Periodontal diseases (also called periodontitis) are those diseases that affect one or more of the periodontal tissues

: 1. alveolar bone 2. periodontal ligament 3. cementum 4. gingiva While many different diseases affect the tooth-supporting structures, plaque-induced inflammatory lesions make up the vast majority of periodontal diseases categories:
[2] [1]

and have traditionally been divided into two

1. gingivitis or 2. periodontitis.

Periodontitis is an infection of the periodontium²causing inflammation of the periodontal ligament, gingiva, cementum, and alveolar bone. It usually presents as a worsening of gingivitis. Symptoms are rare except with HIV or when abscesses develop, in which case pain and swelling are common. Diagnosis is based on inspection, periodontal probing, and x-rays. Treatment involves dental cleaning that extends under the gums and a vigorous home hygiene program. Advanced cases may require antibiotics and surgery.

Periodontitis usually develops when gingivitis, usually with abundant plaque and calculus beneath the gingival margin, has not been adequately treated. In periodontitis, the deep pockets can harbor anaerobic

organisms that do more damage than those usually present in simple gingivitis. The gingiva progressively loses its attachment to the teeth, periodontal pockets deepen, and bone loss begins. With progressive bone loss, teeth may loosen, and gingiva recedes. Tooth migration is common in later stages.

Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis:[1] 1. Localized aggressive periodontitis (LAP) 2. Generalized aggressive periodontitis (GAP) Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form.[2][3] The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis.

In contrast to chronic periodontitis, primary features that are common to both LAP and GAP are as follows:[4]    except for the presence of periodontal disease, patients are otherwise healthy rapid loss of attachment and bone destruction familial aggregation

Moreover, aggressive periodontitis often presents with the following secondary features:  

Amounts of microbial deposits are inconsistent with the severity of the periodontal tissue destruction elevated proportions of Aggregatibacter actinomycetemcomitans, and in some cases, of Porphyromonas gingivalis as well 

phagocyte abnormalities hyperresponsive macrophage phenotype, including elevated levels of prostaglandin E2 (PGE2) and interleukin 1 

progression of pathogenesis may be self limiting


vs. generalized forms of aggressive periodontitis

deep (vertical) bone loss. sometimes before age 3 yr. which show localized. usually shortly after eruption. the signs of inflammation are minor. Aggressive periodontitis may develop as early as childhood. Several studies suggest that these types of cases respond best to a combination of surgical debridement and antibiotics. Regenerative therapy with bone grafting procedures are often selected in these cases due to the favorable morphology of the bony defects which result from the disease. as follows:  Localized aggressive periodontitis     circumpubertal onset robust serum antibody response to infective agents: the dominant serotype antibody is IgG2[5] localized first molar/incisor presentation [4] Generalized aggressive periodontitis     usually affects patients under 30 years of age poor serum antibody response to infective agents pronounced episodic nature of periodontal destruction generalized presentation affecting at least 3 permanent teeth other than first molars and incisors Severity of periodontal tissue destruction is subclassified in the same fashion as is chronic periodontitis.The 1999 Consensus Report published by the American Academy of Periodontology permitted the subdivision of aggressive periodontal disease into localized and generalized forms based on enough individually specific features. In one type of aggressive periodontitis that occurs in healthy adolescents (formerly called localized juvenile periodontitis). its clinical significance is unknown. The disease is detected by periodontal probing or x-rays. Neutrophil function may be defective in aggressive periodontitis. collectively known as aggressive periodontitis. An uncommon type of aggressive periodontitis (formerly called prepubertal periodontitis) affects deciduous teeth. Typically. patients often have significant colonization ofActinobacillus actinomycetemcomitans. [edit]Treatment Treatment generally involves mechanical therapy (non-surgical or surgical debridement) in conjunction with antibiotics. commonly limited to the 1st molars and incisors. Patients may have severe bone loss. often at a rate of 3 to 4 m/day. Aggressive periodontitis: Several more rapidly progressive subtypes of chronic periodontitis exist. Patients also have frequent bouts of otitis media and are usually . Generalized acute proliferative gingivitis and rapid alveolar bone destruction are its hallmarks. even tooth loss. by age 20. Bone loss progresses faster than in adult periodontitis.

