Periodontitis

"Pyorrhea" redirects here. For the Polish band, see Pyorrhoea. For urine containing pus, see Pyuria.
Periodontitis

This radiograph shows significant bone loss between the two roots of a tooth (black region). The spongy bone has receded due to infection under tooth, reducing the bony support for the tooth.
Classification and external resources
Pronunciation Periodontitis /ˌpɛrioʊdɒnˈtaɪtɪs/, pyorrhea /ˌpaɪəˈriə/
Specialty Dentistry
ICD-10 K05.4
DiseasesDB 29362
MedlinePlus 001059
MeSH D010518

Periodontitis, also known as pyorrhea, is a set of inflammatory diseases affecting the periodontium, i.e., 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 over-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 examination) and by evaluating the patient's X-ray films (i.e., a radiographic examination), to determine the amount of bone loss around the teeth.[1] Specialists in the treatment of periodontitis are periodontists; their field is known as "periodontology" or "periodontics".

Classification

The 1999 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases,[2] of which 2-6 are termed destructive periodontal disease, because the damage is 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. midbuccal
  3. distobuccal
  4. mesiolingual
  5. midlingual
  6. distolingual

If up to 30% of sites in the mouth are affected, the manifestation is classified 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:[3]

Signs and symptoms

1: Total loss of attachment (clinical attachment loss, CAL) is the sum of 2: Gingival recession, and 3: Probing depth

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:

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

Associated medical conditions

Periodontitis has been linked to increased inflammation in the body, such as indicated by raised levels of C-reactive protein and interleukin-6.[4][5][6][7] It is linked through this to increased risk of stroke,[8][9] myocardial infarction,[10] and atherosclerosis.[11][12][13][14][15][16][17] It also linked in those over 60 years of age to impairments in delayed memory and calculation abilities.[18][19] Individuals with impaired fasting glucose and diabetes mellitus have higher degrees of periodontal inflammation, and often have difficulties with balancing their blood glucose level owing to the constant systemic inflammatory state, caused by the periodontal inflammation.[20][21] Although no causal association was proven, a recent study showed correlation between chronic periodontitis and erectile dysfunction.[22]

Causes

Periodontitis is an inflammation of the periodontium, i.e., 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 or ineffective oral hygiene, which leads to the accumulation of a mycotic[23][24][25][26] and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes.[27] Diabetics must be meticulous with their homecare to control periodontal disease.[28] New finger prick 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 micro-organisms (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.

Smoking is another factor that increases the occurrence of periodontitis, directly or indirectly,[29][30][31] and may interfere with or adversely affect its treatment.[32][33][34]

Ehlers–Danlos syndrome is a periodontitis risk factor and so is the Papillon-Lefèvre syndrome also known as palmoplantar keratoderma.

If left undisturbed, microbial 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 microbial plaque that adheres to the tooth surfaces, 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.

According to some researchers periodontitis may be associated with higher stress.[35] Periodontitis occurs more often in people from the lower end of the socioeconomic scale than people from the upper end of the socioeconomic scale.[36]

Mechanism

Biofilm image of chronic periodontitis patient with phase contrast microscope at low power 100x magnification on a salivary mount. About 20 black oval objects testifies of the presence of amoebae and their movement forming channels upon displacement. 1000x magnification would confirm diagnostic.

Another line of thinking was introduced in the early 1900s. This one proposes, following a microscopic examination of the biofilm, the existence of a definitive correlation between the presence of the amoeba Entamoeba gingivalis and active periodontal disease then called pyorrhea.[37] This notion has been highlighted half a century later and corroborated by demonstrating that gingival health biofilm consists mostly of non-motile bacteria, gingivitis presenting mostly motile bacteria in the form of bacilli, spirillae and vibrios, accompanied by a significant number of PMN leukocytes and finally, that periodontitis proceeds from a similar bacterial condition but added the absolute presence of protozoan Entamoeba gingivalis, less frequent Trichomonas tenax and more that significant numbers of granulocytes.[38] This theory applied in the 1980s by a Canadian dentist seem to confirm periodontal healing according to him by reestablishing, through hygiene, pharmaceutics and phase contrast microscope monitoring, a commensal biofilm constituted of simple bacteria of various cocoid shapes, motionless filaments and absence of leukocytes.[39][40][41][42] This microscopic correlation has recently been mostly confirmed by PCR molecular biology analysis relating the presence of this protozoan in cases of active periodontal disease and its absence during gingival health, even in local areas of the mouth.[43] This antiparasitic control technique was proposed as an effective therapy to overcome periodontitis.[44] This medical protocol is mainly based on the phagocytosis process of PMN leukocyte nucleus by the amoeba and a resulting enucleated cell spilling its proteolytic enzymes content on the surrounding tissues as being proposed in the amebic liver abscess figuring Entamoeba histolytica pathogen in amoebic dysentery. This particular therapy has the advantage to eliminate concomitant pathogenic bacteria in the same time as the protozoa, being considered at minimum by the dental practitioner and the patient an easy to visualize microscopic target. This phagocytosis process newly called exonucleophagy would account for the local deterioration of the immune system in the deep periodontal pocket and also be present in peri-implantitis infections. Systematic presence of protozoan and the recessed ghost cells exempt of nucleus would then impaired PMN to realise their defense activity Neutrophil extracellular traps. The first data on such an antiparasitic therapy seem effective to heal periodontal sulcus.[45]

