Periodontitis

Periodontal disease
Classification and external resources

This radiograph shows significant bone loss between the two roots of a tooth. The spongy bone has receded due to infection under tooth, reducing the bony support for the tooth.
ICD-10 K05.4
DiseasesDB 29362
MedlinePlus 001059
MeSH D010518

Periodontitis is a set of inflammatory diseases affecting the periodontium — that is, the tissues that surround and support the teeth. Periodontitis involves progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the loosening and subsequent loss of teeth. Periodontitis is caused by microorganisms that adhere to and grow on the tooth's surfaces, along with an overly aggressive immune response against these microorganisms. A diagnosis of periodontitis is established by inspecting the soft gum tissues around the teeth with a probe (i.e. a clinical exam) and by evaluating the patient's x-ray films (i.e. a radiographic exam), to determine the amount of bone loss around the teeth. Specialists in the treatment of periodontitis are periodontists; their field is known as "periodontology" or "periodontics".

The word "periodontitis" comes from peri ("around"), odont ("tooth") and -itis ("inflammation").

Contents

Classification

The 1999 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases,[1] of which the last six are termed destructive periodontal disease because they are essentially irreversible. The seven categories are as follows:

  1. Gingivitis
  2. Chronic periodontitis
  3. Aggressive periodontitis
  4. Periodontitis as a manifestation of systemic disease
  5. Necrotizing ulcerative gingivitis/periodontitis
  6. Abscesses of the periodontium
  7. Combined periodontic-endodontic lesions

Moreover, terminology expressing both the extent and severity of periodontal diseases are appended to the terms above to denote the specific diagnosis of a particular patient or group of patients.

Extent

The extent of disease refers to the proportion of the dentition affected by the disease in terms of percentage of sites. Sites are defined as the positions at which probing measurements are taken around each tooth and, generally, six probing sites around each tooth are recorded, as follows:

  1. mesiobuccal
  2. mid-buccal
  3. distobuccal
  4. mesiolingual
  5. mid-lingual
  6. distolingual

If up to 30% of sites in the mouth are affected, the manifestation is classification as localized; for more than 30%, the term generalized is used.

Severity

The severity of disease refers to the amount of periodontal ligament fibers that have been lost, termed clinical attachment loss. According to the American Academy of Periodontology, the classification of severity is as follows:[2]

Signs and symptoms

Periodontitis manifesting as painful, red, swollen gums, with abundant plaque.

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

Patients should realize that the gingival inflammation and bone destruction are largely painless. Hence, people may wrongly assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that patient.

Effects outside the mouth

Periodontitis has been linked to increased inflammation in the body such as indicated by raised levels of C-reactive protein and Interleukin-6.[3] It is through this linked to increased risk of stroke,[4][5] myocardial infarction,[6] and atherosclerosis.[7] It also linked in those over 60 years of age to impairments in delayed memory and calculation abilities.[8]

Cause

Periodontitis is an inflammation of the periodontium—the tissues that support the teeth. The periodontium consists of four tissues:

This X-ray film displays two lone-standing mandibular teeth, the lower left first premolar and canine, exhibiting severe bone loss of 30–50%. Widening of the periodontal ligament surrounding the premolar is due to secondary occlusal trauma.

The primary etiology (cause) of gingivitis is poor oral hygiene which leads to the accumulation of a mycotic [9][10][11] and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes. New finger nick tests have been approved by the Food and Drug Administration in the US, and are being used in dental offices to identify and screen patients for possible contributory causes of gum disease such as diabetes.

In some people, gingivitis progresses to periodontitis - with the destruction of the gingival fibers, the gum tissues separate from the tooth and deepened sulcus, called a periodontal pocket. Subgingival microorganism (those that exist under the gum line) colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss. Examples of secondary etiology are those things that, by definition, cause microbic plaque accumulation, such as restoration overhangs and root proximity.

The excess restorative material that exceeds the natural contours of restored teeth, such as these, are termed "overhangs", and serve to trap microbic plaque, potentially leading to localized periodontitis.

If left undisturbed, microbic plaque calcifies to form calculus, which is commonly called tartar. Calculus above and below the gum line must be removed completely by the dental hygienist or dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and periodontitis is the microbic plaque that adheres to the tooth surface, there are many other modifying factors. A very strong risk factor is one's genetic susceptibility. Several conditions and diseases, including Down syndrome, diabetes, and other diseases that affect one's resistance to infection also increase susceptibility to periodontitis.

