Chronic and aggressive periodontitis

Sometimes, the diagnosis of periodontal diseases is indeed difficult to make. This is because of the reason that many features of different forms of periodontitis overlap and confuse clinicians to reach a particular diagnosis. This problem is specifically encountered while differentiating generalized chronic and generalized aggressive forms of periodontitis. Although, recent research has clarified most of the aspects of chronic and aggressive forms of periodontitis, but many questions still remain unanswered. In the following discussion, our current understanding of chronic periodontitis and aggressive periodontitis has been highlighted.

What are chronic and aggressive periodontitis?

Chronic periodontitis is an inflammatory process that affects the protective and supportive tissues around the teeth. The primary etiology of this disease is the bacterial plaque on the tooth surface that leads to marginal tissue inflammation, known as gingivitis. Gingivitis is a reversible condition, but if left untreated, it may progress to periodontitis, which is characterized by loss of periodontal attachment support (clinical attachment loss [CAL] / loss of attachment) and bone resorption, eventually resulting in tooth mobility and loss. The characteristic feature of chronic periodontitis is its slow progression rate. Although it may occur in any age group, but most commonly affected are adults and elderly people.

Aggressive Periodontitis is a group of periodontal diseases characterized by localized or generalized loss of alveolar bone usually affecting the individuals under 30 years of age 1. It appears to be etiologically a complex disease. Following characteristics have been proposed to be associated with aggressive periodontitis 2.

Consistent characteristics:

  • Rapid attachment loss and bone destruction.
  • Except for the presence of periodontitis, patients are otherwise clinically healthy.
  • Familial aggregation.

Non-consistent characteristics:

  • Amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction.
  • Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1β,
  • Phagocyte abnormalities.
  • Elevated proportion of Aggeregatibactor actinomycetemcomitans and in some populations Porphyromonas gingivalis may be elevated.
  • Progression of attachment loss and bone loss may be self-arresting.

Both chronic and aggressive periodontitis are further divided into localized or generalized forms:

Localized Chronic/Aggressive periodontitis: Periodontitis is considered as localized, when ≤30% of the sites assessed in the mouth demonstrate attachment loss and bone loss.

Generalized Chronic/Aggressive periodontitis: Periodontitis is considered as generalized, when >30% of the sites assessed in the mouth demonstrate attachment loss and bone loss.

Present data strongly suggest that periodontal diseases are multifactorial diseases where smoking, stress, and genetic factors play a very important role 3-6. It is important to understand host and bacterial interactions before we go into the details of chronic periodontitis. Once the bacteria or their products get an entry into the host tissue, a protective inflammatory response is generated to counter and stop the invasion of these organisms. This inflammatory response is mediated by various chemical mediators, which along with their participation in host-microbial interactions are also responsible for initiation of events that cause host tissue destruction. The immune response in chronic and aggressive forms of periodontitis has been discussed later in this chapter.

Epidemiology of chronic and aggressive periodontitis

Epidemiology and risk factors for chronic periodontitis 7-9 and aggressive periodontitis have been extensively investigated 10, 11. One study estimated that the prevalence of chronic periodontitis in the age group 11-25 years is in the range of 1-3% in West Europe, 2-5% in North America, 4-8% in South America, 5-8% in Asia and 10-20% in Africa 11. Other investigations have demonstrated that race-ethnicity 12-15, gender 13, 16, 17 and socioeconomic status 16, 18 are important risk indicators of chronic periodontitis in adolescents and young individuals.

One study analyzed the data from the Third National Health and Nutrition Examination Survey (NHANES III) conducted on the USA population consisting of 9689 subjects. They concluded that pockets > 5mm were found in 7.6% of non-Hispanic white subjects, 18.4% of non-Hispanic black subjects and 14.4% in Mexican Americans; a total of 8.9% of all subjects had pockets > 5mm. Attachment loss > 5 mm was found in 19.9% of non-Hispanic white subjects, 27.9% of non-Hispanic black subjects and 28.3% of Mexican Americans; a total of 19.9% of all subjects had an attachment loss > 5 mm. The results of this study demonstrated that the severity of the periodontal disease is not uniformly distributed among race, ethnicity or the socioeconomic status 19.

One recent study was done on Brazilian population, where sample consisted of 612 individuals (291 males/321 females) aged 14-29 years. Full-mouth, six sites per tooth clinical examinations was performed. Chronic periodontitis was defined as CAL ≥3mm, affecting two or more teeth. Aggressive periodontitis cases were excluded from the analysis. Results showed that CAL ≥3 and ≥5mm affected 50.4% and 17.4% of subjects and 9.7% and 1.1% of teeth, respectively. Prevalence of chronic periodontitis ranged between 18.2% and 72.0% among subjects 14-19 years and 24-29 years of age, respectively 20.

Importance of case history

The first and foremost step in the diagnosis of chronic and aggressive periodontitis is a detailed case history of the patient. The duration of the disease can be established from the time the patient first observed periodontal problem such as swollen gums/bleeding from gums/ bad breath/ dull gnawing pain deep in jaw bones/ mobility of teeth/ tooth migration etc. A comparision of clinical features of chronic and aggressive periodontitis has been given in Table 24.1

Table 24.1 

Differences between chronic and aggressive periodontitis on the basis of case history and clinical features

Case history & Clinical feature

Chronic periodontitis

Aggressive periodontics

Age of onset or detection  Relatively older and elderly individuals Relatively young individuals
rates of progression Slow Rapid
Signs of inflammation  Consistent with presence of local factors Minimal
Relative amounts of plaque and calculus Consistent with periodontal destruction Not consistent with periodontal destruction
Patterns of destruction Usually uniform with horizontal bone loss. Usually variable with vertical bone loss


In general, generalized aggressive periodontitis is characterized by the widespread destruction of periodontal tissues in a young patient with the rapid rate of disease progression i.e. history of a couple of years. Whereas, generalized chronic periodontitis is characterized by the widespread periodontal damage, but usually in an older individual with a slower rate of disease progression i.e. history of many years.

In the case of generalized aggressive periodontitis most commonly reported complaints are recently noticed flaring and progressing spacing of anterior teeth and bleeding from the gums. Other complaints may include halitosis and pus discharge from the gums. The mobility of the affected teeth will be seen towards the later stages of the infection. The patient is otherwise systemically healthy. The patient may also complain of a dull nagging type of pain in the gums. Rarely, severe pain is experienced by the patients in situations where a periodontal abscess develops or a periodontal-endodontic infection occurs via accessory canals or tooth apex.

Clinical examination

Chronic periodontitis cases present with clinical features like supra-gingival and sub-gingival plaque accumulation which is consistent with the periodontal destruction. Plaque accumulation is usually associated with calculus formation. It is prevalent in adults but may occur in children. Gingival inflammation is usually evident with pocket formation, loss of periodontal attachment and alveolar bone loss (Figure 24.1). Bleeding on probing can be seen from periodontal pockets. In chronic periodontitis cases, gingiva may show a fibrotic appearance which is due to long standing low-grade inflammation. This finding shows that there is sufficient time for repair following active periodontal destruction. Clinical attachment loss (CAL) is evident in the form of periodontal pockets or recession or both. In the case of multi-rooted teeth, furcation is involved. In long standing cases, tooth mobility or tooth loss may be evident (Figure 24.2). The disease can be classified as mild, moderate or severe at a particular site as mild (CAL = 1–2 mm), moderate (CAL = 3–4 mm), and severe (CAL ≥5 mm).

Generalized Chronic Periodontitis

Figure 24.1 The clinical photograph of a generalized chronic periodontitis case. This is a photograph of a 65 years old male patient. The chief complaint of the patient was receding gums. Clinical examination demonstrated generalized recession and generalized periodontal pockets of an average depth of 4-5 mm. The patient gives a history of swollen and bleeding gums for 7-10 years. The patient also reported an increased mobility in some of his teeth during the recent past. Radiographic examination demonstrated generalized bone loss with on an average 50% of bone remaining around most of the teeth. On the basis of these findings, the patient was diagnosed as chronic generalized periodontitis case.