A common regimen isamoxicillin . the disease resolves before the permanent teeth erupt. If pockets are no deeper than 4 mm at this point. Thorough home oral hygiene is necessary. removal of diseased or toxin-affected cementum and dentin followed by smoothing of the root) to remove plaque and calculus deposits. Treatment y y y Scaling and root planing Sometimes oral antibiotics. and exudate are characteristic. swelling.Porphyromonas gingivalis. it resembles acute necrotizing ulcerative gingivitis (see Common Dental Disorders: Acute Necrotizing Ulcerative Gingivitis (ANUG)) combined with rapidly progressive periodontitis. HIV-associated periodontitis is a particularly virulent. Abundant plaque along with redness. the first phase of treatment consists of thorough scaling and root planing (ie. Impaction of food in the pockets can cause pain at meals. Symptoms and Signs Pain is usually absent unless an acute infection forms in one or more periodontal pockets or if HIVassociated periodontitis is present. If deeper pockets persist. and many gram-negative bacilli. Gums may be tender and bleed easily. In some patients. and breath may be foul. Treatment regimens are under study.diagnosed by age 4 yr. rapidly progressing disease. It is often associated with A. antibiotic packs. or both Surgery or extraction For all forms of periodontitis. The patient is reevaluated after 3 wk. Dental x-rays reveal alveolar bone loss adjacent to the periodontal pockets. Some cases result from undiagnosed localized juvenile periodontitis or prepubertal periodontitis. Eikenella corrodens. but others appear independently. Patients may lose 9 to 12 mm of attachment in as little as 6 mo. The prototypical aggressive periodontitis (formerly called rapidly progressive periodontitis) occurs in patients aged 20 to 35 yr. Pockets deeper than 4 mm indicate periodontitis. Diagnosis y y Clinical evaluation Sometimes dental x-rays Inspection of the teeth and gingiva combined with probing of the pockets and measurement of their depth are usually sufficient for diagnosis. the only treatment needed is regular cleanings. Clinically. actinomycetemcomitans. but cause and effect are not clear. systemic antibiotics can be used.

amoxicillin 500 mg qid or metronidazole 250 mg tid for 14 days). In selected situations. usually metronidazole 250 mg po tid for 14 days. Ninety percent of patients with HIV-associated periodontitis respond to irrigation of the sulcus with povidone-iodine (which the dentist applies with a syringe). Splinting of loose teeth and selective reshaping of tooth surfaces to eliminate traumatic occlusion may be necessary. Localized juvenile periodontitis requires periodontal surgery plus oral antibiotics (eg. regenerative surgery and bone grafting are done to encourage alveolar bone growth. . In addition.500 mg po qid for 10 days. a gel containing doxycycline or microspheres of minocycline can be placed into isolated recalcitrant pockets. and systemic antibiotics. regular use of chlorhexidine mouth rinses. Another approach is to surgically eliminate the pocket and recontour the bone so that the patient can clean the depth of the sulcus (pocket reduction/elimination surgery). These are resorbed in 2 wk. Contributing systemic factors should be controlled before initiating periodontal therapy. Extractions are often necessary in advanced disease.

Localized Localized Aggressive Periodontitis Clinical appearance: extreme bone loss around 1st molars and incisors. no plaque or inflammation. large percentage of neutrophils with slow chemotactic response Microbiology: Aa Histopathology: neutrophils with slow chemotactic response Radiographic features: extreme bone loss around 1st molars and incisors . good OH Etiology: Aa. loose. drifting teeth.

inflammation IS present with heavy plaque and calculus . often younger than 20 Treatment/Prognosis: mechanical debridement.Diagnosis: radiographs and probing. periodontal surgery Generalized Aggressive Periodontitis Clinical appearance: affects most or all the teeth with 1st molars and incisors being the most severely involved. systemic antibiotics (tetracycline).