Another factor that makes periodontitis a difficult disease to study is that human host response can also affect the alveolar bone resorption. Host response to the bacterial-mycotic insult is mainly determined by genetics; however, immune development may play some role in susceptibility.

Prevention

Daily oral hygiene measures to prevent periodontal disease include:

Typically dental hygienists (or dentists) use special instruments to clean (debride) teeth below the gumline and disrupt any plaque growing below the gumline. This is a standard treatment to prevent any further progress of established periodontitis. Studies show that after such a professional cleaning (periodontal debridement), microbic plaque tend to grow back to pre-cleaning levels after about 3–4 months. Hence, in theory, cleanings every 3–4 months might be expected to also prevent the initial onset of periodontitis. However, analysis of published research has reported little evidence either to support this or the intervals at which this should occur.[12] Instead, it is advocated that the interval between dental check-ups should be determined specifically for each patient between every 3 to 24 months.[13][14]

Nonetheless, the continued stabilization of a patient's periodontal state depends largely, if not primarily, on the patient's oral hygiene at home as well as on the go. Without daily oral hygiene, periodontal disease will not be overcome, especially if the patient has a history of extensive periodontal disease.

Periodontal disease and tooth loss are associated with an increased risk of cancer [15].

A contributing cause may be low selenium in the diet: "Results showed that selenium has the strongest association with gum disease, with low levels increasing the risk by 13 fold." [16]

Management

This section from a panoramic X-ray film depicts the teeth of the lower left quadrant, exhibiting generalized severe bone loss of 30–80%. The red line depicts the existing bone level, whereas the yellow line depicts where the gingiva was originally (1–2 mm above the bone), prior to the patient developing periodontal disease. The pink arrow, on the right, points to a furcation involvement, or the loss of enough bone to reveal the location at which the individual roots of a molar begin to branch from the single root trunk; this is a sign of advanced periodontal disease. The blue arrow, in the middle, shows up to 80% bone loss on tooth #21, and clinically, this tooth exhibited gross mobility. Finally, the peach oval, to the left, highlights the aggressive nature with which periodontal disease generally affects mandibular incisors. Because their roots are generally situated very close to each other, with minimal interproximal bone, and because of their location in the mouth, where plaque and calculus accumulation is greatest because of the pooling of saliva, mandibular anteriors suffer excessively. The split in the red line depicts varying densities of bone that contribute to a vague region of definitive bone height.

The cornerstone of successful periodontal treatment starts with establishing excellent oral hygiene. This includes twice daily brushing with daily flossing. Also the use of an interdental brush (called a Proxi-brush) is helpful if space between the teeth allows. Persons with dexterity problems such as arthritis may find oral hygiene to be difficult and may require more frequent professional care and/or the use of a powered tooth brush. Persons with periodontitis must realize that it is a chronic inflammatory disease and a lifelong regimen of excellent hygiene and professional maintenance care with a dentist/hygienist or periodontist is required to maintain affected teeth.

Initial therapy

Removal of microbic plaque and calculus is necessary to establish periodontal health. The first step in the treatment of periodontitis involves non-surgical cleaning below the gumline with a procedure called scaling and debridement. In the past, Root Planing was used (removal of cemental layer as well as calculus). This procedure involves use of specialized curettes to mechanically remove plaque and calculus from below the gumline, and may require multiple visits and local anesthesia to adequately complete. In addition to initial scaling and root planing, it may also be necessary to adjust the occlusion (bite) to prevent excessive force on teeth that have reduced bone support. Also it may be necessary to complete any other dental needs such as replacement of rough, plaque retentive restorations, closure of open contacts between teeth, and any other requirements diagnosed at the initial evaluation.

Reevaluation

Multiple clinical studies have shown that non-surgical scaling and root planing is usually successful if the periodontal pockets are shallower than 4–5 mm (See articles by Stambaugh RV, Int J Periodontics Rest Dent, 1981 or Waerhaug J, J Periodontol, 1978).[17][18][19] It is necessary for the dentist or hygienist to perform a reevaluation 4–6 weeks after the initial scaling and root planing, to determine if the treatment was successful in reducing pocket depths and eliminating inflammation. Pocket depths which remain after initial therapy of greater than 5-6mm with bleeding upon probing are indicate continued active disease and will very likely show further bone loss over time. This is especially true in molar tooth sites where furcations (areas between the roots) have been exposed.

