Chronic periodontitis

Chronic periodontitisPresented by :RICHA sharma

Chronic periodontitis formerly known as adult periodontitis or chronic adult periodontitis is the most prevalent form of periodontitis Although it is most frequently seen in adults, but in some cases can also be present in children and in adolescents in response to chronic plaque and calculus accumulation.

It is defined as an inflammatory disease of supporting tissues of teeth caused by specific micro-organism or group of specific micro-organisms resulting in progressive destruction of periodontal ligament and alveolar bone with pocket formation, recession or both.

It is an infectious disease in inflammation within the supporting tissues of the teeth, progressive attachment loss and bone loss. (Carranza 11th edition , Fleming TF)

HISTORICAL PERSPECTIVE

Late 1800s Chronic periodontitis was clinically characterized as a slowly progressive destruction of the periodontium due to the accumulation of Lime Deposits on the teeth (Davis, 1879) . Known as Riggs disease.

Throughout most of the 20th century, this form of periodontitis had been considered an inflammatory disease associated with local irritants and the formation of dental plaque (biofilms) on tooth surfaces. This concept prevails today.

AAP (1999)- based on current clinical and scientific data. General clinical manifestation of periodontitis.1. Chronic periodontitislocalizedgeneralized2. Aggressive periodontitislocalizedgeneralized3.Periodontitis as manifestation of systemic disease4. Two forms of necrotizing disease have been described:NUGNUP

5. Abscesses of the periodontiumGingival abscessPeriodontal abscessPericoronal abscess6. Periodontitis associated with endodontic lesions

Clinical charateristics (Flemming,mombelli; periodontol 1992)Prevalent in adults, but can occur in children.Amount of destruction consistent with local factors.Associated with variable microbial pattern.Subgingival calculus frequently found.Slow to moderate rate of disease progression with possible periods of rapid destruction.

Possibly modified or associated with the following:Systemic diseases such as diabetes mellitus and HIVLocal factors predisposing to periodontitis.Environmental factors such as smoking

CLINICAL FEATURESSupra and subgingival plaque accumulation (frequently associated with calculus)Gingival inflammationPocket formationLoss of periodontal attachment tooth Mobility in advance cases.Furcation involvementOccasional suppuration

Blunted or rolled gingival margins and Flattened or cratered papillae.Gingival bleeding- either spontaneous or in response to probing.In some cases, due to long standing, Low grade inflammation, thickened fibrotic marginal tissues may obscure the underlying inflammatory changes.Both horizontal and vertical bone loss is evident radiographically.

Radiographic signs The following characteristic are indicative of periodontal tissue change.1. The crest of interdental bone will be 2 mm or more apical to the CEJ; this is very important to determine if there is bone loss. 2. The crest of alveolar bone will appear fuzzy in appearance. 3. Lamina dura will be ill-defined .4. Density of interdental bone will be decreased .5. Furcation areas of molar areas will be involved, and you will find radiolucency in that area.

Pattern of bone loss may be vertical or horizontal

VERTICALHORIZONTALWhen attachment & bone loss on one tooth surface is greater than that on an adjacent surface.When attachment and bone loss proceeds at an uniform rate on the majority of tooth surfaces.Vertical bone loss is usually associated with angular bony defects & infrabony pocket formation.Horizontal bone loss is usually associated with suprabony pockets.

PATHOGENESIS OF PERIODONTAL DISEASE

Disease distributionSite specific disease It may occur on one surface and other may be free of symptom.14

15LOCALIZEDWhen < 30%of the sites are involved.

GENERALIZEDWhen > 30% sites are involved.

DISEASE SEVERITY

MILD- 2-3 mm of CAL lossMODERATE- 3-5 mm of CAL lossSEVERE- more than 5mm of CAL loss

Disease progressionUsually slow rate of progression: In the few studies that have been performed on the natural history of progression of chronic periodontitis, the disease was found to progress at a full-mouth average rate of approximately 0.2 mm year. (Brown, Loe 1996; Lindhe Hafajee 1983 et al.)

In a longitudinal study by Loe H, Anerud A, Boysen H, Morrison E (1986) of Sri Lankan workers on a tea plantation, one group of individuals lost, on a full-mouth basis, an average of 0.46 mm year . This group was referred to as rapidly progressive, and would probably be classified as generalized aggressive periodontitis using the current system of nomenclature.

Several models have been proposed to describe the rate of progression by Socransky ,Goodson 1984. These models progression is measured by determining the amount of attachment loss at a given time. This was termed as BURST HYPOTHESIS of disease progression.1- Continuous Models2- Random or Episodic burst model3- Asynchronous , multiple burst model

Continuous model slow and continuous, constantly progressive rate of destruction throughout the duration of the disease.

Random / episodic-burst model short bursts of destruction followed by periods of no destruction, random pattern of disease w.r.t the tooth sites affected.

Asynchronous, multiple-burst model periodontal destruction occurs in bursts, around affected teeth during defined periods of life. The chronology of these bursts of disease is asynchronous for individual teeth or groups of teeth.

