Year : 2011 | Volume
: 15 | Issue : 4 | Page : 318--322
"What is there in a name?": A literature review on chronic and aggressive periodontitis
Sameera G Nath1, Ranjith Raveendran2,
1 Department of Periodontics, Govt. Dental College, Calicut, India
2 Department of Orthodontics, Kerala State Co-Operative Hospital Complex, Academy of Medical Sciences, Pariyaram Dental College, Kannur, Kerala, India
Sameera G Nath
20/1312, «DQ»Krishneeyam«DQ», Thiruvannur Road, Panniyankara, Post Kallai, Calicut, Kerala
The objective of this review is to bring the reader up-to-date on the current understanding of chronic and aggressive forms of periodontitis and the implications for diagnosis and treatment of these diseases. The only difference between chronic periodontitis and aggressive periodontitis with regard to tissue destruction appear to be perhaps the magnitude, sequelae, and control of the response. While there may be some differences in the cellular infiltrate between these two diseases, the molecular mediators and pathologic processes are generally the same.
|How to cite this article:|
Nath SG, Raveendran R. "What is there in a name?": A literature review on chronic and aggressive periodontitis.J Indian Soc Periodontol 2011;15:318-322
|How to cite this URL:|
Nath SG, Raveendran R. "What is there in a name?": A literature review on chronic and aggressive periodontitis. J Indian Soc Periodontol [serial online] 2011 [cited 2021 May 8 ];15:318-322
Available from: https://www.jisponline.com/text.asp?2011/15/4/318/92561
Periodontal diseases range from the relatively benign gingivitis to chronic and aggressive forms of the disease. There is inconsistent use of criteria to define the different forms of periodontitis in literature. Throughout the 20 th century, chronic periodontitis was considered as an inflammatory disease associated with local irritants and dental plaque on tooth surfaces. 
This concept prevails today. What is now known as "generalized aggressive periodontitis" was not clearly described until the latter part of 20 th century. The objective of this review is to update the current understanding of the chronic and aggressive forms of periodontitis and their implications for the diagnosis and treatment.
Clinical Features of Chronic and Aggressive Periodontitis
Chronic and aggressive periodontitis share many clinical features. They are both complex infections that occur in susceptible hosts and are caused by biofilms with indigenous oral microbiota on tooth surfaces.  The host response to the biofilms are primarily responsible for the loss of periodontal attachment and alveolar bone supporting the teeth.  The eventual outcome of these untreated diseases is tooth loss.
In both generalized forms of chronic and aggressive periodontitis, the affected individuals have no known medical or general health conditions that might contribute to the development of their periodontitis. If the systemic disease profoundly impairs the ability of the host to cope with the bacterial challenge associated with periodontitis, the term "periodontitis as a manifestation of systemic disease" should only be used instead of and not "chronic or aggressive" according to the 1999 classification. 
Although similar in many respects, chronic and aggressive forms of periodontitis have a number of significant clinical differences including: (i) age of onset (i.e., detection), (ii) rates of progression, (iii) patterns of destruction, (iv) clinical signs of inflammation, and (v) relative abundance of plaque and calculus. Indeed, combinations of these clinical differences are the primary basis for placing affected individuals into one of the three major categories of periodontitis (i.e., chronic periodontitis, localized aggressive periodontitis, and generalized aggressive periodontitis).
Age of onset
The age of onset is an important feature that has traditionally been used to help place patients either in the aggressive or in the chronic periodontitis category. But there is considerable uncertainty about setting arbitrary upper age limits for certain forms of periodontitis. Given similar amounts of periodontal damage (i.e., probing depths, attachment loss, alveolar bone resorption), people with aggressive periodontitis are significantly younger than individuals with chronic periodontitis.
It is pointless for clinicians to argue about what is the best cut-off age to distinguish between aggressive and chronic periodontitis as the treatment of a 30-year-old patient with severe periodontitis will probably be the same regardless of what the disease is called. However, for research purposes and depending on the research question, it may well be reasonable to include age limits in case definitions to reduce heterogeneity within study groups and to ensure that there is no overlap in disease categories.