Surgery

If non-surgical therapy is found to have been unsuccessful in managing signs of disease activity, periodontal surgery may be needed to stop progressive bone loss and regenerate lost bone where possible. There are many surgical approaches used in treatment of advanced periodontitis, including open flap debridement, osseous surgery, as well as guided tissue regeneration and bone grafting. The goal of periodontal surgery is access for definitive calculus removal and surgical management of bony irregularities which have resulted from the disease process to reduce pockets as much as possible. Long-term studies have shown that in moderate to advanced periodontitis, surgically treated cases often have less further breakdown over time and when coupled with a regular post-treatment maintenance regimen are successful in nearly halting tooth loss in nearly 85% of patients (Kaldahl WB, Long-term evaluation of periodontal therapy: II. Incidence of sites breaking down. J Periodontol. 1996 Feb;67(2):103–8. and Hirschfeld L, Wasserman B. A long-term survey of tooth loss in 600 treated periodontal patients. J Periodontol. 1978 May;49(5):225-37.

Maintenance

Once successful periodontal treatment has been completed, with or without surgery, an ongoing regimen of "periodontal maintenance" is required. This involves regular checkups and detailed cleanings every three months to prevent re-population of periodontitis-causing microorganism, and to closely monitor affected teeth so that early treatment can be rendered if disease recurs. Usually periodontal disease exist due to poor plaque control, therefore if the brushing techniques are not modified, a periodontal recurrence is probable.

Alternative treatments

Periodontitis has an inescapable relationship with subgingival calculus (tartar). The first step in any procedure is to eliminate calculus under the gum line, as it houses destructive anaerobic microorganisms that consume bone, gum and cementum (connective tissue) for food.

Most alternative “at-home” gum disease treatments involve injecting anti-microbial solutions, such as hydrogen peroxide, into periodontal pockets via slender applicators or oral irrigators. This process disrupts anaerobic microorganism colonies and is effective at reducing infections and inflammation when used daily. A number of potions and elixirs that are functionally equivalent to hydrogen peroxide are commercially available but at substantially higher cost. However, such treatments do not address calculus formations, and so are short-lived, as anaerobic microorganism colonies quickly regenerate in and around calculus.

In a new field of study, calculus formations are addressed on a more fundamental level. At the heart of the formation of subgingival calculus, growing plaque formations starve out the lowest members of the community, which calcify into calcium phosphate salts of the same shape and size of the original, organic bacilli. Calcium phosphate salts (unlike calcium phosphate; the primary component in teeth) are ionic and adhere to tooth surfaces via electrostatic attraction. Smaller, free-floating calcium phosphate salt particles are equally attracted to the same areas, as are additional calcified microorganism, growing calculus formations as unorganized, yet strong, “brick and mortar” matrices. The microscopic voids in calculus formations house new anaerobic microorganism, as does the top “diseased layer”.

Because the root cause of subgingival calculus development is ionic attraction, it was hypothesized that the introduction of oppositely charged particles around the formations may chelate calcium phosphate salt components away from the matrix, thus reducing the size of subgingival calculus formations. To accomplish this, a sequestering agent solution consisting partly of sodium tripolyphosphate (STPP) and sodium fluoride (charge -1) was tested on a patient with burnished and new subgingival calculus at a depth of 6 mm. The patient delivered the solution using an oral irrigator, once a day, for 60 days. The results were the successful elimination of all calculus formations studied.[20] This test was conducted using a subgingival endoscopic camera (perioscope) by an independent periodontist.

The promise of this new, alternative treatment is to keep subgingival calculus at bay, in concert with traditional periodontal treatments. In this way, periodontitis may be controlled by the patient, and complete restoration of dental health can be a collaborative effort between the patient and the dental professional.

