Chronic periodontitis

Chronic periodontitis

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.

Chronic periodontitis
Classification and external resources
ICD-10 K05.3
ICD-9 523.4
DiseasesDB 29362
MeSH D055113



It is one of the seven destructive periodontal diseases as listed in the 1999 classification.[1]

Signs and symptoms

In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following:

  • Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g. apples) (though this may occur even in gingivitis, where there is no attachment loss)
  • Gum swelling that recurs
  • Halitosis, or bad breath, and a persistent metallic taste in the mouth
  • Gingival recession, resulting in apparent lengthening of teeth. (This may also be caused by heavy handed brushing or with a stiff tooth brush.)
  • 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, in the later stages (though this may occur for other reasons as well)

Gingival inflammation and bone destruction are often painless. Patients sometimes assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing chronic periodontitis in that patient.

Subgingival calculus is a frequent finding.

There is a slow to moderate rate of disease progression but the patient may have periods of rapid progression ("bursts of destruction"). Chronic periodontitis can be associated with local predisposing factors(e.g. tooth-related or iatrogenic factors). The disease may be modified by and be associated with systemic diseases (e.g. diabetes mellitus, HIV infection) It can also be modified by factors other than systemic disease such as smoking and emotional stress.

Major risk factors: Smoking, lack of oral hygiene with inadequate plaque biofilm control.

Measuring disease progression is carried out by measuring probing pocket depth (PPD) and bleeding indices using a periodontal probe. Pockets greater than 3mm in depth are considered to be unhealthy. Bleeding on probing is considered to be a sign of active disease. Discharge of pus, involvement of the root furcation area and deeper pocketing may all indicate reduced prognosis for an individual tooth.

Age is related to the incidence of periodontal destruction: " a well-maintained population who practises oral home care and has regular check-ups, the incidence of incipient periodontal destruction increases with age, the highest rate occurs between 50 and 60 years, and gingival recession is the predominant lesion before 40 years, while periodontal pocketing is the principal mode of destruction between 50 and 60 years of age."[2]


Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. Major drivers of this aggressive tissue destruction are matrix metalloproteinases (MMPs), cathepsins, and other osteoclast-derived enzymes.


There are two views of the microbiology of periodontitis: the specific plaque hypothesis and the non specific plaque hypothesis.

The disease is associated with a variable microbial pattern.[3]

Anaerobic species of bacteria Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eubacterium sp. have all been implicated in chronic periodontitis.[4]

Microaerophile bacteria Actinomyces actinomycetemcomitans, Campylobacter rectus, and Eikenella corrodens also may play a role in chronic periodontitis.[4]


There is professional agreement among dentists that smoking cessation and good oral hygiene are key to effective treatment and positive outcomes for patients.

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. "In patients with chronic periodontitis, subgingival debridement (in conjunction with supragingival plaque control) is an effective treatment in reducing probing pocket depth and improving the clinical attachment level. In fact it is more effective than supragingival plaque control alone".[5]

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. However, these additional improvements were only modest and there was only a very limited number of studies available for comparison, thus limiting general conclusions about the clinical benefit of full-mouth disinfection."[6]

Open flap debridement is used by some practitioners particularly in deeper pocket areas. The advantages of this approach is better visualization of the root surface to be cleaned. This must be weighed against the risks of surgery. 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. In the treatment of deep pockets open flap debridement results in greater PPD reduction and clinical attachment gain."[7]

Guided tissue regeneration (GTR) using PTFE membranes is favoured by some practitioners, despite its cost and complexity: "GTR has a greater effect on probing measures of periodontal treatment than open flap debridement, including improved attachment gain, reduced pocket depth, less increase in gingival recession and more gain in hard tissue probing at re-entry surgery. However there is marked variability between studies and the clinical relevance of these changes is unknown. As a result, it is difficult to draw general conclusions about the clinical benefit of GTR. Whilst there is evidence that GTR can demonstrate a significant improvement over conventional open flap surgery, the factors affecting outcomes are unclear from the literature and these might include study conduct issues such as bias. Therefore, patients and health professionals need to consider the predictability of the technique compared with other methods of treatment before making final decisions on use."[8]

Enamel matrix derivative (EMD) is favoured by some practitioners despite its high cost: "One year after its application, EMD significantly improved probing attachment levels (1.1 mm) and probing pocket depth reduction (0.9 mm) when compared to a placebo or control, however, the high degree of heterogeneity observed among trials suggests that results have to be interpreted with great caution. In addition, a sensitivity analysis indicated that the overall treatment effect might be overestimated. The actual clinical advantages of using EMD are unknown. With the exception of significantly more postoperative complications in the GTR group, there was no evidence of clinically important differences between GTR and EMD. Bone substitutes may be associated with less gingival recession than EMD." [9]

Adjunctive systemic antibiotic treatment

Systemic antibiotics such as amoxicillin or metronidazole are sometimes used in addition to debridement based treatments.