Chronic periodontitis case

Figure 24.2 The clinical and radiographic images of a 62 years old female patient demonstrating gingival recession and moderately deep periodontal pockets. The patients had a chief complaint of food impaction and dull gnowing pain. On examination, deep pockets were observed with maxillary and mandibular posterior teeth. Tooth mobility was present with maxillary anterior teeth. The patient gave a history of 25 years when she fisrt visited the dentist for gum problem. On the basis of history of the disease, clinical examination and radiographic examination the
patient was diagnosed with chronic generalized periodontitis.

Aggressive periodontitis cases present with minimal supra- and sub-gingival plaque accumulation. Periodontal destruction is not consistent with the amount of local factors present (Figure 24.3). The patient is otherwise systemically healthy as systemic diseases may severely impair host defense leading to periodontal destruction. In cases of periodontal destruction due to systemic diseases, the diagnosis is usually made as a periodontal manifestation of systemic disease. The microbiological analysis shows elevated levels of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans). Other characteristic features include phagocyte abnormalities and hyper-responsive macrophage phenotype, including the elevated production of prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) in response to bacterial endotoxins. Active diseases, as well as periods of inactive disease, are evident during the course of the disease. As described previously, aggressive periodontitis may be localized or generalized.

Localized aggressive periodontitis (LAP):

  • Usually has a circumpubertal onset.
  • Periodontal destruction localized to permanent first molar/incisor with interproximal attachment loss on at least two permanent teeth, one of which is a first molar and involving no more than two teeth other than first molars and incisors.
  • Robust serum antibody response to infecting agents is frequently detected.

Generalized aggressive periodontitis (GAP):

  • Usually affecting people under 30 years of age, but patients may be older.
  • Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors
  • Attachment loss occurs in pronounced episodic periods of destruction.
  • A poor serum antibody response to infecting agents is frequently detected.


Chronic generalized periodontitis case

Figure 24.3 Clinical photographs and radiograph of a 35 years old male patient who reported with the chief complaint of increasing mobility and migration of upper right central incisor . The patient was a smoker for last 17 years. The patient reported that he had gum problems since last 10-12 years. Clinical examination demonstrated moderate to deep pockets throughout the dentition. Radiographic examination demonstrated generalized horizontal bone loss. On the basis of history of the disease, clinical examination and radiographic examination, the case was diagnosed as chronic generalized periodontitis. 

The disease progresses in alternating periods of activity and quiescence 21. Periods of quiescence may remain for weeks to months or even years and are followed by periods of active disease. During the periods of quiescence, patients are free of symptoms and the gingiva appears pink and healthy even though probing reveals deep periodontal pockets. Lack of visible signs of clinical inflammation despite the presence of deep periodontal pockets and severe attachment loss in an otherwise healthy young individual is the classic sign of aggressive periodontitis presenting at this stage. Generalized aggressive periodontitis rarely undergoes spontaneous remission, whereas localized forms of the disease have been known to arrest spontaneously 2. This unexplained curtailment of disease progression has sometimes been referred to as a “burnout” of the disease.

During the periods of the active disease, there is alveolar bone loss and loss of attachment. The gingiva shows all the signs of mild to severe inflammation, which may include tender, fiery red, edematous, soft, and boggy gingiva (Figure 24.4). Bleeding on probing or even spontaneous bleeding and purulent exudation may be evident. Inflammatory gingival enlargement may also be noticed.

Juvenile Periodontitis

Pocket depth measurement


Figure 24.4  A localized aggressive periodontitis case demonstrating the minimal presence of local factors and gingival inflammation. Upon periodontal probing, a deep periodontal pocket was identified on the distal aspect of the lower right first molar. The radiographic examination demonstrated bone loss around the distal root of the molar. Deep periodontal pockets were also recorded around first molars in other three quadrants.

In advanced stages of the disease, there is severe periodontal destruction causing extrusion of teeth, mobility and pathologic migration, furcation involvement, generalized gingival recession, and the loss of several teeth due to spontaneous exfoliation (Figure 24.5).


aggressive periodontitis case

Figure 24.5 A generalized aggressive periodontitis case. The clinical photograph and radiograph of 18 years old female patient who reported with a chief complaint of tooth mobility and tooth migration with increasing gap between upper central incisors. The patient also reported swollen gums and irritation in gums. Clinical examination of the patient demonstrated generalized deep periodontal pockets, the mobility of maxillary 1st molars and incisors, furcation involvement with maxillary and mandibular 1st molars and pathologic tooth migration with respect to maxillary left central and lateral incisor . Radiographic examination demonstrated severe bone loss with an average of 30% bone remaining around most of the teeth. Loss of lamina dura and decreased bone density can be seen in the radiograph. Microbiological examination demonstrated high numbers of A. actinomycetemcomitans, P . gingivalis, and P . intermedia.


Generalized aggressive periodontitis

Figure 24.6 The clinical and radiographic images of a 46 years old male patient who reported for pain and swelling in the lower left back region. On examination deep periodontal pockets were found in the molar region of the third quadrant as well as with all the other teeth in the remaining quadrants. The patient was a chronic smoker and smoked 10-15 cigarretes per day and gave a two and half years history of the gum problems. The radiographic examination, demonstrated a severe periodontal bone loss. On the basis of history of the disease, clinical examination and readiographic examination the patient was diagnosed with generalized aggressive periodontitis.

Radiographic features of chronic and aggressive periodontitis

Chronic periodontitis:

In chronic periodontitis the crest of interdental bone is usually 2 mm or more apical to the CEJ; this is very important to determine if there is bone loss.  The crest of alveolar bone is fuzzy in appearance. Lamina dura will be ill-defined and density of interdental bone is decreased. Furcation areas of molar teeth may be involved, presenting radiolucency in these areas. Patterns of bone loss may be horizontal or vertical. Bone loss is called as vertical when attachment and bone loss on one tooth surface is greater than that on the adjacent surface and is usually associated with the intrabony pocket formation. In the horizontal bone loss, bone loss occurs at a uniform rate on the majority of tooth surfaces and is associated with suprabony pockets.

Aggressive periodontitis:

In the case of generalized aggressive periodontitis, radiographs may show generalized bone destruction ranging from mild crestal bone resorption to severe, extensive alveolar bone destruction, depending upon the severity of the disease. The defects may be a combination of vertical and horizontal defects. Localized aggressive periodontitis cases show “arc-shaped” mirror image radiolucency in the first molars starting from the distal aspect of second premolars to the mesial aspect of the second molar.

Microbiology of chronic and aggressive periodontitis

Periodontal diseases are primarily caused by periodontopathogenic bacteria for which they have been extensively studied 22-31. There are some fundamental problems in studying the microbiology of periodontal diseases. One major problem is the complexity of the microbiota of dental plaque of which only about 50–60% of the subgingival microbiota can be grown in the laboratory using standard culturing techniques. The remaining organisms are categorized as non-cultivable 32, 33. Secondly, it has been demonstrated by many studies that periodontally healthy individuals harbor some periodontal pathogens as a part of their normal supragingival and subgingival microbiota 34-41. These bacteria are present in relatively low number in healthy periodontal sites and they may be present in these sites for a long duration of time without causing disease. On the other hand, it has been suggested that the presence of these organisms is necessary for the development of immunity by the host 42.

Another problem is the development of plaque as a biofilm. When bacteria grow in a biofilm, their characteristics change as compared to their planktonic counterparts. Different colonies in a biofilm communicate by quorum sensing which is important for the maintenance of internal environments in a biofilm. Horizontal gene transfer takes place in a biofilm between different organisms to sustain the virulence factor (details available in â€œDental plaque”).