Prognosis

Dentists and dental hygienists measure periodontal disease using a device called a periodontal probe. This is a thin "measuring stick" that is gently placed into the space between the gums and the teeth, and slipped below the gum-line. If the probe can slip more than 3 millimeters below the gum-line, the patient is said to have a gingival pocket if no migration of the epithelial attachment has occurred or a periodontal pocket if apical migration has occurred. This is somewhat of a misnomer, as any depth is in essence a pocket, which in turn is defined by its depth, i.e., a 2 mm pocket or a 6 mm pocket. However, it is generally accepted that pockets are self-cleansable (at home, by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if there is a pocket which is deeper than 3 mm around the tooth, at-home care will not be sufficient to cleanse the pocket, and professional care should be sought. When the pocket depths reach 6 and 7 mm in depth, the hand instruments and cavitrons used by the dental professionals may not reach deeply enough into the pocket to clean out the microbic plaque that cause gingival inflammation. In such a situation the bone or the gums around that tooth should be surgically altered or it will always have inflammation which will likely result in more bone loss around that tooth. An additional way to stop the inflammation would be for the patient to receive subgingival antibiotics (such as minocycline) or undergo some form of gingival surgery to access the depths of the pockets and perhaps even change the pocket depths so that they become 3 mm or less in depth and can once again be properly cleaned by the patient at home with his or her toothbrush.

If a patient has 7 mm or deeper pockets around their teeth, then they would likely risk eventual tooth loss over the years. If this periodontal condition is not identified and the patient remains unaware of the progressive nature of the disease then, years later, they may be surprised that some teeth will gradually become loose and may need to be extracted, sometimes due to a severe infection or even pain.

According to the Sri Lankan tea labourer study, in the absence of any oral hygiene activity, approximately 10% will suffer from severe periodontal disease with rapid loss of attachment (>2 mm/year). 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10% will not suffer any loss.[21][22]

Epidemiology

Disability-adjusted life year for peridontal disease per 100,000 inhabitants in 2004.[23]
     no data      less than 3.5      3.5-4      4-4.5      4.5-5      5-5.5      5.5-6      6-6.5      6.5-7      7-7.5      7.5-8      8-8.5      more than 8.5

Periodontitis is very common, and is widely regarded as the second most common disease worldwide, after dental decay, and in the United States has a prevalence of 30–50% of the population, but only about 10% have severe forms.

In Israeli population, individuals of Yemenite, North-African, Asian, or Mediterranean origin have higher prevalence of periodontal disease than individuals from European descent.[24] This could be attributed to genetic predisposition as well as social-cultural-behavioral differences (e.g., smoking, oral hygiene, access to dental treatment) between populations.[24]. However, individuals in Eastern Asia have the lowest incident of periodontal disease in the world.

In other animals

Periodontal disease is the most common disease found in dogs and affects more than 80% of dogs aged three years or older. The prevalence of periodontal disease in dogs increases with age but decreases with increasing body weight; therefore, toy and miniature breeds are more severely affected. Systemic disease may develop because the gums are very vascular (have a good blood supply). The blood stream carries these anaerobic microorganisms, and they are filtered out by the kidneys and liver, where they may colonize and create microabscesses. The microorganisms traveling through the blood may also attach to the heart valves, causing vegetative endocarditis (infected heart valves). Additional diseases that may result from periodontitis includes chronic bronchitis and pulmonary fibrosis.[25]