"Systemic antimicrobials in conjunction with scaling and root planing (SRP), can offer an additional benefit over SRP alone in the treatment of periodontitis, in terms of clinical attachment loss (CAL) and probing pocket depth (PPD) change, and reduced risk of additional CAL loss. However, differences in study methodology and lack of data precluded an adequate and complete pooling of data for a more comprehensive analyses. It was difficult to establish definitive conclusions, although patients with deep pockets, progressive or 'active' disease, or specific microbiological profile, can benefit more from this adjunctive therapy."[10]

Locally delivered adjunctive antimicrobial treatment

Chemical antimicrobials may be used by the clinician to help reduce the bacterial load in the diseased pocket.

"Among the locally administered adjunctive antimicrobials, the most positive results occurred for tetracycline, minocycline, metronidazole, and chlorhexidine. Adjunctive local therapy generally reduced PD levels....Whether such improvements, even if statistically significant, are clinically meaningful remains a question." [11]

Minocycline is typically delivered via slim syringe applicators. Chlorhexidine impregnated chips are also available.

Modulating the host response

Sub-antimicrobial doses of doxycycline (SDD) have been used to alter host response to the periodontal pathogens. This is believed to disrupt the action of matrix metalloproteinases and thus minimise host mediated tissue destruction.

"The adjunctive use of SDD with SRP is statistically more effective than SRP alone in reducing PD and in achieving CAL gain."[12]

Current controversies in chronic periodontal disease management

"There is no good evidence to show whether routine scale and polishing prevents chronic periodontitis."[13]

Lasers are increasingly being used in treatments for chronic periodontitis. 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."[14]

Costs of treatment

"Costs for tooth retention via supportive periodontal therapy are relatively low compared with alternatives (e.g. implants or bridgework) even in periodontally impaired teeth.".[15] However, health outcomes of periodontal therapy are not directly comparable with those from implants or bridgework.[16]

Tentative links to other conditions

There is only very weak evidence linking to coronary heart disease.[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, disease progression was not associated with an increased risk for delivering a pre-term or a low birthweight infant."[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 those without periodontitis (32.8% versus 11.5%; P = 0.038)".[19]