It is difficult to categorize any particular micro-organism as the causative agent for chronic or aggressive periodontitis. However, attempts have been made to identify if there is any relationship between specific microorganisms with chronic or aggressive periodontitis. Various investigations done on identifying periodontal pathogens in chronic and aggressive periodontitis have been analyzed in a systematic review by Mombelli et al. (2002) 43 in which the authors concluded with no confirmation of any particular organism specifically associated with chronic or aggressive periodontitis. Here, it is important to remember that we are presently following the infection and host response paradigm. Our present knowledge strongly suggests that host response is equally important for periodontal disease progression. Studies have shown that some of the bacterial species are strongly associated with advanced periodontal lesions. These include A. actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis and Treponema denticola 44. Many other studies have identified A. actinomycetemcomitans along with immunological defects as the main causative agent of localized aggressive periodontitis 45, 46.

Although both chronic and aggressive periodontitis are multi-bacterial infections and many bacteria are common in both the conditions, some authors have tried to categorize bacteria which are more prevalent in periodontal health, gingivitis, chronic periodontitis and aggressive periodontitis 47-50 (Table 24.2).

Table 24.2 Microbiology of various periodontal conditions

Periodontal HealthGingivitisChronic periodontitisAggressive periodontitis
Gram positive organismsGram-positive organismsGram-positive organismsActinobacillus actinomycetemcomitans
Porphyromonas gingivalis
Streptococcus oralis
Streptococcus sanguis
Streptococcus mitis
Actinomyces gerencseriae
Actmomyces naeslundi
Lactobacillus species
Actinomyces naeslundi
Peprostreptococcus micros
Streptococcus onginosus
Eubacterium brachy
Eubacterium nodatum
Mogibacterium timidium
Parvimonas micra
Peptostreptococcus stomatis
Parvimonas micra
Tannerella forsythia
Prevotella intermedia
Campylobacter rectus
Peptostreptococcus micros
Campylobacter concisus
Prevotella nigrescens
Gram-negative organismsGram-negative organismsGram-negative organismsEikenella corrodens
Selenomonas sputigena
Fusobacterium nucleatum
Fusobacterium species
Prevotella nigrescens
Veillonella species
Fusobacterium nucleatum
Prevotella intermedia
Winonalla parvula
Campylobacter species
Haemophilus species
Selenomonas species
Treponema species
Tannerella forsythia
Fusobacterium nucleatum
Porphyromonas gingivalis
Prevotella intermedia
Prevotella loescheii
Dialister pneumosintes
Campylobacter rectus
Treponema species

Immunology of chronic and aggressive periodontitis

Innate immunity:

In innate immunity, the role of neutrophils, Toll-like receptors and Defensins has been well studied.

Role of neutrophils in aggressive and chronic periodontitis:

Polymorphonuclear leukocyte (PMN) appears to play a key role in the maintenance of the periodontal health 51. Individuals with defective PMN function are subjected to increased periodontal breakdown (for more details read “Role of neutrophils in periodontal diseases”).

Neutrophil function in aggressive periodontitis:

There are two kinds of neutrophilic function defects that have been discussed in the literature. One is impaired neutrophil function and the other is primed ⁄ hyperactive neutrophil function. Both of these are opposite to each other. In the former, the neutrophil is unable to do its normal functions such as, chemotaxis and phagocytosis whereas, in the latter, the neutrophil is hyperactive in its function.

Impaired neutrophil function:

There is strong evidence that neutrophils from localized or generalized aggressive periodontitis demonstrate defective chemotaxis and phagocytosis. There are many reasons suggested for impaired chemotaxis including reduced numbers of receptors on the neutrophil cell membrane, defects in neutrophil membrane receptors such as f-Met-Leu-Phe membrane receptor or its co-receptors such as GP110 (glycoprotein 110) or CD38, which participate in the chemotactic response. Neutrophils may also have a combination of reduced number of receptors and defective receptors 52 A Study demonstrated a significantly decreased expression of CD38 in f-Met-Leu-Phe-stimulated neutrophils in localized aggressive periodontitis patients as compared to normal individuals 53.

Various studies have demonstrated defective phagocytosis by neutrophils derived from a patient having localized or generalized form of aggressive periodontitis. One study demonstrated that 53% of patients with localized aggressive periodontitis and 46% of patients with generalized aggressive periodontitis demonstrated neutrophils with the significantly lower percentage of phagocytosis per neutrophil as compared to neutrophils from chronic periodontitis patients 54. In an in vitro investigation, it was observed that neutrophils derived from affected sites in patients with generalized aggressive periodontitis demonstrated significantly lower bacterial phagocytosis when challenged with one strain of Porphyromonas gingivalis and two strains of A. actinomycetemcomitans as compared to neutrophils derived from healthy individuals 55.

Neutrophils are an important source of…………


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Hyperactive or primed neutrophil function:

As discussed above, various studies demonstrated defects in neutrophil chemotaxis and phagocytosis, which could be either inherent and⁄ or acquired, but these findings could not relate neutrophils to fully account for the rapid tissue destruction in aggressive periodontitis. Research in the last decade has emphasized on the presence of hyperactive⁄ primed neutrophil that could cause increased tissue destruction in aggressive forms of periodontitis 61. These hyperactive neutrophils demonstrate increased adhesion and most importantly elevated oxidative burst. It has been demonstrated that neutrophils from patients with aggressive periodontitis have increased intracellular levels of β-glucuronidase, which is present in azurophilic granules of the neutrophils 62. Increased β-glucuronidase levels in GCF have been associated with increased periodontal destruction 63. Another important enzyme secreted by neutrophils, which actively participates in tissue breakdown is myeloperoxidase. The level of this enzyme in GCF sample of aggressive periodontitis patients have been found to be increased in areas with active periodontal destruction. A positive correlation between enzyme levels and presence of bleeding and suppuration has been found 64.

Matrix metalloproteinases (MMPs) participate in tissue remodeling by breaking down various components of the connective tissue. MMP-8 and MMP-9 are derived from neutrophils and have been investigated for their role in the tissue breakdown in aggressive periodontitis. Studies have demonstrated no significant difference in tissue or crevicular fluid levels of MMP-8 enzyme between chronic and aggressive periodontitis patients 65.

Neutrophil function in chronic periodontitis:

As already discussed, neutrophils have an important role in host-microbial interaction in periodontal diseases. Various aspects of neutrophil function have been investigated in chronic periodontitis. Neutrophil cytokine release has been studied in chronic periodontitis. As compared to healthy controls, increased plasma concentrations of IL-8 66, IL-6 67-70 and IL-1β 71, 72 have been demonstrated in patients with chronic periodontitis. Similarly, increased GCF concentrations of IL-8 73, IL-6 74, IL-1β 71, 75 and TNF-α 74, 76 have been reported in chronic periodontitis patients.

There are few studies done to investigate peripheral blood neutrophil cytokine release from patients with chronic periodontitis. Some of them have shown no difference in the release of cytokines (IL-8, IL-1β, and TNF-α) in chronic periodontitis patients as compared to healthy controls 77, 78 while one study demonstrated decreased IL-8 release from isolated neutrophils of patients with chronic periodontitis as compared to healthy controls 79. Another study demonstrated significantly more IL-1β release from neutrophils in patients with chronic periodontitis as compared to healthy controls 80.

A few investigations have been done to investigate neutrophil chemotaxis in chronic periodontitis patients. However, conflicting results have been reported. Two studies have reported significantly, increased chemokinesis of neutrophils towards E. coli supernatant, fMLP, and LPS-activated serum in chronic periodontitis patients 81, 82 whereas two other studies have reported no significant difference between neutrophil chemotaxis in chronic periodontitis patients and controls 83, 84. It has been hypothesized that periodontal disease pathogenesis may also be associated with dysregulated neutrophil extracellular trap release 85. However, more research is required to clarify the dysregulation of neutrophil extracellular trap release in chronic periodontitis patients.