Etiology: neutrophil chemotactic disorder .

A. Eikenella corrodens.Microbiology: P. gingivalis. a .

periodontal surgery Aggressive Periodontitis Clinical Appearance: severe inflammation. antibiotic therapy. scaling and root planing. rapid bone loss.Diagnosis: generally younger than 20 Treatment/Prognosis: improved OH. and early tooth loss Etiology: white blood cell defects .

antibiotics may help but it usually slows rather than stops disease Prognosis: Poor.Radiographic features: advanced bone loss Treatment: responds poorly to conventional treatment such as scaling and root planing. individuals with prepubertal gingivitis frequently become edentulous at an early ag Chronic Periodontitis Clinical Appearance: pockets .





disease activity/patient resistance Microbiology: multibacterial.Etiology: plaque and calculus. primary = Porphyromonas gingivalis .

Histopathology: attachment loss. bone resorption Radiographic features: horizontal bone loss .

education. control of associated factors .Diagnosis: probing depth Treatment and prognosis: remove local etiologic factors.

465.[align=center] [/align] Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that is caused by accumulation of profuse amounts of dental plaque.4 DiseasesDB ? MeSH C07.714.3 ICD-9 523.533. Chronic periodontitis Classification and external resources ICD-10 K05.324 Contents [hide] 1 Diagnosis .

[1] [edit]Signs and symptoms In the early stages. Symptoms may include the following:  Redness or bleeding of gums while brushing teeth. Subgingival calculus is a frequent finding. although this may be a symptom of progressing chronic periodontitis in that patient.)  Deep pockets between the teeth and the gums (pockets are sites where the attachment has been gradually destroyed by collagen-destroying enzymes. . known as collagenases)  Loose teeth. (This may also be caused by heavy handed brushing or with a stiff tooth brush. chronic periodontitis has few symptoms and in many individuals the disease has progressed significantly before they seek treatment. where there is no attachment loss)    Gum swelling that recurs Halitosis.2 Signs and symptoms 3 Pathology 4 Microbiology 5 Treatment 6 Adjunctive systemic antibiotic treatment 7 Locally delivered adjunctive antimicrobial treatment 8 Modulating the host response 9 Current controversies in chronic periodontal disease management 10 Cost/benefit analysis of treatment 11 Tentative links to other conditions 12 References 13 External links [edit]Diagnosis It is one of the seven destructive periodontal diseases as listed in the 1999 classification. or bad breath. resulting in apparent lengthening of teeth. using dental floss or biting into hard food (e. Patients sometimes assume that painless bleeding after teeth cleaning is insignificant. apples) (though this may occur even in gingivitis. in the later stages (though this may occur for other reasons as well) Gingival inflammation and bone destruction are often painless.g. and a persistent metallic taste in the mouth Gingival recession.

g. and gingival recession is the predominant lesion before 40 years. Measuring disease progression is carried out by measuring probing pocket depth (PPD) and bleeding indices using a periodontal probe. [5] . [4] Microaerophile bacteria Actinomyces actinomycetemcomitans.g. diabetes mellitus. the highest rate occurs between 50 and 60 years. [edit]Microbiology There are two views of the microbiology of periodontitis: the specific plaque hypothesis and the non specific plaque hypothesis. Discharge of pus. Bleeding on probing is considered to be a sign of active disease. The disease may be modified by and be associated with systemic diseases (e. Fusobacterium nucleatum. Prevotella intermedia. cathepsins. Major drivers of this aggressive tissue destruction are matrix metalloproteinases (MMPs).There is a slow to moderate rate of disease progression but the patient may have periods of rapid progression ("bursts of destruction"). In response to endotoxin derived fromperiodontal pathogens. Bacteroides forsythus. tooth-related or iatrogenic factors).. the incidence of incipient periodontal destruction increases with age. Age is related to the incidence of periodontal destruction: ". and other osteoclastderived enzymes. Chronic periodontitis can be associated with local predisposing factors(e. lack of oral hygiene with inadequate plaque biofilm control. [3] Anaerobic species of bacteria Porphyromonas gingivalis. HIV infection) It can also be modified by factors other than systemic disease such as smoking and emotional stress. Eubacterium species have all been implicated in chronic periodontitis. Pockets greater than 3mm in depth are considered to be unhealthy."[2] [edit]Pathology Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response. Treponema denticola. while periodontal pocketing is the principal mode of destruction between 50 and 60 years of a well-maintained population who practises oral home care and has regular check-ups. involvement of the root furcation area and deeper pocketing may all indicate reduced prognosis for an individual tooth.. Major risk factors: Smoking. Campylobacter rectus. several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. The disease is associated with a variable microbial pattern. and Eikenella corrodens also may play a role in chronic periodontitis. which results in bone and soft tissue destruction.