Rates of progression
The rate at which loss of supporting periodontal tissues occurs has long been considered an important characteristic by which chronic and aggressive forms of periodontitis can be clinically distinguished. Chronic periodontitis has traditionally been viewed as a slowly progressing disease, whereas aggressive forms of periodontitis progress at a rapid rate. The most compelling argument indicating that aggressive periodontitis progresses at a rapid rate comes from case series and epidemiological reports showing extensive periodontal damage at some sites in adolescents and young adults. ,
Rates of progression of various forms of periodontitis are difficult to study since there are many factors that influence how rapidly periodontal tissues are destroyed like the effectiveness of oral hygiene habits, access to dental care, genetic susceptibility to periodontal infections, systemic diseases (e.g., diabetes mellitus), and other powerful host-response modifiers (e.g., smoking).
Patterns of destruction
In cases of chronic periodontitis, there is no consistent pattern to the number and types of teeth involved. The disease can be localized to a few teeth or can affect the entire dentition. In cases of generalized aggressive periodontitis, most permanent teeth are usually affected. There are no evidence-based criteria to determine when a localized periodontal infection becomes generalized.
The consensus at the 1999 Classification Workshop suggested the extent of the disease be considered localized if < 30% of the sites (or teeth) are affected and generalized if > 30% of the sites (or teeth) are involved to facilitate communication among colleagues as to the general location of the problem. The fallacy of rigidly using the 30% cut-off point between localized and generalized patterns of disease can be nicely demonstrated in a classic case of localized aggressive periodontitis in which 12 teeth are affected (i.e., all incisors and first molars). If such a patient has only 28 teeth, then 12 ⁄ 28 or 42.9% teeth have the disease. Therefore, if the 30% figure is rigidly applied, some individuals with localized aggressive periodontitis paradoxically have generalized disease!
Clinical signs of inflammation
One of the features of localized aggressive periodontitis is the relatively low level of gingival inflammation (e.g., redness, swelling) compared with other forms of periodontitis.  In contrast, patients with generalized aggressive or chronic forms of periodontitis usually present with relatively intense gingival inflammation.
Plaque and calculus formation
In many patients with localized aggressive periodontitis, there are only thin deposits of dental plaque (i.e., biofilm) with little or no calculus. ,, However, sites affected by the disease are not biofilm- free. In contrast, teeth with chronic periodontitis usually have very complex and thick deposits of polymicrobial communities on affected root surfaces and this may hold true for generalized aggressive periodontitis cases as well.
Histopathological Features of Chronic and Aggressive Periodontitis
Chronic periodontitis and gingivitis are initiated by plaque , and has been classically described as progressing through a series of stages, i.e., the initial, early, established, and advanced lesions with predominant plasma cells.  There are no studies examining the initiation of aggressive periodontitis. The histopathology of aggressive periodontitis is not as well characterized as that of chronic periodontitis, particularly with regard to development of the lesion.
Chronic periodontitis is characterized by cycles of progression and stability. Currently, however, there is little evidence that aggressive periodontitis follows the typical cyclical course of chronic periodontitis (from gingival T-cell lesion to progressive B-cell lesion). Additionally, aggressive periodontitis appears to differ from chronic periodontitis in that clinically the gingival lesion is often absent , suggesting that the lesion may not follow the same sequence of chronic periodontitis.
Although the stages in development of the aggressive periodontitis lesion are unknown, the fully developed lesion is characterized by a plasma cell-dominated inflammatory infiltrate in the connective tissue with neutrophils migrating through the pocket-lining epithelium and forming a layer between the tissues and the plaque biofilm. Although this profile is identical to the histopathology of chronic periodontitis, it does not necessarily mean that they are not different diseases. This profile may just represent the response of the periodontium to varying plaque biofilms in susceptible individuals with the subsequent loss of tooth support being a consequence of this inflammatory process.