Toll-like receptor (TLR) in aggressive and chronic periodontitis:

Toll-like receptor (TLR) family, which plays a fundamental role in pathogen recognition and activation of innate immunity. Members of this family are responsible for the recognition of pathogen-associated molecular patterns (PAMPs) expressed by a wide spectrum of infectious agents. To date, ten proteins have been identified that belong to the human TLR family 86, of which TLR2 and TLR4 have been extensively studied. TLR2 has been identified as a receptor that is central to the innate immune response to lipoproteins of Gram-negative bacteria, several Gram-positive bacteria, as well as a receptor for peptidoglycan and lipoteichoic acid and other bacterial cell membrane products. TLR4 physically associates with another molecule called MD-2, and together with CD14, this complex is responsible for LPS recognition and signaling. It has been shown that TLR2 and TLR4 are expressed in healthy oral epithelium but the expression of both is markedly upregulated during inflammation 87 TLR2 stimulation has been shown to be associated with porphyromonas gingivalis lipopolysaccharides and Gram-negative periodontal bacteria 88-90. A study done by Kikkert et al. (2007) 88 showed that only A. actinomycetemcomitans and Veillonella parvula were capable of stimulating both TLR2 and TLR4.

Various studies have investigated the expression of TLR2 and TLR4 in chronic and aggressive periodontitis.  A study showed increased expression of both TLR2 and TLR4 in chronic periodontitis cases as compared to healthy tissues, there was only a weak expression of TLR2 and no expression of TLR4 was detected 91. Various studies have demonstrated TLR2 and TLR4 mutations/polymorphisms and their positive association with chronic and aggressive periodontitis 92-95, whereas, many others have not found any relation 96-98. So, this is a matter of further research at the molecular level to explain the exact mechanism of this association, if any.

Role of defensins in aggressive and chronic periodontitis:

The epithelium along with acting as a physical barrier also contains substances that kill pathogens or inhibit their growth. Most abundant among them are the antimicrobial peptides, called defensins. Human defensins are divided into two subgroups……


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The levels of cathelicidin LL-37 were found to be reduced or absent and levels of neutrophil peptide 1-3 defensin were found to be reduced in gingival crevicular fluid (GCF) samples derived from aggressive periodontitis patients as compared to GCF samples derived from chronic periodontitis patients 102. In another investigation, it was found that in neutrophils derived from patients with generalized aggressive periodontitis, levels of human neutrophil peptide 3 defensin were significantly reduced 103 However, in this study, it was proposed that reduced levels of neutrophil peptide 3 defensin had only a minor role in the pathogenesis of aggressive periodontitis.

Acquired immunity

The adaptive immune response in periodontitis has been extensively studied. It has been shown that Th1 cells play an important role in an early or stable lesion of chronic periodontitis whereas, advanced lesion of chronic periodontitis is dominated by B-cells and plasma cells, which are activated byTh2 cytokines 104-107. Details about Th1 and Th2 cell response can be studied in â€œHost-microbial interactions in periodontal diseases”. The role of acquired immunity has been discussed in details in the same chapter.

The difference in the acquired immune response in chronic and aggressive periodontitis appears to be in the disease progression. Aggressive periodontitis may not follow the same sequence of initiation and progression as chronic periodontitis i.e. initial lesion dominated by T-cells to a progressive B-cell and plasma cell dominated lesion. This may be because of the reason that the clinical course of the disease in case of aggressive periodontitis is quite different from chronic periodontitis. The basic functions of cells, which are involved in acquired immune response, e.g. TH0, Th1, Th2, Treg, Th17 etc. are discussed in â€œHost-microbial interactions in periodontal diseases”.

Role of Genetics in Chronic and aggressive Periodontitis

Chronic periodontitis:

Although research work has shown that genetic factors may be associated with chronic periodontitis but no clear genetic determinants have been described 108. The twin model is probably the most powerful method to study genetic aspects of periodontal diseases. Initial studies recognized that the periodontal conditions of identical twins were often similar 109. In one of the largest twin study 4908, twin pairs were studied using a questionnaire data. 349 (116 Monozygotic and 233 Dizygotic) pairs reported a history of periodontal disease in one or both pair members. The concordance rates ranged from 0.23 to 0.38 for monozygotic twins and 0.08 to 0.16 for dizygotic twins 110.

In another study Michalowicz et al. (1991) 4 studied the periodontal condition (attachment loss, pocket depth, gingival index, and plaque index) of 110 adult twin pairs with a mean age of 40 years. The results of the study concluded that 38% to 82% of the population variance for these measures may be attributed to genetic factors. In a subsequent study, the authors conclude that after making other variables constant (smoking and utilization of dental care) the chronic (adult) periodontitis had approximately 50% heritability 3.  Also in a Dutch population, epidemiological studies have suggested that chronic (adult) periodontitis aggregates in families 111.

Various single nucleotide polymorphisms have been shown to be associated with the disease progression in chronic periodontitis cases. These include

  • Polymorphisms in the IL1 Gene Cluster,
  • Polymorphisms in the TNF-α Gene,
  • Polymorphisms in the IL4 and IL4RA Genes,
  • Polymorphisms in the IL6 and IL6R genes,
  • Polymorphisms in the IL10 gene,
  • Polymorphisms in the FcγR Gene,
  • Polymorphisms in the VDR Gene,
  • Polymorphisms in the Pattern Recognition Receptor Genes,
  • Polymorphisms in the CD14 Gene,
  • Polymorphisms in the TLR2 and TLR4 Genes,
  • Polymorphisms in Miscellaneous Genes

These polymorphisms have been described in detail in “Role of genetics in pathogenesis of periodontal diseases”.

Aggressive periodontitis:

Evidence for the genetic link of aggressive periodontitis has been clearly established.  The initial research work showed that the prevalence of aggressive periodontitis was disproportionately high among certain families 112-114. One study done by Marazita et al. (1994) 115 in young patients with severe periodontitis showed that their siblings often suffered from severe periodontitis. These findings were followed by a systematic genetic research work which included three genetic analysis methods that can be used to study modes of inheritance: pedigree analysis, segregation analysis, and linkage analysis.

Pedigree analysis studies the transmission of disease in families from one generation to the other. Both X-linked dominant and autosomal-recessive inheritance of aggressive periodontitis has been proposed. Many studies have shown an increased prevalence of aggressive periodontitis among female family members which supports the X-linked dominant inheritance 116-119. On the other hand, certain features like affected siblings of unaffected parents support autosomal-recessive inheritance of aggressive periodontitis 120, 121. Although different modes of inheritance have been proposed by different researchers, it is difficult to assess the mode of transmission in one family and the appearance of the disease in a particular individual 122.

Segregation analysis is based on Mendel’s laws 123. In this analysis, it is expected that the genes segregate from parents to their offspring’s in a predictable manner. For autosomal dominant inheritance the segregation ratios are 1:2 and for autosomal recessive inheritance these are 1:4. A segregation analysis study was done on families affected with aggressive periodontitis. The authors concluded that the mode of inheritance was most probably an X-linked dominant trait with a decreased penetrance of 78%, and the female:male ratio of affected persons was approximately 2:1 124.

Linkage analysis is based upon the fact that alleles present in close proximity on a chromosome tend to be passed together from one generation to the other generation. These genes which are “linked” violate Mendel’s law of independent assortment. Boughman et al. (1985) 125 first reported linkage between aggressive periodontitis and a specific chromosomal region (4q11-13) near the gene for dentinogenesis imperfecta. Another linkage reported was of localized aggressive periodontitis to a marker on chromosome 1(1q25) 126. The linkage analysis of genetic variations in IL-1 was also associated with aggressive periodontitis 127.

