The diagnosis of periodontal diseases is indeed difficult to make. This is basically because of the reason that many features of different forms of periodontitis confuse clinicians to reach a particular diagnosis. Because of the same reason a complete “periodontology 2000″ volume has recently been dedicated to chronic and aggressive periodontitis 1. My aim in the following discussion is to highlight our current understanding of chronic periodontitis and aggressive periodontitis.
It is an inflammatory process that affects the protective and supportive tissues around teeth. Primary etiology for this disease is 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.
It is a group of periodontal diseases characterized by localized or generalized loss of alveolar bone usually affecting individuals under 30 years of age 2. It appears to be etiologically a complex disease. Following characteristics have been proposed to be associated with aggressive periodontitis 3.
- Rapid attachment loss and bone destruction.
- Except for the presence of periodontitis, patients are otherwise clinically healthy.
- Familial aggregation.
- 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 Actinobacillus 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 divide as localized or generalized forms:
Localized Chronic/Aggressive periodontitis: Periodontitis is considered localized when ≤30% of the sites assessed in the mouth demonstrate attachment loss and bone loss.
Generalized Chronic/Aggressive periodontitis: Periodontitis is considered generalized when >30% of the sites assessed in the mouth demonstrate attachment loss and bone loss.
Present data strongly suggests that periodontal diseases are multifactorial diseases where smoking, stress and genetic factors play a very important role 4-7. It is important to understand host and bacterial interactions before we go in details of chronic and aggressive periodontitis. Readers are advised to study “Immunology of periodontal diseases” and “Host response in periodontal disease” to understand the background of periodontal diseases. Equally important are “Role of genetics in pathogenesis of periodontal diseases”, “Smoking and periodontal diseases” and “The role of Stress in periodontal diseases and wound healing”.
Epidemiology of chronic and aggressive periodontitis:
Epidemiology and risk factors for chronic periodontitis 8-10 and aggressive periodontitis have been extensively investigated 11-12. 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 12. Other investigations have demonstrated that race–ethnicity 13-16, gender 14, 17-18 and socioeconomic status 17, 19 are important risk indicators of chronic periodontitis in adolescents and young individuals.
One study analysed data from the Third National Health and Nutrition Examination Survey (NHANES III) conducted on 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 > 5mm 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 attachment loss > 5mm. Results of this study demonstrated that severity of periodontal disease is not uniformly distributed among race, ethnicity or the socioeconomic status 20.
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 and 24–29 years old, respectively 21.
Importance of case history:
The first and foremost important step in diagnosis of chronic and aggressive periodontitis is 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. Following are the differences between chronic and aggressive periodontitis based upon clinical features,
Differences between chronic and aggressive periodontitis on the basis of case history and clinical features
Case history & Clinical feature
|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 widespread destruction of periodontal tissues in a young patient with rapid rate of disease progression i.e. history of couple of years. Whereas, generalized chronic periodontitis is characterized by widespread periodontal damage, but usually in an older individual with a slow rate of disease progression i.e. history of many years.
In case of generalized aggressive periodontitis most common reported complaints are recently noticed flaring and progressing spacing of anterior teeth and bleeding from gums. Other complaints may include halitosis and pus discharge from gums. Mobility of the affected teeth will be seen towards the later stages of the infection. The patient is otherwise systemically healthy. Patient may also complain of a dull nagging type of pain from 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.
These 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. Bleeding on probing can be seen from periodontal pockets. In chronic periodontitis cases gingiva may shows 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 case of multi-rooted teeth furcation is involved. In long standing cases tooth mobility or tooth loss may be evident. 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 case
This is clinical 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 average depth of 4-5 mm. Patient gives a history of swollen gums and bleeding gums for many 7-10 years. Patient also reported the feeling of increased mobility in some of his teeth during 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 patient was diagnosed as chronic generalized periodontitis case.
These cases present with minimal supra and sub-gingival plaque accumulation. Periodontal destruction is not consistent with the amount of local factors present. The patient is otherwise systemically healthy as systemic diseases may severely impair host defence leading to periodontal destruction. In cases of periodontal destruction due to systemic diseases the diagnosis is usually made as periodontal manifestation of systemic disease. Microbiological analysis shows elevated levels of aggregatibacter actinomycetemcomitans. Other characteristic features include phagocyte abnormalities and hyper-responsive macrophage phenotype, including 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 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.