Immunopathology of Chronic and Aggressive Periodontitis
The immune response in periodontal disease is governed by the net effect of T-helper 1 (Th1) and T helper 2 (Th2) cytokines. In chronic periodontitis, the early ⁄ stable lesion is characterized by a Th1 response and the advanced ⁄ progressive lesion is associated with a Th2 response (B cell/plasma cell nature). Because of the B-cell ⁄ plasma-cell nature of the aggressive periodontitis lesion, it is likely that aggressive periodontitis is also a Th2-mediated lesion.
Even though it is now generally agreed that chronic periodontitis is a Th2 response,  the role of Th1 ⁄ Th2 responses in both chronic periodontitis and aggressive periodontitis, however, remains unresolved. At present, it is not possible to identify real differences in the immunopathology of the two diseases. This may be because there are no differences or because the differences only reflect variations in the degree of severity or susceptibility rather than actual different immunopathologies.
A third helper T-cell subset, defined as Th17, has been recently identified  and these cells appear to add a further dimension to the Th1 ⁄ Th2 paradigm of immune regulation in periodontal disease. Th17 cells express genes associated with chronic inflammation that may lead to the production of metalloproteinases with resultant osteoclast formation and bone destruction. In this context, the role of Th17 cells in tissue destruction and their role in Th1 ⁄ Th2 responses have to be checked in all forms of periodontitis.
Microbiological Features of Chronic and Aggressive Periodontitis
The one pathogen⁄one disease model does not apply in cases of periodontal infections as they are caused by an extremely diverse consortium of microorganisms that are part of the endogenous microbiota of most people.  Many individuals harbor potential periodontal pathogens as part of the commensal or normal oral microbiota for long periods of time without developing periodontal disease. 
In the past decade, there has been an explosion in our understanding of periodontal microbiology and the list of putative periodontal pathogens has grown considerably. Both conditions appear to be associated with certain cultivable pathogens listed by the 1996 World Workshop in Periodontics,  including P. gingivalis, T. forsythia, C. rectus, Eubacterium sp., P. micra, and Treponema sp. A major impediment to understanding the nature of periodontal infections is that the pathogens do not act alone in the biofilm. Instead, their biochemical and physiological properties are modified by their interactions with other members of the biofilm community.  In this sense, all periodontal infections have a diverse polymicrobial etiology.
The microbiological picture of chronic and aggressive periodontitis is further complicated by the fact that only about 50-60% of the subgingival microbiota can be grown in the laboratory using culturing techniques. The remainder of the microbiota is in "not-yet-cultivated" category.  Comparisons of the microbiology of chronic and generalized aggressive forms of periodontitis are in the early phases.
Application of culture independent microbiological methods is beginning to reveal a longer and more diverse list of pathogens than was possible even a few years ago. It is now clear that chronic and generalized aggressive periodontitis are not simply gram-negative anaerobic infections, but that gram-positive bacteria and even non-bacterial microbes from the Archaea domain may have an etiological role. Preliminary studies have suggested that individuals with generalized aggressive periodontitis have higher subgingival levels of Selenomonas sp.  and T. lecithinolyticum compared to patients with chronic periodontitis.
Also, research during the past 15 years has implied that herpes viruses are involved in the etiopathogeny of destructive periodontal disease. Co-infection with Epstein-Barr virus and cytomegalovirus shows a particularly close link with progressive periodontitis. The current paradigm of the pathogenesis of periodontitis needs to be revisited based upon the concept of a herpesviral- bacterial co-infection. Viral studies may lead to clarification of the clinical and biological features of periodontitis and to new strategies for managing the disease.
Based on the available preliminary data, generalized aggressive periodontitis and chronic periodontitis appear to be different from a microbiological perspective. However, more microbiological data generated by combined culture and culture-independent methods are required from patients with unambiguously defined cases of generalized aggressive periodontitis or chronic periodontitis.