[edit]Treatment There is professional agreement among dentists that smoking cessation and good oral hygiene are key to effective treatment and positive outcomes for patients. the factors affecting outcomes are unclear from the literature and these might include study conduct issues such as bias. less increase in gingival recession and more gain in hard tissue probing at re-entry surgery. Whilst there is evidence that GTR can demonstrate a significant improvement over conventional open flap surgery. In fact it is more effective than supragingival plaque control alone".1 mm) and probing pocket depth . As a result. This must be weighed against the risks of surgery.and complexity: "GTR has a greater effect on probing measures of periodontal treatment than open flap debridement. The typical initial treatment known to be effective is scaling and root planing (SRP) to mechanically debride the depths of the periodontal pocket and disturb the biofilm present. This is done using a powered ultrasonic or sonic scaler or unpowered hand instruments. despite its cost. The advantages of this approach is better visualization of the root surface to be cleaned. including improved attachment gain. EMD significantly improved probing attachment levels (1."[7] Open flap debridement is used by some practitioners particularly in deeper pocket areas. reduced pocket depth. However."[8] Guided tissue regeneration (GTR) using PTFE membranes is favoured by some practitioners."[9] Enamel matrix derivative (EMD) is favoured by some practitioners despite its high cost: "One year after its application. Open flap surgery is more effective than non-surgical periodontal therapy in deep pocketing : "Both scaling and root planing alone and scaling and root planing combined with flap procedure are effective methods for the treatment of chronic periodontitis in terms of attachment level gain and reduction in gingival inflammation. patients and health professionals need to consider the predictability of the technique compared with other methods of treatment before making final decisions on use. "In patients with chronic periodontitis. it is difficult to draw general conclusions about the clinical benefit of GTR. these additional improvements were only modest and there was only a very limited number of studies available for comparison. subgingival debridement (in conjunction with supragingival plaque control) is an effective treatment in reducing probing pocket depth and improving the clinical attachment level. In the treatment of deep pockets open flap debridement results in greater PPD reduction and clinical attachment gain.[6] Full mouth disinfection protocols are favoured by some clinicians: "In patients with chronic periodontitis in moderately deep pockets slightly more favourable outcomes for pocket reduction and gain in probing attachment were found following FMD compared to control. Therefore. However there is marked variability between studies and the clinical relevance of these changes is unknown. thus limiting general conclusions about the clinical benefit of full-mouth disinfection.