Other studies which have shown a genetic link of aggressive periodontitis include

  • The study of inherited disorders and genetic syndromes.
  • Twin studies.
  • Population studies.
  • Single nucleotide polymorphism.

 Role of risk factors in chronic periodontitis and aggressive periodontitis

Risk factors for chronic and aggressive periodontitis can be divided into two categories viz. modifiable and non-modifiable risk factors. Modifiable risk factors are those which can be eliminated or reduced such as smoking, which is a well-established modifiable risk factor. Whereas, factors like genetic factors, immunological abnormalities are designated as non-modifiable as they cannot be modified. Some common risk factors for both chronic and aggressive periodontitis include smoking and psychological stress. Following is a brief description of risk factors for chronic and aggressive periodontitis.

Risk factors for chronic periodontitis:

Prior history of periodontitis:

Prior history of periodontitis puts the patient at more risk of developing periodontitis. The periodontal bone loss is caused by the accumulation of microbial plaque. An improperly treated patient or patients with poor postoperative maintenance are the candidates, which can develop periodontitis after treatment. Here lies the importance of bone re-contouring during periodontal surgery. The architecture of the periodontal tissues should be modified in a manner that patient can easily maintain oral hygiene and there are minimal chances for re-pocket formation.


Usually, chronic periodontitis occurs in adults, although younger patients may be affected. The disease has a slow progression and patients usually present with a history of many years. So, it is expected that older patients are more commonly affected with chronic periodontitis.

Oral hygiene:

Poor oral hygiene is a risk factor for the development of periodontitis. Many randomized controlled trials have demonstrated the cause-effect relationship of plaque on gingivitis 128-130. Application of antimicrobial therapy and agents such as chlorhexidine also reduces the gingival inflammation, which indicates the imporance of maintaining good oral hygiene to reduce periodontal disease activity. Other investigations have shown that periodontal surgical procedures accompanied by regular professional tooth cleaning halt the progression of periodontal diseases 131-133.  All these findings suggest that bacterial plaque is the primary risk factor for the development of periodontal disease and maintenance of oral hygiene is required to return to periodontal health.


It is an important risk factor for periodontal disease progression as well as response to periodontal therapy.  Many investigations have shown that smokers have an increased prevalence and severity of periodontal disease, as well as a higher prevalence of tooth loss and edentulism 134-140. The reported odds ratios for developing periodontal disease as a result of smoking are 2.5 141, 3.97 for current smokers and 1.68 for former smokers 142 and 3.25 for light smokers to 7.28 for heavy smokers 135. It has also been shown that periodontal treatment is less likely to be successful in smokers than in non-smokers 143, 144.

How smoking affects the periodontal disease progression has been discussed in detail in â€œSmoking as a risk factor for periodontitis”.


Many clinical investigations have demonstrated a possible relationship between psychological stress and periodontitis and have suggested that stress may play a role in the development of periodontal disease 145-147. The hypothalamic-pituitary-adrenal (HPA) axis and the systemic adreno-medullary sympathetic nervous system plays an important role in periodontal disease progression. Details about this relationship have been discussed in “Stress as a risk factor for periodontal diseases”.


It has been a consistent finding that the severity of periodontal diseases is generally more in males than in females. It is confirmed by all the national health surveys conducted in the United States 148-150. The reason for this variation is that males usually exhibit poorer oral hygiene than females, whether measured as calculus or soft plaque deposits. Poor oral hygiene is the basis of this variation in the severity of periodontal diseases between the two genders. So, gender may not be considered as an absolute risk factor, but poor oral hygiene must be.

Genetic factors:

Genetics and its role in periodontal disease have been well investigated and present data strongly suggest that genetic factors play an important role in the progression of periodontal diseases. Various genetic factors have already been discussed in the previous sections. The complete detail of genetic factors is available in â€œRole of genetics in the pathogenesis of periodontal diseases”.

Role of systemic factors:

There is wide evidence in the support of the association of systemic diseases and periodontal diseases 151-157. Systemic diseases like diabetes not only influence the pathogenesis of the periodontal disease but also affect the course and the outcome of the disease. Healing and post-operative maintenance are also affected by systemic diseases. They play an important role in disease progression in both chronic and aggressive periodontitis. So, they act as an important risk factor for periodontal diseases.

Socioeconomic Status (SES):

Studies have clearly demonstrated more prevalence of destructive periodontal diseases among people with low SES 149, 150. It is believed that well-educated people with a good SES have better oral health status than the less educated and poorer segments of the society. The reason for this is the positive attitude toward oral hygiene and a greater frequency of dental visits among the more dentally aware and those with dental insurance. Gingivitis has been clearly associated with low SES.

Risk factors for aggressive periodontitis:

Pathogenesis of aggressive periodontitis is quite different from chronic periodontics. Some risk factors like smoking, stress and SES are same for chronic and aggressive periodontitis but major risk factors for aggressive periodontitis are as follows,

Microbiological risk factors:

Bacteriology of aggressive periodontitis indicates that certain bacterial species are prevalent in these cases. Commonly isolated organisms from aggressive periodontitis cases include Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Prevotella nigrescens, Eikenella corrodens, Selenomonas sputigena, Fusobacterium nucleatum, Campylobacter rectus. Although the presence of these organisms in the periodontal pocket does not confirm aggressive periodontitis but in their number above certain levels certainly predisposes the patient to the development of aggressive periodontitis.

Genetic and Immunological risk factors:

Many studies have demonstrated immunological abnormalities in aggressive periodontitis cases.

Abnormalities in neutrophil functions have been proposed for rapid tissue destruction in aggressive periodontitis. It has been suggested that overly active or “primed” neutrophils may be responsible for mediating much of the tissue destruction that is observed in localized aggressive periodontitis 158. Single nucleotide polymorphisms such as IL-1 gene polymorphisms have been linked to periodontal disease. Specific IL-1 genotypes have been linked to the presence of pathogenic microorganisms in rapidly progressive periodontitis cases 159. A population study demonstrated an odds ratio of 18.9 associated with a specific IL-1 genotype 160. A detailed description of cytokine polymorphism and its effect on host response has been discussed in â€œRole of genetics in the pathogenesis of periodontal diseases”.

Diagnosis of chronic and aggressive periodontitis

Chronic periodontitis:

The diagnosis of chronic periodontitis is made on the basis of dental history, medical history, radiographic examination and clinical examination. The chief complaint of the patients may not always be diagnostic of chronic periodontitis. However, relevant questions should be asked which can be useful in making a diagnosis. The past dental record of the patient is very useful in establishing a diagnosis. The dental treatment done in the past should be recorded. Past dental treatment can be helpful in establishing the nature of dental diseases the patient is suffering from. A dental treatment in the past for chief complaints of bleeding from the gums, swollen gums, oral malodor or deep gnawing pain in the gums is indicative of past periodontal problems.

The patient should be asked about any pre-existing conditions like diabetes, hypertension, smoking, use of medications and other conditions which may impact periodontal disease progression. If the patient is unable to provide adequate information, concerned health care provider should be consulted.

After the dental and medical history is over, routine dental and periodontal examination is done. A detailed description of history taking and clinical examination has been given in “The art of history taking in periodontics”. The patient should be thoroughly examined for all the positive dental and periodontal findings. Periodontal findings, which specifically relate to chronic or aggressive periodontitis include gingival examination (color, contour, consistency, surface texture, exudation or any other specific finding) and periodontal examination, which includes distribution and depth of periodontal pockets, tooth mobility, furcation involvement, recession, tooth migration or any other significant finding.