See also

Further reading

Footnotes

  1. Armitage, GC. "Development of a classification system for periodontal diseases and conditions." Ann Perio 1999;4:1-6.
  2. The Periodontal Disease Classification System of the American Academy of Periodontology — An Update
  3. D'Aiuto F, Parkar M, Andreou G, Suvan J, Brett PM, Ready D, Tonetti MS. (2004). Periodontitis and systemic inflammation: control of the local infection is associated with a reduction in serum inflammatory markers. J Dent Res. 83(2):156-60. PMID 14742655
  4. Pussinen PJ, Alfthan G, Jousilahti P, Paju S, Tuomilehto J. (2007). Systemic exposure to Porphyromonas gingivalis predicts incident stroke. Atherosclerosis. 193(1):222-8. PMID 16872615
  5. Pussinen PJ, Alfthan G, Rissanen H, Reunanen A, Asikainen S, Knekt P. (2004). Antibodies to periodontal pathogens and stroke risk. Stroke. 35(9):2020-3.PMID 15232116
  6. Pussinen PJ, Alfthan G, Tuomilehto J, Asikainen S, Jousilahti P. (2004). High serum antibody levels to Porphyromonas gingivalis predict myocardial infarction. Eur J Cardiovasc Prev Rehabil. 11(5):408-11. PMID 15616414
  7. Ford PJ, Gemmell E, Timms P, Chan A, Preston FM, Seymour GJ. (2007). Anti-P. gingivalis response correlates with atherosclerosis. J Dent Res. 86(1):35-40. PMID 17189460
  8. Noble JM, Borrell LN, Papapanou PN, Elkind MS, Scarmeas N, Wright CB. (2009). Periodontitis is associated with cognitive impairment among older adults: analysis of NHANES-III. J Neurol Neurosurg Psychiatry. 80(11):1206–11. PMID 19419981
  9. Aubrey Crich; Sawhney, RC; Rastogi, GK (1932). "Blastomycosis of the gingiva and jaw". Can Med Assoc J. 26 (6): 662–665. PMID PMC402380. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC402380/pdf/canmedaj00119-0016.pdf. 
  10. Urzúa B, Hermosilla G, Gamonal J, Morales-Bozo I, Canals M, Barahona S, Cóccola C, Cifuentes V. (2008). "Yeast diversity in the oral microbiota of subjects with periodontitis: Candida albicans and Candida dubliniensis colonize the periodontal pockets.". Med Mycol. 46 (8): 783–93. doi:10.1080/13693780802060899. PMID 18608938. http://www.ncbi.nlm.nih.gov/pubmed/18608938. 
  11. Matsuo T, Nakagawa H, Matsuo N. (1995). "Endogenous Aspergillus endophthalmitis associated with periodontitis.". Ophthalmologica 209 (2): 109–11. doi:10.1159/000310592. PMID 7746643. http://www.ncbi.nlm.nih.gov/pubmed/7746643. 
  12. Beirne P, Forgie A, Clarkson J, Worthington HV (2005). "Recall intervals for oral health in primary care patients". Cochrane Database for Systematic Reviews (2): CD004346. doi:10.1002/14651858.CD004346.pub2. ISSN 1469-493X. PMID 15846709. 
  13. National Institute for Health and Clinical Excellence (27 October 2004). "NICE guidance issued on frequency of dental check-ups". National Library for Health (UK). http://www.library.nhs.uk/oralhealth/viewResource.aspx?resID=64336. Retrieved 2006-05-07. 
  14. BBC News (27 October 2004). "Call for tailored dental checks - Routine six-monthly dental check-ups should become a thing of the past, new guidance recommends". http://newswww.bbc.net.uk/1/low/health/3950587.stm. Retrieved 2006-05-07. 
  15. Michaud DS, Liu Y, Meyer M, Giovannucci E, Joshipura K. (2008). "Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study.". Lancet Oncol. 9 (6): 550–8. doi:10.1016/S1470-2045(08)70106-2. PMID 18462995. PMC 2601530. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2601530/pdf/nihms51673.pdf. 
  16. First Evidence Found Of Link Between Gum Disease And High Alcohol Consumption, Low Dietary Antioxidants
  17. Stambaugh RV, Dragoo M, Smith DM, Carasali L (1981). "The limits of subgingival scaling". Int J Periodontics Restorative Dent 1 (5): 30–41. PMID 7047434. 
  18. Waerhaug J (January 1978). "Healing of the dento-epithelial junction following subgingival plaque control. I. As observed in human biopsy material". J Periodontol. 49 (1): 1–8. PMID 340634. 
  19. Waerhaug J (March 1978). "Healing of the dento-epithelial junction following subgingival plaque control. II: As observed on extracted teeth". J Periodontol. 49 (3): 119–34. PMID 288899. 
  20. http://www.youtube.com/watch?v=3wXaL-PkLqk
  21. Preus HR, Anerud A, Boysen H, Dunford RG, Zambon JJ, Loe H (1995). "The natural history of periodontal disease. The correlation of selected microbiological parameters with disease severity in Sri Lankan tea workers". J Clin Periodontol 22 (9): 674–8. doi:10.1111/j.1600-051X.1995.tb00825.x. PMID 7593696. 
  22. Ekanayaka A (1984). "Tooth mortality in plantation workers and residents in Sri Lanka". Community Dent Oral Epidemiol 12 (2): 128–35. doi:10.1111/j.1600-0528.1984.tb01425.x. PMID 6584263. 
  23. "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. http://www.who.int/entity/healthinfo/statistics/bodgbddeathdalyestimates.xls. 
  24. 24.0 24.1 Zadik Y, Bechor R, Shochat Z, Galor S (April 2008). "Ethnic origin and alveolar bone loss in Israeli adults" (in Hebrew). Refuat Hapeh Vehashinayim 25 (2): 19–22, 72. PMID 18780541. 
  25. Muller-Esnault, Susan, DVM. "Periodontal Disease in the Dog and Cat" (2009). http://www.critterology.com/articles/periodontal-disease-dog-and-cat

External links