Whether such improvements. the high degree of heterogeneity observed among trials suggests that results have to be interpreted with great caution. can benefit more from this adjunctive therapy. [edit]Modulating the host response Sub-antimicrobial doses of doxycycline (SDD) have been used to alter host response to the periodontal pathogens. Chlorhexidine impregnated chips are also available. are clinically meaningful remains a question. "Among the locally administered adjunctive antimicrobials. there was no evidence of clinically important differences between GTR and EMD.. Bone substitutes may be associated with less gingival recession than EMD. can offer an additional benefit over SRP alone in the treatment of periodontitis. a sensitivity analysis indicated that the overall treatment effect might be overestimated. progressive or 'active' disease.. This is believed to disrupt the action of matrix metalloproteinases and thus minimise host mediated tissue destruction. differences in study methodology and lack of data precluded an adequate and complete pooling of data for a more comprehensive analyses."[13] . metronidazole. Adjunctive local therapy generally reduced PD levels. although patients with deep pockets."[11] [edit]Locally delivered adjunctive antimicrobial treatment Chemical antimicrobials may be used by the clinician to help reduce the bacterial load in the diseased pocket. minocycline. even if statistically significant. or specific microbiological profile. and reduced risk of additional CAL loss.." [edit]Adjunctive [10] systemic antibiotic treatment Systemic antibiotics such as amoxicillin or metronidazole are sometimes used in addition to debridement based treatments.reduction (0. The actual clinical advantages of using EMD are unknown." [12] Minocycline is typically delivered via slim syringe applicators. in terms of clinical attachment loss (CAL) and probing pocket depth (PPD) change. however. and chlorhexidine. "The adjunctive use of SDD with SRP is statistically more effective than SRP alone in reducing PD and in achieving CAL gain. With the exception of significantly more postoperative complications in the GTR group. It was difficult to establish definitive conclusions. However. In addition. the most positive results occurred for tetracycline.9 mm) when compared to a placebo or control. "Systemic antimicrobials in conjunction with scaling and root planing (SRP).

J. Incidence. Clin. . Holdeman LV.g. 42 (2): 510±5. Infect. characteristics and time of occurrence of the initial periodontal lesion".[edit]Current controversies in chronic periodontal disease management "There is no good evidence to show whether routine scale and polishing prevents chronic periodontitis. Löe H. et al. implants or bridgework) even in periodontally impaired teeth. Periodontol. Immun.8% versus 11."[14] Lasers are increasingly being used in treatments for chronic periodontitis.30 (10): 902±8. "Development of a classification system for periodontal diseases and conditions.4:1-6.[17] There is little evidence linking progression of periodontal disease to low birth weight or preterm birth: "In these women with periodontitis and within this study's limitations."[16] = [edit]Tentative links to other conditions There is only very weak evidence linking to coronary heart disease. II. ^ Armitage. PMC 264458." Ann Perio 1999. Ranney RR (November 1983). "Clinical course of chronic periodontitis.[19] References 1. disease progression was not associated with an increased risk for delivering a pre-term or a low birthweight infant. "Bacteriology of moderate (chronic) periodontitis in mature adult humans". ^ Moore WE."[15] [edit]Cost/benefit analysis of treatment "Costs for tooth retention via supportive periodontal therapy are relatively low compared with alternatives (e. 3. 2. P = 0. ^ Heitz-Mayfield LJ. (October 2003)."[18] There is recently emerged evidence linking chronic periodontitis with head and neck squamous cell carcinoma: "Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than t hose without periodontitis (32.038)".5%. PMID 14710770.PMID 6642641. Smibert RM. However there is some controversy over their use: "No consistent evidence supports the efficacy of laser treatment as an adjunct to non-surgical periodontal treatment in adults with chronic periodontitis. GC. Schätzle M. Burmeister JA. Cato EP.