Neutrophil Functions in Aggressive and Chronic Periodontitis
The earliest pioneering work on neutrophil functions and periodontal diseases in general and aggressive periodontitis in particular ,, indicated impairment of neutrophil functions responsible for host protection. The prevailing view was that impaired neutrophil functions as well as impaired functions of other cells of the host response were a central mechanism in the progression of chronic and aggressive forms of periodontitis.
Several complex issues emerged when comparing the roles of neutrophil functions in aggressive periodontitis, chronic periodontitis, and periodontal health. There is clear evidence that patients who have low counts of circulating neutrophils due to rare conditions such as cyclic neutropenia present with a pattern and progression of loss of periodontal attachment that is similar to that of aggressive forms of periodontitis.  However, low neutrophil counts have not been demonstrated in either chronic or aggressive forms of periodontitis. , Some authors have reported elevated neutrophil counts in patients with generalized aggressive periodontitis.  Others found that the numbers and proportions of neutrophils in serum are similar in aggressive and chronic forms of periodontitis.  Thus, the relevance of neutrophil counts in aggressive periodontal diseases remains unresolved.
In a study that compared neutrophil chemotaxis in chronic and aggressive periodontitis patients, the patients in the chronic periodontitis group exhibited either a normal or elevated chemotaxis response  and impaired chemotaxis in aggressive periodontitis. The consensus is that the chemotaxis defect may involve faulty surface receptors for chemotactic stimulants. In addition to impaired chemotaxis, some early studies demonstrated impaired phagocytosis and killing in patients with localized or generalized aggressive periodontitis compared to individuals with chronic periodontits.
Most of the earlier studies on aggressive periodontitis neither could not fully explain the possible role of neutrophils in aggressive periodontitis nor could they fully account for the rapid tissue destruction in aggressive compared to chronic forms of periodontitis. These observations led investigators to examine other possible alterations of neutrophil function that may lead to the more rapid breakdown of the periodontal support in aggressive forms of periodontitis compared to chronic forms.
In recent decades, a new concept of a hyperactive ⁄ "primed" neutrophil that leads to increased tissue destruction in aggressive forms of periodontitis  has emerged which could involve increased neutrophil adhesion, enzyme release, and perhaps most importantly, an elevated oxidative burst.
Evidence for increased neutrophil enzyme release is supported by studies showing greater beta-glucuronidase and myeloperoxidase activity in periodontitis patients than periodontally healthy controls. ,, Perhaps the most characteristic event in neutrophil priming or hyperactivity is an increase in the synthesis and release of oxidative burst products, such as superoxide, hydroxyl radicals, and hydrogen peroxide, from both resting and stimulated cells. As in other neutrophil function studies in aggressive and ⁄ or chronic periodontitis, there is no clear consensus as to whether the oxidative burst is increased, decreased, or unchanged neutrophils of periodontitis patients than in individual patients.
Whether be it defective neutrophil functions or primed neutrophils with elevated functions that are the predominant contributor to progression of aggressive and chronic forms of periodontitis, we must take into consideration that the neutrophil per se is just one component of the immune system in the periodontal tissues. Nevertheless, despite these complexities in determining the inflammatory and immune pathways in these diseases, an understanding of neutrophil function can aid in the development of new diagnostic and treatment approaches.
Response of Chronic and Aggressive Periodontitis to Treatment
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. 
The clinical response and the microbiological response to nonsurgical therapy in the treatment of chronic periodontitis have been well documented. The response to periodontal treatment in aggressive periodontitis is much less well understood. The bottom line is that the patient with generalized aggressive periodontitis requires careful monitoring and close collaboration is necessary between all the members of a treatment team.
While the use of antibiotics in periodontal treatment will probably always be controversial, reports from both the American Academy of Periodontology  and the European Federation of Periodontology  suggests that patients with aggressive periodontitis appear to benefit from the adjunctive use of systemic antibiotics during treatment; however, both also emphasized that knowledge of the optimal drug, dosage and duration providing the greatest effect was unknown at this time.
