance visit – yearly radiographs of at-risk teeth* – assessment of oral hygiene. This may guide the periodontist in recommending extractions of questionable teeth. and (ii) that root planing is performed over the short time period during which the antibiotic is prescribed. especially those who have experienced attachment loss that has exposed furcations and root concavities. then extending to 3 months* – probing. 50). Finally. Continued Surgical phase (if indicated. then bimonthly until 12 months. Furthermore. but may be more difﬁcult in the aggressive patient if chlorhexidine rinses are prescribed frequently during treatment. The combination of metronidazole 500 mg three times daily plus amoxicillin 500 mg three times daily is probably the most popular antibiotic regimen in the current literature. because aggressive periodontitis often demonstrates a familial pattern. in our view there is value in any reasonable protocol that enhances patient and provider conﬁdence.Response of chronic and aggressive periodontitis to treatment Table 1.
In general. as with more knowledge of the mechanisms of disease it is possible that patients currently classiﬁed as having aggressive periodontitis may be found not to represent a single diagnostic entity. 164 . then proceeding to either a maintenance phase or a surgical phase. Becker W. Subgingival scaling in combination with local delivery of antibiotics is a good way to manage isolated sites of recurring disease. J Periodontol 1996: 67: 1143–1158. osseous surgery. Genco RJ. Armitage GC. Quireynen M. Lange DE. we recommend a return to the initial phase for additional data collection and treatment. a clinicianÕs success in treating patients with aggressive periodontitis may be most dependent on the maintenance program. regenerative therapy. J Periodontol 1987: 58: 540–545. J Periodontol 1983: 54: 148–150. J Periodontol 2002: 73: 675–683. At this point. It seems critical to very slowly extend the maintenance interval in these patients. If. If the patient is stable during this ﬁrst year. Baker RL. the clinician would expect at least some resolution of disease indicators. References 1. Aggressive periodontitis: 5 year follow-up of treatment. as indicated in each individual case. The formation and healing of osseous lesions in a patient with localized juvenile periodontitis. Bollen CM. while full-mouth scaling and systemic antibiotics. bacterial culture and sensitivity testing of the deepest pockets may be warranted. Ochsenbein C. Morrison E. II. Van Dyke TE. seems justiﬁed. the patient may be referred to his physician for evaluation of his metabolic status. Becker BE. possibly using the enhanced scaling and root planing techniques referred to previously. and we do not clearly understand the reasons for this variable response. regardless of whether the initial diagnosis is chronic periodontitis or aggressive periodontitis. Nunn ME. by proceeding to a surgical phase in patients who have demonstrated little or no improvement in clinical indices following well-delivered initial therapy. risk factors. and modiﬁed Widman procedures: results after 5 years. Prichard J. Depending on the results of the 2-h postprandial test. with very careful monitoring of probing depths. Depending on the outcome. Periodontal diseases: diagnosis. Caffesse R. which is a more sensitive test for diabetes mellitus than either fasting or casual glucose tests. Barnett ML. respective therapy and even tooth extraction. Zambon JJ. depending on the response. 4. along with a 2-h postprandial glucose test. 3. We think it likely that this research could result in further alterations to the classiﬁcation of periodontal diseases. the clinician may choose to repeat subgingival scaling with a different antibiotic regimen. Kerry G. Buchmann R. It is possible that new research into the resolution of inﬂammation may reveal basic differences between patients with chronic periodontitis and those with aggressive disease. Correlation between immunoﬂuorescence and culture techniques. A review of the literature. If the response to initial therapy is equivocal. we recommend monthly maintenance for the ﬁrst 6 months after completing active treatment. isolated area and to monitor healing during a period of trial maintenance before proceeding to other sites. Microbiologic response to mechanical treatment in combination with adjunctive therapy. then bimonthly for 6 more months. Ultimately. there is little to be gained. Summary and future directions Patients with aggressive periodontitis can be both rewarding and frustrating to treat in clinical practice. In our opinion. Wikesjo UM. maintenance intervals can be extended to 3 months. At this point. or host-modulation therapy. 