Radiographic examination is done to evaluate the amount of bone destruction that has already occurred. If the past dental record of the patient is available, the present radiographs should be compared with the past dental radiographs. It gives very useful information regarding the rate of disease progression. The patient is diagnosed for chronic periodontitis if the patient has a slow rate of disease progression and local factors are consistent with the amount of destruction that has taken place. Other findings, which are used to make a diagnosis of chronic periodontitis have already been discussed in previous sections.

Aggressive periodontitis:

As already discussed, consistent and non-consistent features of aggressive periodontitis have been well defined. The patient should be examined thoroughly for the presence of these features.  The most important finding in aggressive periodontitis is severe and rapid periodontal destruction in an otherwise healthy patient. The periodontal destruction is not consistent with the amount of local factors present. The radiographic examination demonstrates excessive bone loss with vertical or horizontal bone loss patterns.  The patient may demonstrate furcation involvement in posterior teeth. Varying degree of tooth mobility is usually present in advanced periodontal destruction.

Treatment of chronic and aggressive periodontitis

Chronic periodontitis:

The treatment planning of chronic periodontitis is done on the basis of severity and extent of periodontal involvement. The treatment of chronic periodontitis is initiated with non-surgical periodontal therapy. If required, the nonsurgical therapy phase is followed by surgical therapy. Once the desired results are achieved, the patient is scheduled for supportive periodontal therapy. The first step in the treatment of chronic periodontitis is patient education. The patient is informed about the relationship between deposits on teeth and periodontal destruction and is educated about adequate maintenance of oral hygiene and appropriate brushing technique is instructed for oral home care.  Once, the patient understands the significance of maintaining oral hygiene and is well motivated, treatment of chronic periodontitis is initiated with non-surgical therapy.

Non-surgical therapy:

The non-surgical therapy consists of SRP, aimed at the mechanical elimination of plaque, calculus, and other deposits. SRP are performed in multiple sittings to ensure that teeth are absolutely free from plaque and other deposits and patient is maintaining an adequate oral hygiene. A detailed description of SRP have been given in “Principles of scaling and root planing”. If the patient is not maintaining a good oral hygiene, he/she should be re-informed and motivated to do so. There is evidence that in the absence of periodic professional reinforcement, self-administered plaque control programs alone are inconsistent in providing long-term inhibition of plaque-induced gingival inflammation 161-163. All the local factors which facilitate plaque accumulation (such as overhanging restorations) should be corrected so that plaque control is facilitated. It has been demonstrated that desired results are achieved when professional plaque control measures are executed along with adequate personal plaque control 164, 165. The application of self-applied or professionally applied subgingival irrigation is recommended for reduction of bacterial load in the subgingival areas. It has been demonstrated that in patients who are not efficiently maintaining a good oral hygiene, supragingival irrigation with or without anti-bacterial agent significantly reduce gingival inflammation as compared to tooth brushing alone 166.

Once, the non-surgical phase is over, there should be a marked reduction in gingival inflammation and all the signs and symptoms of inflammation should significantly reduce. The patient is re-examined for periodontal findings and further treatment is planned according to the findings. There are various therapies which can be planned, if open flap debridement is not planned. These include,

Systemic antibiotic therapy:

Systemic antibiotics and their combinations have been used for many years in the treatment of periodontal diseases. Systemic antibiotic treatment with a combination of metronidazole and amoxicillin has been shown to be beneficial in the treatment of chronic and aggressive periodontitis 167-169. However, it must be remembered that systemic antibiotic therapy is not indicated in all cases of periodontitis. Systemic antibiotic therapy as an adjunct to mechanical debridement can be utilized in specific situations such as patients with multiple sites unresponsive to mechanical debridement, acute infections, medically compromised patients, the presence of tissue-invasive organisms and ongoing disease progression 170-173. Ideally, the systemic antibiotic therapy should be instituted following bacterial culturing and sensitivity test. A detailed description of antibacterial chemotherapeutic agents has been given in â€œChemotherapeutic agents used in periodontal therapy”.

Local drug delivery (LDD):

Local delivery of therapeutic agents have been used in the treatment of periodontitis. If the patient has few moderately deep localized pockets, LDD is the treatment of choice. This therapy includes placement of various chemotherapeutic agents in the periodontal pocket with or without a protective dressing. The carrier/vehicle releases the agent slowly so that the effective concentration of the agent is maintained in the periodontal pocket for a desired duration of time after which it is either degraded or is removed manually. It has been demonstrated that pathogenic flora is significantly altered and periodontal pocket depth improves after the use of these agents 174-182. However, the cost-benefit ratio of LDD agents should be critically evaluated before they are applied to a particular patient. In patients where aggressive periodontal destruction is observed, LDD is not indicated and conventional therapy should be executed. A detailed description of LDD has been given in the “Local drug delivery in periodontics”.

Host modulation therapy:

It has been well established that during host- bacterial interaction in periodontal diseases, enzymes derived from host immune cells are responsible for connective tissue destruction.  Various agents have been used as host modulation agents that directly or indirectly reduce host cell mediated connective tissue destruction 183-189.  Well, investigated host modulation agents include non-steroidal anti-inflammatory drugs (NSAIDS), chemically modified tetracyclines (CMT’s) and bisphosphonates. The first United States Food and Drug Administration (FDA) approved host modulation agent is systemically delivered collagenase inhibitor “Periostat” which contains Doxycycline Hyclate (20 mg capsule). Its application has been recommended as an adjunct to SRP in the treatment of periodontitis. Statistically, significant improvement in the periodontal status of patients has been reported with the use of Periostat 187, 188.

Overall research on host modulation agents has shown significant, but limited improvement in the periodontal status of patients. The proper protocol for the application of these agents in periodontitis cases still needs to be established. A detailed description of various host modulation agents and their clinical benefit in periodontitis patients has been given in â€œHost response modulation therapeutic agents in periodontics”.

Photodynamic therapy (PDT):

The PDT was initially introduced in the medical field for the inactivation of microorganisms on the basis of photosensitizer attachment to target cells. This therapy works on the principle of photon energy. When a photon of light is absorbed by a molecule of the photosensitizer in its ground singlet state (S), it is excited to the singlet state (S*) after it receives the energy of the photon. The lifetime of the S* state is very small (in nanosecond range) and it rapidly releases energy in the form of light (fluorescence) or by internal conversion with energy lost as heat. Photosensitizer is absorbed by microorganisms and following exposure to light of the appropriate wavelength, it becomes activated to an excited state.  Then it transfers its energy from light to molecular oxygen to generate singlet oxygen and free radicals that are cytotoxic to the bacterial cells. The PDT also has stimulating effects on fibroblasts, hence helpful in wound healing. Photosensitizer molecules have been attached to antibodies directed against various periodontal pathogens.

Most of the photosensitizers used basically have tetrapyrrole nucleus. These include porphyrins, chlorins, bacteriochlorins, and phthalocyanines. This tetrapyrrole ring structure is named porphin and derivatives of porphins are named porphyrins. Following photosensitizers are presently available for clinical use

  1. Mesotetra-hydroxyphenyl-chlorin (mTHPC, temoporfin,Foscan®; Biolitec Pharma Ltd., Dublin, Ireland),
  2. Benzoporphyrin derivative monoacid A (BPD-MA, Visudyne®; QLT Inc., Vancouver, Canada and Novartis Opthalmics, Bulach, Switzerland)
  3. 5- or daminolevulinic acid (ALA, Levulan®; DUSA Pharmaceuticals Inc., Wilmington, MA, USA)
  4. Methyl ester of ALA (Metvix®; Photocure ASA, Oslo, Norway)

Research on PDT has been done to evaluate its effect on subgingival microbiota in periodontitis cases. The therapy has demonstrated bactericidal effects on subgingival periodontopathogenic bacterial species 190-195. The therapy can be used as an adjunct to non-surgical treatment modalities in the treatment of chronic periodontitis cases.