PERIODS OF DESTRUCTION1- Bursts of destructive activity are associated with sub gingival ulceration, acute inflammatory reaction resulting in rapid bone loss. 2- Conversion of T lymphocyte lesion to B- Lymphocyte plasma cell infiltrates3- Increase in loose unattached motile Gram ve anaerobic pocket flora and remission with dense unaltered non motile Gram +ve flora. Tissue invasion by one or several bacterial species followed by an advanced local host defense that controls the attack (Saglie RF, et al 1987)

Categories of Risk Elements for Periodontal DiseaseRisk Defined as is the probability that an individual will get a specific disease in a given period.

RISK FACTORS:Tobacco smokingDiabetesPathogenic bacteriaMicrobial tooth deposits

RISK DETERMINANTS:Genetic factorsAgeGenderSocioeconomic statusstressRISK INDICATORS:HIV/AidsOsteoporosisInfrequent dental visits

RISK MARKERS/PREDICTORS:Previous history of periodontal diseaseBleeding on probing

SmokingUndoubtedly one of the main and most prevalent, risk factors for chronic periodontitis, risk calculations suggesting 40% of the cases of chronic periodontitis may be attributable to smoking...Several cross sectional and longitudnal studies performed over the years by Kinane & Chestnutt 2000 have found that tobacco is a risk factor for chronic periodontitis.It is not only the risk of developing the disease that is enhanced by smoking but also response to periodontal therapy is impaired in smokers.

A further feature in smokers is that their signs and symptoms of both gingivitis and chronic periodontitis, mainly gingival redness and bleeding on probing , are masked by the dampening of inflammation seen in smokers as compared to non-smokers.

MECHANISMVascular alterationsAltered neutrophil functionDecreased IgG productionDecreased lymphocyte proliferationIncreased prevalence of periopathogensAltered fibroblast attachment and functionDifficulty in eliminating pathogens by mechanical therapyNegative local effects on cytokine and growth factor products

When combined with plaque-induced chronic periodontitis, an increase in the rate of periodontal destruction may be observed in patients who smoke and have chronic periodontitis.As a result, smokers with chronic periodontitis have more attachment and bone loss, more furcation involvements and deeper pockets. In addition they appear to form more supragingival than sub-gingival calculus and demonstrate less bleeding on probing than non-smokers.

DIABETES

Diabetes can increase the severity of the disease. NIDDM or type II is the most prevalent factor. In addition, Type II diabetes is most likely to develop in an adult population at the same time as chronic periodontitis. The synergistic effect of plaque accumulation and modulation of an effective host response through the effect of diabetes can lead to severe and extensive periodontal destruction that may be difficult to manage with standard clinical techniques without controlling the systemic condition.In 2001, Taylor conducted a comprehensive Medline search of studies examining periodontal diseases as a complication of diabetes and the effect of periodontal therapy on glycemic control.

Most reports indicated that subjects with diabetes have increased prevalence, extent, severity or progression of periodontal diseases.

Micro vascular changes Hyperglycemia Glycosylation of basement membrane proteins Thickening of basement membrane Altered structural and physical properties of BM Disruption of collagen fibers in BM, swelling of endothelium Impedes oxygen diffusion, metabolic waste elimination, PMN migration diffusion of serum factor including antibodies Susceptibility to infection

(Brownlee et al 1994)

MECHANISM Hyperglycemia + collagen AGEs

Increases cross linking between collagen molecules

Reduced solubility and turnover of collagen

Failure in periodontal repair and regeneration

In addition, type 1 diabetes, or insulin-dependent diabetes mellitus, is observed in children, teenagers, and young adults and may lead to increased periodontal destruction when it is uncontrolled. It is likely that chronic periodontitis, aggravated by the complications of type1 and type 2 diabetes, will increase in prevalence in the near future and will provide therapeutic challenges to the clinician.

MICROORGANISMSChronic periodontitis is generally progressive, with some patients having increased susceptibility to attachment and bone loss and pocketing. A specific group of micro-organisms is seen in sub-gingival bio-film of patients with ongoing bone associated with chronic periodontitis, including Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola.

The identification and characterization of these and other pathogenic micro-organisms and their association with attachment and bone loss have led to the specific-plaque hypothesis for development of chronic periodontitis.

This hypothesis implies that although a general increase occurs in the proportion of gram-negative micro-organisms in the sub-gingival plaque in periodontitis, it is the presence of increased proportion of members of gram-negative micro-organisms, that precipitate attachment and bone loss.

World Workshop in Periodontology consensus report 1996Designated A.a., P.gingivalis and B. forsythus as periodontal pathogens1)A.a- small, non-motile, gram negative, sacchrolytic, capnophilic rond ended rodIt has ability to invade the epithelial and endothelial cells.

2) P. gingivalisGram negative, anaerobic, non-motile, asaccharolytic rod-member of black bacteriods brown black colonies on blood agar group.- elaborate a variety of proteolytic enzymes to invade host defense mechanism to cause tissue destruction.Various proteases:-GingipainsProlyl tripeptidaseProlyl dipeptidasecollagenase

3) Bacteroid forsythusIt was first described in 1979 as fusiform bacteroidsDifficult to grow- gram negative anaerobic- spindle shapeHighly pleomorphic rod- its growth get enhanced by co cultivation with F. nuceatum- shows trypsin like proteolytic activity- detected more frequently and in higher no. in active periodontal leions than inactive lesions.