2. If this is the case. Ann Periodontol 1996: 1: 37–215. Interindividual variation in response to therapy can be widespread. Armitage GC. Albini B. 5. A longitudinal study comparing scaling. future research involving modulation of host inﬂammatory responses may clarify the reasons for the differences in clinical outcomes between patients. there is no signiﬁcant positive response to initial therapy. J Periodontol 2001: 72: 1675–1684. Case report. oral hygiene techniques and clinical indices. Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. ¨ 7. Ann Periodontol 1999: 4: 1–6. can be used to treat a generalized recurrence. Development of a classiﬁcation system for periodontal diseases and conditions. and potentially much to be lost. If the response to initial therapy supports proceeding to a surgical phase. risk factors and signs of inﬂammation. Surgical modalities are selected according to these goals and include all forms of treatment such as ﬂap debridement. Better understanding of the true nature of patients currently identiﬁed as having aggressive periodontitis may therefore lead to more effective treatment approaches. In addition. the goals of surgical treatment are similar to those in a patient with chronic periodontitis. Christersson LA. 6. then it may be prudent to perform surgery in a limited.Deas & Mealey medical history. however.
Haffajee AD. Gottlow J. 39. J Periodontol 1999: 70: 711–723. Ann Periodontol 1996: 1: 443–490. Periodontosis: treatment results in 15-year old girl. J Clin Periodontol 1982: 9: 1–21. 33. A case report. Primary health care assessment and intervention in the dental ofﬁce. Jafﬁn RA. Heitz F. Herrera D. Treatment of intrabony defects by different surgical procedures. Mergenhagen SE. Clinical indicators of probing attachment loss following initial periodontal treatment in advanced periodontitis patients. Curtis MA. Rosenberg ES. Genco RJ. DC: ASM. 165 . J Periodontol 1984: 55: 261–267. Jepsen S. Bostanci N. J Clin Periodontol 2002: 29(suppl 3): 92– 102. Kleber BM. Hodge PJ. Kornman KS. Hung HC. Tinoco EM. A systematic review on the effect of antimicrobials as an adjunct to scaling and root planing in periodontitis patients. Chen R. Amsterdam M. Cooper LC. Croucher RE. Kamma JJ. non-surgical debridement for the treatment of chronic periodontitis. Burmeister JA. Cobb CM. J Periodontol 2007: 78: 1201–1208. Mabry TW. Schenkein HA. Echeverria JJ. 43. Aggressive periodontitis is likely inﬂuenced by a few small effect genes. J Periodontol 1998: 69: 507–520. Alexander SA. J Periodontol 1993: 64: 243–253. J Periodontol 1970: 41: 683–684. J Clin Periodontol 2009: 36: 468–473. Advances in the pathogenesis of periodontitis. Bernimoulin JP. Tedesco LA. Timing effects the clinical outcome of adjunctive systemic antibiotic therapy for generalized aggressive periodontitis. Dunford RG. J Clin Periodontol 2005: 32(Suppl 6): 130–131. J Am Dent Assoc 2000: 131: 1580–1592. Zinney WB. J Periodontol 1964: 35: 63–69. Needleman I. Hoge HW. 20. Guarnelli ME. Treatment of molar teeth with juvenile periodontitis. Yukna RA. Freeze dried bone allografts combined with tetracycline in the treatment of juvenile periodontitis. 24. Berman CL. Manfrini R. J Clin Periodontol 1995: 22: 690–696. 25. In: Genco RJ. Roldan S. Kirkham DB. Egelberg J. Lang NP. Kaner D. A systematic review. Bleeding on probing. Van Dyke TE. J Clin Periodontol 2002: 29(suppl 3): 136–159. 13. Tonetti MS. Scaletta LJ. Host–parasite interactions in periodontal disease. Marazita ML. Liljenberg B. 12. Results after 5 years. Rudney JD. J Periodontol 1998: 69: 303–313. J Clin Periodontol 2006: 33: 663–670. J Periodontol 2008: 79: 2305–2312. Laurell L. Polson A. Hinrichs JE. Sanz M. Viera AR. Kinane DF. Kaner D. 29. 