29.pub310. Vol.14. ^ Herrera D. Jepsen S. ^ Heitz-Mayfield LJ.4. ^ Clinical Microbiology Reviews.pub310. 8.1128/CMR.pub210.2001 Periodontal Disease as a Specific. Gunsolley JC (December 2003).pub210. albeit Chronic. 14. "A systematic review of the effect of surgical debridement vs non-surgical debridement for the treatment of chronic periodontitis".pub3.727-752. AJ et al (August 2005). and bone-sparing agents.* and Natalie S. A systematic review". Worthington HV (2009). 4 0893-8512/01/$04. Tucker RJ (2006).doi:10. p.2. Loesche1.1002/14651858.14. J.1034/j. PMID 16625546. Periodontol. 29 (Suppl 3): 92±102. PMID 19821315.s3.CD001724. Periodontol.1002/14651858.12. 727-752. Worthington HV. Roldán S (2002). October 2001.doi:10.pub3.CD004622. J. Coulthard P. Sanz M. Timmerman MF.doi:10. Worthington HV (2008). PMID 18254056.1128/CMR.pub2. J. No. discussion 160±2.1. 11.00+0 DOI: 10. 14. Clarkson JE (2007).727-752. ^ Bonito. 7. "Enamel matrix derivative (Emdogain(R)) for periodontal tissue regeneration in intrabony defects". Geurs NC. 12. 727-752. 4 0893-8512/01/$04. Loesche1.CD001724.8.CD004625.4. Cochrane Database Syst Rev (4): CD003875.1902/annals.4. ^ Needleman IG.1600-051X. Heitz F. "Periodontal host modulation with antiproteinase. PMID 12787211. 14. discussion 160±2. Needleman I. 9. Giedrys-Leeper E. Papanikolaou N. Needleman I. Clin.doi:10.CD004622. "A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients". doi:10.2001 Periodontal Disease as a Specific.CD003875. 10. anti-inflammatory. Cochrane Database Syst Rev (4): CD004625. . ^ Eberhard J. Periodontol. Clin. 29 (Suppl 3): 136±59. Worthington HV. "A systematic review on the clinical efficacy of subgingival debridement in the treatment of chronic periodontitis". ^ Reddy MS. October 2001.doi:10. PMID 14971246. Infection: Diagnosis and Treatment Walter J. Clin.CD004625. albeit Chronic. Grossman2 6. ^ Beirne P. Moles D (2002). 13.1002/14651858. ^ Van der Weijden GA. "Guided tissue regeneration for periodontal infra-bony defects".* and Natalie S. Cochrane Database Syst Rev (1): CD004622. "Impact of Local Adjuncts to Scaling and Root Planing in Periodontal Disease Therapy: A Systematic Review".2. PMID 12787214. Journal of Periodontology 76. Ann. Infection: Diagnosis and Treatment Walter J. p. "Routine scale and polish for periodontal health in adults". Vol. Periodontol. "Full-mouth disinfection for the treatment of adult chronic periodontitis". Jervøe-Storm PM.CD003875. 8 (1): 12± 37. No. ^ Clinical Microbiology Reviews. Cochrane Database Syst Rev (2): CD001724. 8. No. Jepsen S.pub2.00+0 DOI: 10.x.1002/14651858. Needleman I.2003. ^ Esposito M.1002/14651858.1002/14651858. 29 (S3): 55± 71.1002/14651858. PMID 17943824. Grusovin MG. Trombelli L.3.1002/14651858. Grossman2 5.

Clin. et al.1902/jop. 36 (8): 669± 76. "Change in periodontitis during pregnancy and the risk of pre-term birth and low birthweight". ^ Karlsson MR.x. 79 (11): 2021±8. Biomarkers Prev. "The effect of laser therapy as an adjunct to non-surgical periodontal treatment in subjects with chronic periodontitis: a systematic review". "Effort and costs of tooth preservation in supportive periodontal treatment in a German population".1111/j. Cosgarea R. Hodges JS. (September 2009). PMID 19566541. (April 2009). et al. 36 (4): 308±14. PMID 12085722. ^ Tezal M. Diogo Löfgren CI. et al. J. 17.doi:10. doi:10. Jansson HM (November 2008). Periodontol. J. ^ Michalowicz BS.15.2008.1111/j. Novak MJ. Clin. J Am Dent Assoc 133 (Suppl): 31S±36S.01409. 18. 16. PMID 19745222.2009. Wiedemann D. (August 2009). Hyland A.1600051X.1600-051X.doi:10. PMID 18980508. 19.doi:10. ^ Hujoel PP (June 2002). 18 (9): 2406± 12. PMID 19426177.01385. Cancer Epidemiol. ^ Pretzl B. Periodontol. Sullivan MA. "Chronic periodontitis and the incidence of head and neck squamous cell carcinoma". .1158/1055-9965.080197.2009.EPI-09-0334.J. Periodontol. "Does chronic periodontitis cause coronary heart disease? A review of the literature".x.

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