Local contributing factorsAnatomical factors Proximal contactCervical enamel projectionIntermediate bifurcation ridgesCemental tearAccessory canalsRoot proximity. Intermediate bifurcation ridgesAccessory canalsRoot anatomy- palatogingival groove, attachment area, root trunk length31

Restorative contributing factorsOverhanging restorationMargin locationCrown contoursPontic formRestorative materialsOrthodontic contributing factorsCrowding, malocclusion, bands and brackets

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Risk determinants/background characteristics

Genetics Multifactorial diseaseIn contrast to aggressive periodontitis , chronic periodontitis does not typically follow a simple pattern of familial transmission.Twin studies it has familial component but transmission of bacteria among family members and due to common environmental factors is difficult to interpret.Polymorphism in genes encoding for IL-1alpha and beta is associated with aggressive form of chronic periodontitis in Northern America. (Korman1998)

A study by McGuire et al,1999 suggested that patients with the IL-1 genotype increased the risk for tooth loss by 2.7 times; those who were heavy smokers and IL-1 genotype negative increased the risk for tooth loss by 2.9 times.The combined effect of the IL-1 genotype and smoking increased the risk of tooth loss by 7.7 times ( McGuire et al 1999).As it is accepted that the immune system plays an important role in the pathogenesis of periodontitis, most genes that are considered to be responsible for the development of periodontitis are also linked to the immune response.These include that genes that affect the expression of interlukin-1, interlukin-6, TNF, interlukin-10, toll-like receptors.

AGEBoth the prevalence and severity of periodontal disease increases with age. (Burt 1994, Papapanou 1994, 1998).Lindhe (1991, 1992)Minimal loss of attachment in aging subjects enrolled in preventive programs throughout their lives.

PREGNANCY

Hormonal changes during pregnancy can aggravate existing gingivitis, which typically worsens around the second month and reaches a peak in the eighth month.

Pregnancy itself does not cause disease, and simple preventive oral hygiene can help maintain healthy gums. Any pregnancy-related gingivitis usually resolves within a few months of delivery. (Offenbacher et al.)

Stress

Psycho physiological response of the organism to a perceived challenge or threat. (Breivik et al 1996).

Has direct anti-inflammatory or anti immune effects on body defenses.Increasing evidence suggest that emotional stress may also influence the extent and severity of chronic periodontitis.(Glaser et al.2002) However, stress is currently considered as a risk indicator for periodontal disease (Genco RJ.1996).

The mechanisms by which stress could affect periodontal disease progression and wound healing have been divided into two main categories: Psychosocial stress Behaviour change

Poor Oral Hygiene Poor compliance

Bacterial infection Periodontal disease

SmokingOver-eating

Cortisol

i) health-impairing behaviours such as poor oral hygiene, increased tobacco and alcohol consumption and poor nutritional intake;ii) patho-physiological factors that lead to higher glucocorticoid and catecholamine levels which indirectly affect hormonal, inflammatory and immunological profiles, leading to an increased susceptibility to periodontal disease (Boyapati L, 2007)

Treatment planning

Preliminary phase/ emergency phasePhase I therapyPlaque control and patient educationRemoval of calculus and root planingOcclusal therapy, orthodontic movementRe evaluationSurgical Phase ( Phase II therapy)Restorative phase (Phase III)Maintenance Phase ( Phase IV)

TREATMENT OF MILD CHRONIC PERIODONTITIS

Scaling and root planingClosed curettage andSubgingival scalingOral hygiene measure

TREATMENT OF MODERATE CHRONIC PERIODONTITISPlaque control Scaling and root planing proceduresProbing depth reduction procedures Gingivectomy Repositioned flaps1.Apically positioned flap without osseous resection 2.Apically positioned flap with osseous resection

SEVERE CHRONICChemical agents that modify the root surface, while promoting new attachment, have shown variable results when used in humans. Bone grafting and guided tissue regeneration techniques, with or without bone replacement grafts, may be successful when used at selected sites with advanced attachment loss. The use of biologically engineered tissue inductive proteins (eg, growth factors, extracellular matrix proteins, and bone morphogenic proteins) to stimulate periodontal or osseous regeneration has also shown promising results.

Bone grafting with a variety of materials has been estimated to decrease probing depths and lead to gains in clinical attachment of 0.51 mm beyond that of surgical debridement alone (Reynolds MA,2003).

A comprehensive meta-analysis of regeneration studies by (Laurell L,1998) found that guided tissue regeneration generally improved attachment levels and bone fill by 2.7 and 2.1 mm respectively, beyond surgical debridement alone.

CONCLUSION

The effective management of periodontal diseases in clinical practice presents many challenges to the clinician, some of which can not be over come by clinical treatment alone.

It is increasingly recognized that periodontal disease cannot at present be cured but rather must be controlled in order to stabilize the progression of the destructive process in the long term.