16.Response of chronic and aggressive periodontitis to treatment 8. Friedmann A. Grossi SG. De Carvalho FM. DiBattista P. Patil KD. A preliminary report on the treatment of osseous defects in periodontosis. J Periodontol 1995: 66: 673–678. 27. Everett FG. 15. Socransky SS. Treatment of localized juvenile periodontitis. 30. Trombelli L. Needleman I. Int J Periodontics Restorative Dent 2000: 20: 336–357. J Am Dent Assoc 1980: 101: 795–797. Changing periodontal paradigms: therapeutic implications. Greenstein G. J Periodontol 1995: 66: 321–328. Group B consensus report of ﬁfth European Workshop in Periodontology. The use of autogenous hip marrow in the treatment of juvenile periodontitis. Evian CI. 1981: 382–394. 42. Clinical and microbiological effects of scaling and root planing in smoker and non-smoker chronic and aggressive periodontitis patients. Moles D. A review of longitudinal studies that compared periodontal therapies. 22. Longitudional assessment of early onset periodontitis. Douglass CW. Robertson PB. Koertge TE. Gunsolley JC. Meta-analysis of the effect of scaling and root planing. editors. Comparative effectiveness of various regenerative modalities for the treatment of localized juvenile periodontitis. J Periodontol 1985: 56: 74–81. Persson R. Lindhe J. Washington. Systemic antiinfective periodontal therapy. J Periodontol 1985: 56: 443–446. Hughes FJ. Lamster IB. Nonsurgical periodontal therapy in 2000: a literature review. Baer PN. Ho AW. J Clin Periodontol 2003: 30: 562–572. 38. Bernimoulin JP. Ann Periodontol 2003: 8: 115–181. Riggio MP. 31. J Clin Periodontol 2002: 29: 975–986. Attstrom R. Lindhe J. Incomplete adherence to an adjunctive systemic antibiotic regimen decreases clinical outcomes in generalized aggressive periodontitis patients: a pilot retrospective study. Heitz-Mayﬁeld LJ. Int J Periodontics Restorative Dent 2009: 29: 89–97. surgical treatment and antibiotic therapies on periodontal probing depth and attachment loss. Fritz ME. J Clin Periodontol 2007: 34: 897–902. J Clin Periodontol 2008: 35: 333–341. Guerrero A. A parameter for monitoring periodontal conditions in clinical practice. Four case reports. J Clin Periodontol 1984: 11: 399–410. Zhang G. Adjunctive effect of chlorhexidine in ultrasonic instrumentation of aggressive periodontitis patients: a pilot study. Relationship of stress. The role of local drug delivery in the management of periodontal diseases: a comprehensive review. Minimally invasive ﬂap surgery and enamel matrix derivative in the treatment of localized aggressive periodontitis: case report. Wolf DL. Kaldahl WB. Ricchetti PA. 36. 9. 19. Greenstein G. J Periodontol 2008: 79: 1825–1832. J Clin Periodontol 1994: 21: 402–408. Claffey N. Prognostic factors in the treatment of generalized aggressive periodontitis: I. Persistance of extracrevicular bacterial reservoirs after treatment of aggressive periodontitis. Five-year maintenance follow-up of early onset periodontitis patients. Clinical features and initial outcome. Koshy B. A literature review. De Marco TJ. Califano JV. Sepe WW. Treatment of localized juvenile periodontitis. 21. 28. J Dent Res 1989: 68: 883. Zybutz M. Gunsolley JC. 41. Joss A. Hameroff JA. Adler R. distress and inadequate coping behaviors to periodontal disease. 18. Friedmann A. 17. Marcenes W. Marinho V. Treatment of juvenile periodontitis patients by control of infection and inﬂammation. Lenton PA. Dietrich T. Clinical and microbiological evaluation of therapy for juvenile periodontitis. 10. 11. McKay IJ. J Clin Periodontol 2005: 32: 200–206. Lamster I. 40. Greenstein G. ´ 26. 14. 23. Kinane DF. Kalkwarf KL. A systematic review of surgical debridement vs. 34. ¨ 32. 37. Franceschetti G. Bissada NF. 35. Juvenile periodontitis – healing following therapy to control inﬂammatory and traumatic etiologic components of the disease. Greenstein G. Kleber BM. Darby IB. Govil M. Syed M. Non-surgical pocket therapy: mechanical. Baehni PC. Christian C. Trombelli L. Johnson JD.