Beyond isolated case reports, very little has been published about the surgical treatment of generalized aggressive periodontitis. There could be several logical reasons for this: Severe attachment loss on presentation; possible links with covert or undetected systemic disease; the inability to control risk factors; and a history of poor surgical outcomes with previous patients with generalized aggressive periodontitis.
Although little has been written about prognostic factors in aggressive disease,  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. These tooth-level factors could be 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.
In general, it is likely that risk factors have similar long-term influences on both chronic periodontitis and aggressive periodontitis and they may dictate a poorer long-term prognosis in aggressive disease. Regardless, modulating and correcting these risk factors are critical in the treatment of both chronic periodontitis and aggressive periodontitis. If risk factors, especially smoking, can be eliminated and if compliance with maintenance care is high, then therapy can be as beneficial to the patient with generalized aggressive periodontitis as it is to any other patient. The relatively high rate of sites breaking down over time in aggressive periodontitis patients suggests a likely need for retreatment during the maintenance phase.
Overall, while most clinicians would agree that aggressive forms of periodontitis exist as clinical entities, the clinical distinction between chronic and aggressive periodontitis (especially generalized) is not clear cut. However, from a research perspective, it is essential that these diseases be clearly distinguished in order to gain a complete understanding of their etiology and pathogenesis. The relative lack of clinical inflammation and the localized molar-and-incisor form is typical for localized aggressive periodontitis. In contrast, the presence of clinical inflammation in generalized aggressive periodontitis appears to be similar to that observed in chronic periodontitis, and in this situation, age of onset and family history are important additional criteria for either diagnosis or classification. Moreover, chronic periodontitis could subsequently be superimposed on both localized and generalized forms of aggressive periodontitis. This may have little bearing on the treatment of such cases, but it could have an enormous impact on both the design and interpretation of research studies, whether basic science or clinical.
|1||Armitage GC. Classifying periodontal diseases-a long-standing dilemma. Periodontol 2000 2002;30:9-23.|
|2||Armitage GC. Comparison of the microbiological features of chronic and aggressive periodontitis. Periodontol 2000;53:70-88.|
|3||Schenkein HA. Host responses in maintaining periodontal health and determining periodontal disease. Periodontol 2000 2006;40:77-93.|
|4||Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6.|
|5||Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971;42:516-20.|
|6||Burmeister JA, Best AM, Palcanis KG, Caine FA, Ranney RR. Localized juvenile periodontitis and generalized severe periodontitis: Clinical findings. J Clin Periodontol 1984;11:181-92.|
|7||Listgarten MA. Structure of the microbial flora associated with periodontal health and disease in man. A light and electron microscopic study. J Periodontol 1976;47:1-18.|
|8||Liljenberg B, Lindhe J. Juvenile periodontitis. Some microbiological, histopathological and clinical characteristics. J Clin Periodontol 1980;7:48-61.|
|9||Loe H, Theilade E, Jensen SB. Experimental Gingivitis in Man. J Periodontol 1965;36:177-87.|
|10||Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest 1976;34:235-49.|
|11||Ruben MP. Periodontosis. An analysis and clarification of its status as a disease entity. J Periodontol 1979;50:311-5.|