  1. ^ Armitage GC (1999). "Development of a classification system for periodontal diseases and conditions". Ann. Periodontol. 4 (1): 1–6. doi:10.1902/annals.1999.4.1.1. PMID 10863370. 
  2. ^ Heitz-Mayfield LJ, Schätzle M, Löe H, et al. (October 2003). "Clinical course of chronic periodontitis. II. Incidence, characteristics and time of occurrence of the initial periodontal lesion". J. Clin. Periodontol. 30 (10): 902–8. doi:10.1034/j.1600-051X.2003.00399.x. PMID 14710770. 
  3. ^ Moore WE, Holdeman LV, Cato EP, Smibert RM, Burmeister JA, Ranney RR (November 1983). "Bacteriology of moderate (chronic) periodontitis in mature adult humans". Infect. Immun. 42 (2): 510–5. PMC 264458. PMID 6642641. 
  4. ^ a b Loesche WJ, Grossman NS (October 2001). "Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment". Clin. Microbiol. Rev. 14 (4): 727–52, table of contents. doi:10.1128/CMR.14.4.727-752.2001. PMC 89001. PMID 11585783. 
  5. ^ Van der Weijden GA, Timmerman MF (2002). "A systematic review on the clinical efficacy of subgingival debridement in the treatment of chronic periodontitis". J. Clin. Periodontol. 29 (S3): 55–71. doi:10.1034/j.1600-051X.29.s3.3.x. 
  6. ^ Eberhard J, Jepsen S, Jervøe-Storm PM, Needleman I, Worthington HV (2008). Eberhard, Jörg. ed. "Full-mouth disinfection for the treatment of adult chronic periodontitis". Cochrane Database Syst Rev (1): CD004622. doi:10.1002/14651858.CD004622.pub2. PMID 18254056. 
  7. ^ Heitz-Mayfield LJ, Trombelli L, Heitz F, Needleman I, Moles D (2002). "A systematic review of the effect of surgical debridement vs non-surgical debridement for the treatment of chronic periodontitis". J. Clin. Periodontol. 29 (Suppl 3): 92–102; discussion 160–2. doi:10.1034/j.1600-051X.29.s3.5.x. PMID 12787211. 
  8. ^ Needleman IG, Worthington HV, Giedrys-Leeper E, Tucker RJ (2006). Needleman, Ian. ed. "Guided tissue regeneration for periodontal infra-bony defects". Cochrane Database Syst Rev (2): CD001724. doi:10.1002/14651858.CD001724.pub2. PMID 16625546. 
  9. ^ Esposito M, Grusovin MG, Papanikolaou N, Coulthard P, Worthington HV (2009). Esposito, Marco. ed. "Enamel matrix derivative (Emdogain(R)) for periodontal tissue regeneration in intrabony defects". Cochrane Database Syst Rev (4): CD003875. doi:10.1002/14651858.CD003875.pub3. PMID 19821315. 
  10. ^ Herrera D, Sanz M, Jepsen S, Needleman I, Roldán S (2002). "A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients". J. Clin. Periodontol. 29 (Suppl 3): 136–59; discussion 160–2. doi:10.1034/j.1600-051X.29.s3.8.x. PMID 12787214. 
  11. ^ Bonito AJ, Lux L, Lohr KN (August 2005). "Impact of local adjuncts to scaling and root planing in periodontal disease therapy: a systematic review". J. Periodontol. 76 (8): 1227–36. doi:10.1902/jop.2005.76.8.1227. PMID 16101353. 
  12. ^ Reddy MS, Geurs NC, Gunsolley JC (December 2003). "Periodontal host modulation with antiproteinase, anti-inflammatory, and bone-sparing agents. A systematic review". Ann. Periodontol. 8 (1): 12–37. doi:10.1902/annals.2003.8.1.12. PMID 14971246. 
  13. ^ Beirne P, Worthington HV, Clarkson JE (2007). Beirne, Paul V. ed. "Routine scale and polish for periodontal health in adults". Cochrane Database Syst Rev (4): CD004625. doi:10.1002/14651858.CD004625.pub3. PMID 17943824. 
  14. ^ Karlsson MR, Diogo Löfgren CI, Jansson HM (November 2008). "The effect of laser therapy as an adjunct to non-surgical periodontal treatment in subjects with chronic periodontitis: a systematic review". J. Periodontol. 79 (11): 2021–8. doi:10.1902/jop.2008.080197. PMID 18980508. 
  15. ^ Pretzl B, Wiedemann D, Cosgarea R, et al. (August 2009). "Effort and costs of tooth preservation in supportive periodontal treatment in a German population". J. Clin. Periodontol. 36 (8): 669–76. doi:10.1111/j.1600-051X.2009.01409.x. PMID 19566541. 
  16. ^ Pennington M, et al. (August 2009). "Making the leap from cost analysis to cost-effectiveness". J. Clin. Periodontol. 36 (8): 667–668. doi:10.1111/j.1600-051X.2009.01424.x. 
  17. ^ Hujoel PP (June 2002). "Does chronic periodontitis cause coronary heart disease? A review of the literature". J Am Dent Assoc 133 (Suppl): 31S–36S. PMID 12085722. 
  18. ^ Michalowicz BS, Hodges JS, Novak MJ, et al. (April 2009). "Change in periodontitis during pregnancy and the risk of pre-term birth and low birthweight". J. Clin. Periodontol. 36 (4): 308–14. doi:10.1111/j.1600-051X.2009.01385.x. PMC 2741139. PMID 19426177. 
  19. ^ Tezal M, Sullivan MA, Hyland A, et al. (September 2009). "Chronic periodontitis and the incidence of head and neck squamous cell carcinoma". Cancer Epidemiol. Biomarkers Prev. 18 (9): 2406–12. doi:10.1158/1055-9965.EPI-09-0334. PMID 19745222. 

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