LASER application:

With the introduction of LASER in dentistry, its use in different fields has been investigated.  In periodontics, LASER has been used for various purposes, including debridement of root surfaces, removal of the diseased pocket epithelium, for hemostasis during surgical procedures, for its bactericidal effects and for various periodontal surgical procedures. Low-power pulsed Nd:YAG laser has been shown to be capable of removing the pocket lining epithelium in moderately deep pockets 196. LASER application has been shown to suppress and eradicate putative periodontal pathogens from periodontal pockets 197, 198. So, lasers can be effectively used in conjunction with routine SRP in the treatment of both chronic and aggressive periodontitis cases.

Surgical therapy:

After execution of non-surgical therapy, if it is observed that multiple sites with moderate to deep pockets are remaining and surgical access is required to facilitate mechanical instrumentation of the root surfaces; surgical therapy is planned. The primary aims of surgical therapy are 199-201,

  1. To provide better access for the removal of etiologic factors
  2. To reduce deep probing depths
  3. To regenerate or reconstruct lost periodontal tissues

It has been well established that both non-surgical and surgical therapies are capable of halting periodontal disease progression and effectively achieve stability of clinical attachment levels 202-207. The primary advantage of surgical therapy is that it increases operators access to the root surfaces and furcation areas, thereby facilitating effective and efficient debridement of these surfaces 208-213 The surgical therapy provides access to the bone defects, thus facilitating osseous resection and recontouring, and periodontal regenerative procedures. There are various periodontal flap surgeries described in the literature. A detailed description of these surgeries has been given in â€œHistory of periodontal surgeries” and “Periodontal flap surgeries: current concepts”. Various periodontal regenerative procedures and techniques used presently in the treatment of periodontal diseases include guided tissue regeneration (GTR) (chapter 62), bone grafting (chapter 63), root surface biomodification (chapter 65) and newly introduced tissue engineering techniques (chapter 69).

Periodontal maintenance after active treatment of chronic periodontitis:

Once the active treatment of chronic periodontitis is over and desirable clinical results have been achieved, the patient is scheduled for the periodontal maintenance program. It involves the periodic evaluation of the patient and assessment of the results obtained from active periodontal treatment 214.  The schedule for periodontal maintenance varies from patient to patient. The patients who are more prone to periodontal destruction or those who already have advanced periodontal destruction need frequent maintenance visits than patients who have minimal periodontal destruction. A detailed description of the protocol that is followed during periodontal maintenance has been given in the chapter 89 “Periodontal maintenance”.

Treatment of aggressive periodontitis:

The classical sign of aggressive periodontitis is the rapid progression of disease which causes severe periodontal destruction in a relatively short duration of time. Thus, the diagnosis of the condition should be prompt and treatment planning should be done as soon as possible. Because of the difficulties in controlling the aggressive nature of the disease, the treatment of aggressive periodontitis should preferably be carried out by a periodontist. However, general practitioners play an important role in early identification of the diseases and timely referral. As discussed earlier in chronic periodontitis, the treatment of aggressive periodontitis also consists of non-surgical and surgical phases.

Before any treatment is initiated, the patient is educated regarding the nature of the disease and its treatment protocol. The patient should be assured that the condition is treatable and has a good prognosis in most of the cases provided a good patient compliance and periodontal maintenance protocol is followed. The patient should be informed about the etiological factors related to the disease, different treatment phases and probable outcome of the treatment. Most importantly, the patient should be educated regarding his/her role in the treatment of the disease. Appropriate oral hygiene instructions should be given to the patient. The patient should be educated regarding appropriate bushing technique and other oral hygiene measures suitable for the patient. If the patient has habits such as smoking or tobacco chewing, a habit cessation protocol should be instituted.

The aggressive periodontitis patients usually have some severely periodontally compromised teeth, which have a questionable prognosis. A decision should be made regarding whether to keep these teeth or to extract them. If the teeth are to be extracted, the patient should be explained about it and future restorative treatment in that area should be discussed.

Once this pre-treatment protocol is over, active periodontal treatment of the patient is started with non-surgical periodontal therapy.

Non-surgical therapy:

The effectiveness of non-surgical periodontal therapy in the treatment of chronic periodontitis is well established 215. However, its effectiveness in the treatment of aggressive periodontitis is not as clear as in chronic periodontitis. Two aspects of non-surgical periodontal therapy that need to be assessed while determining its effectiveness in the treatment of aggressive periodontitis are changes in clinical parameters following the therapy and long-term maintenance of the results.

Slots and Rosling (1983) 216 conducted a study on six patients with localized aggressive periodontitis and treated teeth associated with 20 deep pockets with SRP. They reported a small reduction of 0.3 mm in the probing pocket depth 16 weeks after the treatment. In another study, Kornman and Robertson (1985) 173 observed only 0.1 mm probing depth reduction in eight patients with aggressive periodontitis, 2 months following SRP. Many other studies also have reported only a marginal improvement in the clinical parameters following non-surgical therapy in aggressive periodontitis patients 217-220.

On the other hand, there is only a limited data regarding the long-term effects of non-surgical periodontal therapy on clinical parameters in aggressive periodontitis patients. Mixed results have been reported in this view. Many studies have reported probing pocket depth reductions and gain in clinical attachment during the initial 6 months following treatment 169, 221-224. However, in studies with longer follow-up, an increase in pocket depth as well as a decrease in attachment gain that was achieved after therapy has been reported after 6 months 223, 225. These results suggest that aggressive periodontitis responds well to non-surgical treatment up to 6 months following the treatment. Thus, the treatment of aggressive periodontitis should be started with SRP. The patient should be evaluated after the initial therapy for improvement in the clinical parameters.

Systemic antibiotics:

The rationale behind the systemic administration of antibiotics in aggressive periodontitis cases is to reach and destroy bacteria present in difficult to reach areas such as furcations, deeper areas of periodontal pockets and dentinal tubuli 226-228 and to reach bacteria in periodontal tissues 229, 230. Furthermore, bacteria present in areas other than periodontal tissues such as oral mucosa, tongue, and tonsils may translocate to and reinfect periodontal sites after mechanical instrumentation 231. Studies have demonstrated additional beneficial effects of adjunctive antibiotic therapy to SRP in aggressive periodontitis cases 232, 233. Whether to use antibiotics or their combinations in every case of aggressive periodontitis, choice of antibiotics and duration of therapy are still debatable questions. However, it is clear from the present data that those patients who continue to demonstrate attachment loss despite diligent mechanical therapy are prime candidates for systemic antibiotics 234-237. Although, initiation of antibiotic administration prior to or after mechanical therapy is an issue which is still being investigated 23, 232 but most of the current literature suggests that mechanical instrumentation must always precede antimicrobial therapy 238. Mombelli (2006)239 has suggested that antibiotics should be administered only after ………


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Local drug delivery (LDD):

There are many advantages associated with the use of LDD (read more in “Local drug delivery in periodontics”) which establish a clear rationale for their use in aggressive periodontitis. However, there is scanty literature regarding their application in aggressive periodontitis cases. One study 219 investigated the effects of SRP + 1% chlorhexidine gel (subgingivally administered) and SRP + 40% tetracycline gel (subgingivally administered) as compared to control group with only SRP. After the 12-week observation period, there was no significant improvement in clinical parameters observed in any of the test groups as compared to control group. Another study 248 was done in generalized aggressive periodontitis cases where the effect of tetracycline fibers was investigated in a split-mouth design. 10 patients were included in the study with six-month follow-up period. The results of the study demonstrated an additional periodontal pocket depth reduction of 0.6 mm and in gains of clinical attachment of 0.7 mm, up to 6 months after therapy.