Sirirat M. Tew JG. Feres-Filho EJ. Zucchelli G. J Periodontal Res 1977: 12: 120–128. Glockman E. Moreira RM. Savitt E. Nagy RJ. Cytokines and inﬂammatory factors regulating immunoglobulin production in aggressive periodontitis. Lana M. editors. Periodontol 2000 2007: 45: 113–127. necrotizing ulcerative periodontitis. A systematic review. Campedelli F. 67. Nibali L. Microbial changes in periodontics successfully treated by mechanical plaque removal and systemic amoxicillin and metronidazole. Modulation of clinical expression of plaque-induced gingivitis: response in aggressive periodontitis subjects. Veihelmann S. Slots J. Sakellari D. Minenna L. 70. 57. Salvi GE. 73. J Clin Periodontol 2008: 35: 685– 695. 48. 64. Guntsch A. 59. J Periodontol 1986: 57: 94–99. J Clin Periodontol 1993: 20: 166–171. Branch-Mays GL. Goodson JM. Xajigeorgiou C. De Sanctis M. Rams TE. J Periodontol 1996: 67: 603–607. Sigusch BW. Vogel U. Philidelphia. Tripodi LS. Aichelmann-Reidy ME. Int J Periodontics Restorative Dent 2002: 22: 323–333. Konstantinidis A. Loureiro CA. Barbour SE. Slini T. Sugarman MM. Purucker P. Vouros I. J Periodontol 2001: 72: 275–283. Levine MJ. Bernimoulin JP. Comparison between 2 surgical techniques for the treatment of early onset periodontitis. Sugarman EF. Schreiber D. 71. Thomas MV. 46. In: Rose LF. J Periodontol 2001: 72: 1241–1245. The acquisition of antibiotic resistance in the periodontal microﬂora. 51. J Periodontol 2002: 73: 1188–1196.Deas & Mealey 44. Nahoum HI. Mandell RL. Shah K. Tatakis DN. 52. 74. A familial analysis of aggressive periodontitis – clinical and genetic ﬁndings. Mertes H. Slots J. Mealey BL. Jeffcoat MK. Karpina K. J Periodontol 2005: 76: 991–997. Takei HH. In: Newman MG. Zwahlen M. Goodson JM. J Int Acad Periodontol 2003: 5: 52–60. Walker CB. Tichy D. Polson AM. Int J Periodontics Restorative Dent 1982: 2: 8–21. 63. Fores-de-Jacoby L. J Am Dent Assoc 1957: 55: 651–658. 166 . St Louis. Baka A. 53. Rams TE. 66. Rosling BG. 49. Lang NP. The use of tetracycline ﬁbres in the treatment of generalized aggressive periodontitis: clinical and microbiological ﬁndings. Metronidazole in the treatment of localized juvenile periodontitis. Grifﬁths GS. Bragger U. Clinical and radiographic evaluation of Emdogain as a regenerative material in the treatment of interproximal vertical defects in chronic and aggressive periodontitis patients. Vandana KL. editors. ¨ 45. Mengel R. Tinoco NM. Saxen L. 62. Beldi MI. Treatment of refractory periodontitis. 9th edn. Bellini HT. 50. Prakash S. Tenenbaum B. 1st edn. Peplies J. Periodontol 2000 1996: 10: 45–78. van Winklehoff AJ. Clinical and microbiological effects of different antimicrobials on generalized aggressive periodontitis. Walker CB. Adair SM. Socransky SS. Schmidlin K. Local versus systemic adjunctive antibiotic therapy in 28 patients with generalized aggressive periodontitis. 69. 47. Pﬁster W. Int J Med Microbiol 2009: 299: 427–438. Preus HR. Slots J. Novak MJ. ¨ 58. 