The disease progresses in alternating periods of activity and quiescence 22. 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 3. This unexplained curtailment of disease progression has sometimes been referred to as a “burnout” of the disease.
During the periods of active disease there is alveolar bone loss and loss of attachment. The gingiva shows all signs of mild to severe inflammation which may include tender, fiery red, edematous, soft, and boggy gingiva. Bleeding on probing or even spontaneous bleeding and purulent exudation may be evident. Inflammatory gingival enlargement may also be noticed.
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 loss of several teeth due to spontaneous exfoliation.
Generalized Aggressive Periodontitis case
These are 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. Patient also reported swollen gums and irritation in gums. clinical examination of the patient demonstrated generalized deep periodontal pockets, mobility of maxillary 1st molars and incisors, furcation involvement with maxillary and mandibular 1st molars and pathologic tooth migration w.r.t. 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 levels of A. actinomycetemcomitans, P. gingivalis and P. intermedia.
Radiographic features of chronic and aggressive 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 appears fuzzy in appearance. Lamina dura will be ill-defined and density of interdental bone is decreased. Furcation areas of molar areas 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 an adjacent surface and is usually associated with intrabony pocket formation. In horizontal bone loss, bone loss occurs at a uniform rate on the majority of tooth surfaces and is associated with suprabony pockets.
In case of generalized aggressive periodontitis radiographs may show generalized bone destruction ranging from mild crestal bone resorption to severe extensive alveolar bone destruction depending on 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 23-32. There are some fundamental problems in studying the microbiology of periodontal diseases. One major problem is the complexity of 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 33-34.
Secondly, it has been demonstrated by many studies that periodontally healthy individuals some periodontal pathogens as part of their normal supragingival and subgingival microbiota 35-42. These bacteria are present in relatively low number in healthy periodontal sites and they may be present inthese sites for long duration of time without causing disease. On the other hand it has been suggested that presence of these organisms is necessary for development of immunity by the host 43.
Another problem is the development of plaque as biofilm. When bacteria grow in a biofilm, their characteristics change as compared 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 virulent factor. Please read “Plaque as biofilm and the ecological plaque hypothesis” for more details on this topic.
It is difficult to categorize any particular micro-organism as the causative agent for chronic or aggressive periodontitis. Various investigations done on identifying periodontal pathogens in chronic and aggressive periodontitis have been analysed in a systematic review which concluded with no confirmation of any particular organism association with any of chronic or aggressive periodontitis 44. 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. Read in details about these facts in “Microbiology of periodontal diseases” and “Host response”.
Studies have shown that some of the bacterial species are strongly associated with advanced periodontal lesions. These include aggregatibactor actinomycetemcomitans, porphyromonas gingivalis, tannerella forsythensis and treponema denticola 45. Many other studies have identified aggregatibactor actinomycetemcomitans along with immunological defects as the main causative agent of localized aggressive periodontitis 46-47.
Although both chronic and aggressive periodontitis are multibacterial infections and many bacteria are common in both conditions, some authors have tried to categorize bacteria which are more prevalent in periodontal health, gingivitis, chronic periodontitis and aggressive periodontitis.
Microbiology of various periodontal conditions 48-51
|Gram positive organisms||Gram-positive organisms||Gram-positive organisms||Actinobacillus actinomycetemcomitans
|Lactobacillus species |
|Eubacterium brachy |
|Gram-negative organisms||Gram-negative organisms||Gram-negative organisms||Eikenella corrodens
|Fusobacterium nucleatum |
Immunology of chronic and aggressive periodontitis:
In innate immunity the role of neutrophils, Toll like receptors and Defensins has been well studied.
Role of neutrophils:
Polymorphonuclear leukocyte (PMN) appears to play a key role in the maintenance of the periodontal health 52. Individuals with defective PMN function are subjected to increased periodontal breakdown. Role of PMN’s in periodontal diseases has been discussed in detail in “Role of neutrophils in periodontal diseases”.