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), microbial plaque tends to grow back to precleaning levels after about three to four months. 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, in male patients, of cancer.[47]

Contributing causes may be high alcohol consumption or a diet low in antioxidants.[48]

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 located 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 is helpful if space between the teeth allows. For smaller spaces, products such as narrow picks with soft rubber bristles provide excellent manual cleaning. 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 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 microbial plaque and calculus is necessary to establish periodontal health. The first step in the treatment of periodontitis involves nonsurgical 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 nonsurgical scaling and root planing are usually successful if the periodontal pockets are shallower than 4–5 mm (0.16–0.20 in).[49][50][51] The dentist or hygienist must perform a re-evaluation four to six weeks after the initial scaling and root planing, to determine if the patient's oral hygiene has improved and inflammation has regressed. Probing should be avoided then, and an analysis by gingival index should determine the presence or absence of inflammation. The monthly reevaluation of periodontal therapy should involve periodontal charting as a better indication of the success of treatment, and to see if other courses of treatment can be identified. Pocket depths of greater than 5–6 mm (0.20–0.24 in) which remain after initial therapy, with bleeding upon probing, indicate continued active disease and will very likely lead to further bone loss over time. This is especially true in molar tooth sites where furcations (areas between the roots) have been exposed.

Surgery

If nonsurgical 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. Many surgical approaches are used in treatment of advanced periodontitis, including open flap debridement and 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, 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.[52][53]

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 repopulation of periodontitis-causing microorganism, and to closely monitor affected teeth so early treatment can be rendered if disease recurs. Usually, periodontal disease exists 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 antimicrobial solutions, such as hydrogen peroxide, into periodontal pockets via slender applicators or oral irrigators. This process disrupts anaerobic micro-organism colonies and is effective at reducing infections and inflammation when used daily. A number of other products, 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 microbial colonies quickly regenerate in and around calculus.

Doxycycline may be given alongside the primary therapy of scaling (see § initial therapy).[54] Doxycycline has been shown to improve indicators of disease progression (namely probing depth and attachment level).[54] Its mechanism of action involves inhibition of matrix metalloproteinases (such as collagenase), which degrade the teeth's supporting tissues (periodontium) under inflammatory conditions.[54] To avoid killing beneficial oral microbes, only small doses of doxycycline (20mg) are used.[54]

Prognosis

Dentists and dental hygienists measure periodontal disease using a device called a periodontal probe. This thin "measuring stick" is gently placed into the space between the gums and the teeth, and slipped below the gumline. If the probe can slip more than 3 mm (0.12 in) below the gumline, the patient is said to have a gingival pocket if no migration of the epithelial attachment has occurred or a periodontal pock 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, pockets are generally accepted as self-cleansable (at home, by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if a pocket 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 to 7 mm (0.24 to 0.28 in) in depth, the hand instruments and cavitrons used by the dental professionals may not reach deeply enough into the pocket to clean out the microbial 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 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 patients have 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 patients remain 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). About 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10% will not suffer any loss.[55][56]

Epidemiology

Disability-adjusted life year for peridontal disease per 100,000 inhabitants in 2004.[57]
  no data
  <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
  >8.5

Periodontitis is very common, and is widely regarded as the second most common dental 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.

Chronic periodontitis affects about 750 million people or about 10.8% of the population as of 2010.[58]

Like other conditions intimately related to access to hygiene and basic medical monitoring and care, periodontitis tends to be more common in economically disadvantaged populations or regions. Its occurrence decreases with higher standard of living. In Israeli population, individuals of Yemenite, North-African, South Asian, or Mediterranean origin have higher prevalence of periodontal disease than individuals from European descent.[59] Periodontitis is frequently reported to be socially patterned, i.e. people from the lower end of the socioeconomic scale suffer more often from it than people from the upper end of the socioeconomic scale.[60]

Society and culture

Etymology

The word "periodontitis" (Greek: περιοδοντίτις) comes from the Greek peri, "around", odous (GEN odontos), "tooth", and the suffix -itis, in medical terminology "inflammation".[61] The word pyorrhea (alternative spelling: pyorrhoea) comes from the Greek pyorrhoia (πυόρροια), "discharge of matter", itself from pyon, "discharge from a sore", rhoē, "flow", and the suffix -ia.[62] In English this term can describe, as in Greek, any discharge of pus; i.e. it is not restricted to these diseases of the teeth.[63]

Economics

It is estimated that periodontitis results in worldwide productivity losses in the size of about US$54 billion yearly.[64]

Other animals

Periodontal disease is the most common disease found in dogs and affects more than 80% of dogs aged three years or older. Its prevalence in dogs increases with age, but decreases with increasing body weight; i.e., 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 micro-organisms, and they are filtered out by the kidneys and liver, where they may colonize and create microabscesses. The micro-organisms traveling through the blood may also attach to the heart valves, causing vegetative endocarditis (infected heart valves). Additional diseases that may result from periodontitis include chronic bronchitis and pulmonary fibrosis.[65]