|12||Page RC, Baab DA. A new look at the etiology and pathogenesis of early-onset periodontitis. Cementopathia revisited. J Periodontol 1985;56:748-51.|
|13||Kramer JM, Gaffen SL. Interleukin-17: A new paradigm in inflammation, autoimmunity, and therapy. J Periodontol 2007;78:1083-93.|
|14||Paster BJ, Olsen I, Aas JA, Dewhirst FE. The breadth of bacterial diversity in the human periodontal pocket and other oral sites. Periodontol 2000 2006;42:80-7.|
|15||Slack E, Hapfelmeier S, Stecher B, Velykoredko Y, Stoel M, Lawson MA, et al. Innate and adaptive immunity cooperate flexibly to maintain host-microbiota mutualism. Science 2009;325:617-20.|
|16||Consensus report. Periodontal diseases: pathogenesis and microbial factors. Ann Periodontol 1996;1:926-32.|
|17||Socransky SS, Haffajee AD. Periodontal microbial ecology. Periodontol 2000 2005;38:135-87.|
|18||Paster BJ, Dewhirst FE. Molecular microbial diagnosis. Periodontol 2000 2009;51:38-44.|
|19||Faveri M, Mayer MP, Feres M, de Figueiredo LC, Dewhirst FE, Paster BJ. Microbiological diversity of generalized aggressive periodontitis by 16S rRNA clonal analysis. Oral Microbiol Immunol 2008;23:112-8.|
|20||Riep B, Edesi-Neuss L, Claessen F, Skarabis H, Ehmke B, Flemmig TF, et al. Are putative periodontal pathogens reliable diagnostic markers? J Clin Microbiol 2009;47:1705-11.|
|21||Cainciola LJ, Genco RJ, Patters MR, McKenna J, van Oss CJ. Defective polymorphonuclear leukocyte function in a human periodontal disease. Nature 1977;265:445-7.|
|22||Page RC, Sims TJ, Geissler F, Altman LC, Baab DA. Abnormal leukocyte motility in patients with early-onset periodontitis. J Periodontal Res 1984;19:591-4.|
|23||Van Dyke TE, Horoszewicz HU, Cianciola LJ, Genco RJ. Neutrophil chemotaxis dysfunction in human periodontitis. Infect Immun 1980;27:124-32.|
|24||Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996;67:1041-9.|
|25||Buchmann R, Hasilik A, Van Dyke TE, Lange DE. Amplified crevicular leukocyte activity in aggressive periodontal disease. J Dent Res 2002;81:716-21.|
|26||Hidalgo MM, Avila-Campos MJ, Trevisan W Jr, Mocelin TT, Itano EN. Neutrophil chemotaxis and serum factor modulation in Brazilian periodontitis patients. Arch Med Res 1997;28:531-5.|
|27||Kantarci A, Van Dyke TE. Lipoxin signaling in neutrophils and their role in periodontal disease. Prostaglandins Leukot Essent Fatty Acids 2005;73:289-99.|
|28||Pippin DJ, Swafford JR, McCunniff MD. Morphology of azurophil lysosomes in polymorphonuclear leukocytes from humans with rapidly progressive periodontitis. J Periodontal Res 2000;35:26-32.|
|29||Kaner D, Bernimoulin JP, Kleber BM, Heizmann WR, Friedmann A. Gingival crevicular fluid levels of calprotectin and myeloperoxidase during therapy for generalized aggressive periodontitis. J Periodontal Res 2006;41:132-9.|
|30||Albandar JM, Kingman A, Lamster IB. Crevicular fluid level of beta-glucuronidase in relation to clinical periodontal parameters and putative periodontal pathogens in early-onset periodontitis. J Clin Periodontol 1998;25:630-9.|
|31||Xajigeorgiou C, Sakellari D, Slini T, Baka A, Konstantinidis A. Clinical and microbiological effects of different antimicrobials on generalized aggressive periodontitis. J Clin Periodontol 2006;33:254-64.|
|32||Walker C, Karpinia K. Rationale for use of antibiotics in periodontics. J Periodontol 2002;73:1188-96.|
|33||Herrera D, Alonso B, Leon R, Roldan S, Sanz M. Antimicrobial therapy in periodontitis: the use of systemic antimicrobials against the subgingival biofilm. J Clin Periodontol 2008;35:45-66.|
|34||Hughes FJ, Syed M, Koshy B, Marinho V, Bostanci N, McKay IJ, et al. Prognostic factors in the treatment of generalized aggressive periodontitis: I. Clinical features and initial outcome. J Clin Periodontol 2006;33:663-70.|