Toll-like receptor (TLR):
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 53 of which TLR-2 and TLR-4 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 whole 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 TLR-2 and TLR-4 are expressed in healthy oral epithelium but the expression of both is markedly upregulated during inflammation54. TLR-2 stimulation has been shown to be associated with porphyromonas gingivalis lipopolysaccharides and gram-negative periodontal bacteria 55-57. Study done by Kikkert et al showed only Aggregatibacter actinomycetemcomitans and Veillonella parvula were capable of stimulating both toll-like receptor-2 and toll-like receptor-4 55.
Various studies have investigated expression of toll like receptor-2 and toll-like receptor-4 in chronic and aggressive periodontitis. A study showed increased expression of both toll-like receptor-2 and toll-like receptor-4 in chronic periodontitis cases as compared to healthy tissues, there was only weak expression of toll-like receptor-2 and no expression of toll-like receptor-4 was detected 58. Various studies have demonstrated TLR-2 and TLR-4 mutations/polymorphisms and their positive association with chronic and aggressive periodontitis 59-62. Whereas, many others have not found any relation 63-65. So, this is a matter of further research at molecular level to explain exact mechanism of this association if any.
The epithelium along with acting as physical barrier also contains substances that kill pathogens or inhibit their growth. Among the most abundant of these are antimicrobial peptides, called defensins. Human defensins are divided into two subgroups: α- and β-defensins. Both α- and β-defensins consist of a triple-stranded β-sheet structure, and have a molecular weight between 3 and 6 kDa. Six alpha-defensins (hND-1 to hND-6) and four beta-defensins (hBD-1 to hBD-4) have been defined in humans.
α-defensins along with cathelicidin LL37 are present in high levels in neutrophils that migrate through the junctional epithelium to the gingival sulcus where they act as anti-microbial peptides. The oral sulcular pocket and junctional epithelia of the gingival are all associated with the expression of defensin, more specifically β-defensins hBD-1, hBD-2 and hBD-3 66 It has been shown that P. gingivalis stimulates hBD-2 expression in gingival epithelial cells 67. One study demonstrated significantly higher expression of hBD-3 in chronic periodontitis 68. Another study showed increased hBD-2 gene expression in aggressive periodontitis cases as compared to healthy patients who had lower expression of hBD-1 and hBD-2 genes. Interestingly expression of hBD-1 and hBD-2 genes were lower in gingivitis cases as compared to healthy patients 69. The exact differences in defensin expression in chronic and aggressive periodontitis are still a matter of further investigations.
The adaptive immune response in periodontitis has been extensively studied. It has been shown that Th1 cells play an important role in early or stable lesion of chronic periodontitis whereas advanced lesion of chronic periodontitis is dominated by B-cells and plasma cells which are activated by Th2 cytokines 70-73.
The difference in 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 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 “Host response in periodontal disease”.
Role of Genetics in Chronic Periodontitis:
Although research work has show that genetic factors may be associated with chronic periodontitis but no clear genetic determinants have been described 74. 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 75. 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 76.
In another study Michalowicz et al 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 occluded that 38% to 82% of the population variance for these measures may be attributed to genetic factors 5. In a subsequent study authors conclude that after making other variables constant (smoking and utilization of dental care) the chronic (adult) periodontitis had approximately 50% heritability 4. Also in a Dutch population epidemiological studies have suggested that chronic (adult) periodontitis aggregates in families 77.
Various single nucleotide polymorphisms have been shown to be associated with 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”.
Evidence for genetic link of aggressive periodontitis has been clearly established. Initial research work showed that the prevalence of aggressive periodontitis was disproportionately high among certain families 78-80.
One study done on young patients with severe periodontitis showed that their siblings often suffered from severe periodontitis 81. 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 increased prevalence of aggressive periodontitis among female family members which supports the X-linked dominant inheritance 82-85. On the other hand certain features like affected siblings of un-affected parents support autosomal-recessive inheritance of aggressive periodontitis 86-87. 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 disease in a particular individual 88.
Segregation analysis is based on Mendel’s laws 89. 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. 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 90.
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 first reported linkage between Aggressive Periodontitis and a specific chromosomal region (4q11-13) near the gene for Dentinogenesis Imperfecta 91. Another linage reported was of Localised Aggressive Periodontitis to a marker on chromosome 1(1q25)(13) 92. The linkage analysis of genetic variations in IL-1 was also associated with aggressive periodontitis 93.