61. A 2 step non-surgical procedure and systemic antibiotics in the treatment of rapidly progressive periodontitis. and periodontitis associated with systemic diseases. Periodontol 2000 1996: 10: 79–88. Valenza G. 68. aggressive periodontitis. J Clin Periodontol 2006: 33: 79–85. Predominant cultivable microbiota in periodontosis. Linger G. Genco RJ. Socransky SS. Schlagenhauf U. Periodontal therapy in humans. J Periodontol 2006: 77: 1781–1787. Glockmann E. PA: WB Saunders. J Periodontal Res 2008: 43: 627–634. J Clin Periodontol 2006: 33: 254–264. Parkar M. MO: Elsevier Mosby. GTR treatment of intrabony defects in patients with early-onset and chronic adult periodontitis. J Periodontol 1979: 23: 260–269. Suppression of the periodontopathic microﬂora in localized juvenile periodontitis by systemic tetracycline. Pﬁtzner A. Ellinas T. 60. Formulating a periodontal diagnosis and prognosis. Brett PM. Inﬂuence of residual pockets on progression of periodontitis and tooth loss: results after 11 years of maintenance. Rational for use of antibiotics in periodontics. Gjermo P. Pjetursson BE. Mashimo P. Llorente M. J Periodontol 1988: 59: 366–372. Beube FE. Newman MG. Wiener R. Carranza FA. Tetracycline therapy in patients with early juvenile periodontitis. Reynolds MA. ´ 55. Tinoco EM. 2004: 172–199. I Microbiological and clinical effects of a single course of periodontal scaling and root planing and of adjunctive tetracycline therapy. J Periodontol 2007: 78: 1683–1688. Konstantinidis A. Enhanced scaling and root planing and systemic metronidazole administration improve clinical and microbiological outcomes in a two-step treatment procedure. Systemic antibiotic therapy in periodontics. Del Carmen Roldan-Pareja M. Results of several types of treatment of periodontosis. Beier M. Kasetsuwan J. 65. 2002: 558–566. Trombelli L. Sigusch BW. Ann Periodontol 2003: 8: 227–265. Periodontics. Int J Periodontics Restorative Dent 2004: 24: 185–191. The effect of treatment on Actinobacillus actinomycetemcomitans in localized juvenile periodontitis. Karshan M. 56. Asikainen S. Scapoli C. Gunsolley JC. 54. 72. J Periodontol 1998: 69: 1355–1363. J Periodontol 1977: 48: 397–409. The efﬁcacy of bone replacement grafts in the treatment of periodontal osseous defects. Donos N. Newman MG. CarranzaÕs clinical periodontology. Comparison between full mouth scaling and root planing and quadrant wise basic therapy of aggressive periodontitis: 6 month clinical results. Brini C. Clinical and microbiologic effects of adjunctive antibiotics in treatment of localized juvenile periodontitis. Matuliene G. A controlled clinical trial. Bioabsorbable membrane and bioactive glass in the treatment of intrabony defects in patients with generalized aggressive periodontitis: results of a 5-year clinical and radiological study. Sepe WW. Schenkein HA. J Clin Periodontol 1983: 10: 465–486. Clinical evaluation of localized periodontosis defects treated with freeze dried bone allografts combined with local and systemic tetracyclines. Precocious periodontitis: a clinical entity and a treatment responsibility. Mealey BL. Sakellari D. Yukna RA.
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.