Some studies have compared LDD with systemic drug delivery in aggressive periodontitis cases. In one study 249, LDD using tetracycline fibers and systemic administration of amoxicillin/clavulanic acid was evaluated in aggressive periodontitis over a 52-week period in 28 patients. The therapies were started 8 weeks after completion of SRP. No significant difference was found in either treatment modality. Another study 250 compared the effect of chlorhexidine chip with systemically administered amoxicillin (1500 mg/day) plus metronidazole (750 mg/day) in generalized aggressive periodontitis cases. After six month observation period, SRP plus adjunctive chlorhexidine chips demonstrated clinical improvement, but these were not maintained over the entire observation period. On the other hand, systemic antibiotic therapy was more effective in reducing pocket depth and gain in clinical attachment.

Hence, it can be concluded that the use of LDD in aggressive periodontitis is not as clear as it is in the cases of chronic periodontitis.

LASER application:

Various studies have investigated the effectiveness of lasers as compared to other therapies in the treatment of aggressive periodontitis. One study 251 compared SRP alone, diode laser treatment (LAS) alone, and SRP combined with LAS on clinical and microbial parameters in patients with aggressive periodontitis. A 980-nm diode laser was used in continuous mode at 2 W power, in this study. The results demonstrated significant improvement in microbial and clinical parameters in patients with aggressive periodontitis over the 6-months observation period. Another study 252 compared surgical therapy with Nd:YAG laser application in aggressive periodontitis cases. No significant difference in clinical parameters was found between the two treatment modalities. It was concluded that laser application can be used as an alternative to surgical therapy.

However, more research is required to evaluate the long-term effectiveness of lasers in aggressive periodontitis cases.

Photodynamic therapy (PDT):

PDT has been recently evaluated as an adjunct to SRP and alternative to conventional surgical therapy in the treatment of aggressive periodontitis. In a study 253, the cytokine profile in GCF of aggressive periodontitis patients was evaluated after PDT or SRP. A split-mouth design was used in the study. The results of the study demonstrated similar effects on crevicular TNF-α and RANKL levels. Another study 254 compared the effects of PDT and systemic antibiotics in the nonsurgical treatment of aggressive periodontitis. The results of the study demonstrated significant clinical improvement with both the therapies. However, systemic antibiotic therapy resulted in a significantly higher reduction of pocket depth and a lower number of deep pockets as compared to PDT.

There are only a few photodynamic studies done in aggressive periodontitis cases, most of which have shown beneficial effects of the therapy in the treatment of these cases.  However, clinical data are insufficient to authenticate the exact utilization of this therapy in the treatment of aggressive periodontitis cases and more research is required in this direction.

Surgical therapy:

As already stated, due to the aggressive nature of the disease, patients with aggressive periodontitis usually have a lot of bone loss at the time of diagnosis. Consequently, after the initial non-surgical treatment, residual pockets often remain which require a surgical treatment. Furthermore, infrabony defects are usually encountered in these cases which may be suitable for regenerative therapy. Osseous corrections may also be required in certain areas. All these goals can be achieved only after surgical entry into the area.

Detailed descriptions of various flap designs used for gaining surgical access have been discussed in â€œHistory of periodontal surgeries” and â€œPeriodontal flap surgeries: current concepts”. Various studies have been done to evaluate the effectiveness of surgical therapy and its comparison with non-surgical therapy in the treatment of aggressive periodontitis. One study 255 compared SRP alone; SRP + soft tissue curettage; or, modified Widman flap surgery for treating 25 deep periodontal lesions in 7 patients. 16 weeks after the treatment, microbiological and clinical effects were evaluated. The results of the study demonstrated that SRP alone did not effectively suppress A. actinomycetemcomitans in periodontal pockets. On the other hand, SRP + soft tissue curettage and modified Widman flap surgery were able to effectively suppress A. actinomycetemcomitans. Another longitudinal study compared the effects of systemic tetracycline administration, SRP and modified Widman flap surgery in patients who were enrolled in a 5-year maintenance program. 16 patients with localized aggressive periodontitis were enrolled in the study. The healing response in these patients was compared with chronic periodontitis patients. The results of the study demonstrated that the healing response in aggressive periodontitis patients was similar to that observed in chronic periodontitis patients 256.

Mandell and Socransky (1988) 257 did a study on 8 patients with localized aggressive periodontitis. The treatment performed included modified Widman flap surgery and a doxycycline regimen. The results of the study demonstrated that the treatment done not only effectively eliminated A. actinomycetemcomitans from periodontal pockets, but also resulted in the reduction of pocket probing depth and a mean clinical attachment gain of 1.3 mm.

These findings suggest that surgical periodontal therapy is effective in not only suppressing A. actinomycetemcomitans in periodontal pockets, but is also able to facilitate regeneration of the lost tissue.  Thus, appropriate execution of surgical periodontal therapy is helpful is halting the disease progression and achieving periodontal health in aggressive periodontitis cases.

Regenerative therapy:

As discussed earlier, various regenerative techniques such as guided tissue regeneration (GTR), bone grafting, etc. have been used to regenerate the lost periodontal structures in aggressive periodontitis. Sirirat et al. (1996) 258 in a randomized controlled trial, compared GTR and resective (osseous surgery) surgical techniques in the treatment of aggressive periodontitis. Paired defects in the same patient were included in the study, thus each patient served as their own control, thus the response to surgery and healing could be better controlled and evaluated. Twelve months after the surgical procedures it was found that the GTR group demonstrated probing depth reduction of 2.60+1.30 mm and clinical attachment gain of 2.20+1.42 mm. On the other hand, osseous surgery group that showed a probing reduction of 1.73+0.96 mm and the attachment gain of 1.20+1.01 mm. Thus, GTR significantly improved the periodontal status of the patient.  It must be remembered that pattern of bone loss and type of bone defects play an important role in regenerative therapy. In general, horizontal bone loss, furcation defects, and increased tooth mobility are poor prognostic factors for regeneration 259.

The recent advancement that may be helpful in achieving regeneration in aggressive periodontitis patients is tissue engineered biologically active molecule carrier systems. These may deliver various growth factors at the site where regeneration is desired.

Maintenance therapy:

The patients with aggressive periodontitis should be motivated to provide a good compliance to periodontal maintenance therapy. This is because these patients are at more risk of disease reactivation and continued periodontal destruction.  A recent study has reported a mean tooth loss, of 0.13 teeth/year in patients with aggressive periodontitis 260. Furthermore, it was observed that in generalized aggressive periodontitis cases, the mean tooth loss was 0.14 teeth/ year and in localized aggressive periodontitis it was 0.02 teeth/year. The study also compared the patients who were compliant with the maintenance schedule and those who were not. It was observed that patient compliant with a maintenance schedule demonstrated only 0.075 teeth/ year, whereas patients who were irregular in periodontal care had a tooth loss of 0.15 teeth/ year. Thus, periodontal maintenance is essential for the overall success of the therapy in aggressive periodontitis patients and should be planned according to patient’s requirement. The patient should be motivated to religiously follow the maintenance schedule.


A clear understanding of chronic and aggressive periodontitis is important to correctly diagnose a patient. Although some features of both the conditions may overlap, but by going into details of the history of the patient and clinical, radiographic and microbiological analysis, we can come to a correct diagnosis. Recent advances in the microbiological and immunological investigations have provided us with new methods of diagnosing and treating periodontal diseases. Risk factors play an important role in disease progression. While risk prediction is still not a precise science in periodontology, enough advances in our knowledge of risk factors have been made to permit the development of a risk calculator that is offered to practitioners to help assess a patient’s risk for periodontal disease 261. Disease progression is a combination of multiple factors. In future, the scope is wide for research in this field to identify the magnitude to which these factors affect periodontal disease progression and treatment options by which we can efficiently treat patients.

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Periobasics: A textbook of periodontics and implantology

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