Other studies which have shown genetic link of aggressive periodontitis include
- The study of inherited disorders and genetic syndromes.
- Twin studies.
- Population studies.
- Single nucleotide polymorphism.
For detailed description of these please read “Role of genetics in pathogenesis of periodontal diseases”.
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.
Prior history of periodontitis:
Prior history of periodontitis puts patient on more risk of developing periodontitis. Periodontal bone loss is caused by accumulation of microbial plaque. An improperly treated patients or patients with poor post-operative 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.
Poor oral hygiene is a risk factor for development of periodontitis. Many randomized controlled trials have demonstrated the cause–effect relationship of plaque on gingivitis 94-96. Application of anti-microbial therapy and agents such as chlorhexidine also reduce the gingival inflammation which indicates the maintenance of good oral hygiene to reduce periodontal disease activity. Other investigations have shown that periodontal surgical procedures accompanied by twice monthly professional tooth cleaning halt the progression of periodontal diseases 97-99. All these findings suggest that bacterial plaque is the primary risk factor for 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 100-106. Odds ratios for developing periodontal disease as a result of smoking range from 2.5 107 , 3.97 for current smokers and 1.68 for former smokers 108 and 3.25 for light smokers to 7.28 for heavy smokers 109. It has also been shown that periodontal treatment is less likely to be successful in smokers than in non-smokers 110-111.
How smoking affects the periodontal disease progression has been discussed in detail in “Smoking 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 112-114. The hypothalamic – pituitary – adrenal (HPA) axis and the systemic adreno – medullary sympathetic nervous system play important role in periodontal disease progression. Details about this relationship have been discussed in “The role of stress in periodontal disease and wound healing”.
It has been a consistent finding that severity of periodontal diseases is generally more in males than in females. It is confirmed by all the national health surveys conducted in United States 115-117. Reason for this variation is that males usually exhibit poorer oral hygiene than females, whether measured as calculus or soft plaque deposits. Data also suggests that this finding may be related to gender dependent genetic predisposing factors or other socio-behavioral factors 118.
Poor oral hygiene is the basis of this variation in severity of periodontal diseases between two genders. So, gender may not be considered as absolute risk factor but poor oral hygiene must be.
Genetics and its role in periodontal disease have been well investigated and present data strongly suggests that genetic factors play an important role in progression of periodontal diseases. Various genetic factors have already been discussed in previous sections. Complete detail is available in “Role of genetics in pathogenesis of periodontal diseases”.
Role of systemic factors:
There is wide evidence in the support of association of systemic diseases and periodontal diseases 119-125. Systemic diseases like diabetes not only influence the pathogenesis of the 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 socioeconomic Status (SES) 116-117. It is believed that well educated people with a good socioeconomic Status (SES) have better oral health status than the less educated and poorer segments of society. Reason for this is the positive attitudes 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 socioeconomic Status (SES).
Pathogenesis of aggressive periodontitis is quite different from chronic periodontics. Some risk factors like smoking, stress and socioeconomic Status (SES) are common 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 presence of these organisms in periodontal pocket does not confirm aggressive periodontitis but in there number above certain levels certainly predisposes the patient for development of periodontitis.
Genetic and Immunological risk factors:
Many studies have demonstrated immunological abnormalities in aggressive periodontitis cases 126-129. 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 the tissue destruction that is observe in localized aggressive periodontitis 130. 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 131. A population study demonstrated an odd ratio of 18.9 associated with a specific IL-1 genotype 132. Detailed description of cytokine polymorphism and its effect on host response has been discussed in “Role of genetics in pathogenesis of periodontal diseases”.
Treatment of chronic and aggressive periodontitis:
For treatment of chronic and aggressive periodontitis please read “Treatment of Chronic Periodontitis” and “Treatment of Aggressive periodontitis”.
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 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 development of a risk calculator that is offered to practitioners to help assess a patient’s risk of disease 133. 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 our patients.
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|Know more…………..Historical names of periodontitis:• Loculosis
• Blennorrhea gingivae
• Alveolodental periostitis
• Infectious arthrodental gingivitis
• Phagedenic pericementitis
• Expulsive gingivitis
• Symptomatic alveolar arthritis
• Smutz pyorrhea
• Riggs disease
• Pyorrhea alveolaris