See also

Footnotes

  1. ↑ Savage, Amir; Eaton, Kenneth A.; Moles, David R.; Needleman, Ian (2009). "A systematic review of definitions of periodontitis and methods that have been used to identify this disease". Journal of Clinical Periodontology 36 (6): 458–467. doi:10.1111/j.1600-051X.2009.01408.x. PMID 19508246.
  2. ↑ Armitage, Gary C. (1999). "Development of a classification system for periodontal diseases and conditions". Annals of Periodontology 4 (1). pp. 1–6. doi:10.1902/annals.1999.4.1.1.
  3. ↑ "The Periodontal Disease Classification System of the American Academy of Periodontology — An Update". American Academy of Periodontology.
  4. ↑ D'Aiuto, Francesco; Parkar, Mohammed; Andreou, Georgios; Suvan, Hannu; Brett, Peter M.; Ready, Derren; Tonetti, Maurizio S. (2004). "Periodontitis and systemic inflammation: control of the local infection is associated with a reduction in serum inflammatory markers". J Dent Res 83 (2): 156–160. doi:10.1177/154405910408300214. PMID 14742655.
  5. ↑ Nibali, Luigi; D'Aiuto, Francesco; Griffiths, Gareth; Patel, Kalpesh; Suvan, Jean; Tonetti, Maurizio S. (2007). "Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study". Journal of Clinical Periodontology 34 (11): 931–7. doi:10.1111/j.1600-051X.2007.01133.x. PMID 17877746.
  6. ↑ Paraskevas, Spiros; Huizinga, John D.; Loos, Bruno G. (2008). "A systematic review and meta-analyses on C-reactive protein in relation to periodontitis". Journal of Clinical Periodontology 35 (4): 277–290. doi:10.1111/j.1600-051X.2007.01173.x. PMID 18294231.
  7. ↑ D'Aiuto, Francesco; Ready, Derren; Tonetti, Maurizio S. (2004). "Periodontal disease and C-reactive protein-associated cardiovascular risk". Journal of Periodontal Research 39 (4): 236–241. doi:10.1111/j.1600-0765.2004.00731.x. PMID 15206916.
  8. ↑ Pussinen PJ, Alfthan G, Jousilahti P, Paju S, Tuomilehto J (2007). "Systemic exposure to Porphyromonas gingivalis predicts incident stroke". Atherosclerosis 193 (1): 222–8. doi:10.1016/j.atherosclerosis.2006.06.027. PMID 16872615.
  9. ↑ Pussinen PJ, Alfthan G, Rissanen H, Reunanen A, Asikainen S, Knekt P (September 2004). "Antibodies to periodontal pathogens and stroke risk". Stroke 35 (9): 2020–3. doi:10.1161/01.STR.0000136148.29490.fe. PMID 15232116.
  10. ↑ Pussinen PJ, Alfthan G, Tuomilehto J, Asikainen S, Jousilahti P (October 2004). "High serum antibody levels to Porphyromonas gingivalis predict myocardial infarction". European Journal of Cardiovascular Prevention & Rehabilitation 11 (5): 408–11. doi:10.1097/01.hjr.0000129745.38217.39. PMID 15616414.
  11. ↑ 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. doi:10.1177/154405910708600105. PMID 17189460.
  12. ↑ Beck, James D.; Eke, Paul; Heiss, Gerardo; Madianos, Phoebus; Couper, David; Lin, Dongming; Moss, Kevin; Elter, John; Offenbacher, Steven (2005). "Periodontal Disease and Coronary Heart Disease : A Reappraisal of the Exposure". Circulation 112 (1): 19–24. doi:10.1161/CIRCULATIONAHA.104.511998. PMID 15983248.
  13. ↑ Scannapieco, Frank A.; Bush, Renee B.; Paju, Susanna (2003). "Associations Between Periodontal Disease and Risk for Atherosclerosis, Cardiovascular Disease, and Stroke. A Systematic Review". Annals of Periodontology 8 (1): 38–53. doi:10.1902/annals.2003.8.1.38. PMID 14971247.
  14. ↑ Wu, Tiejian; Trevisan, Maurizio; Genco, Robert J.; Dorn, Joan P.; Falkner, Karen L.; Sempos, Christopher T. (2000). "Periodontal Disease and Risk of Cerebrovascular Disease: The First National Health and Nutrition Examination Survey and Its Follow-up Study". Archives of International Medicine 160 (18): 2749–2755. doi:10.1001/archinte.160.18.2749. PMID 11025784.
  15. ↑ Beck, James D.; Elter, John R.; Heiss, Gerardo; Couper, David; Mauriello, Sally M.; Offenbacher, Steven (2001). "Relationship of Periodontal Disease to Carotid Artery Intima-Media Wall Thickness : The Atherosclerosis Risk in Communities (ARIC) Study". Arteriosclerosis, Thrombosis, and Vascular Biology 21 (21): 1816–1822. doi:10.1161/hq1101.097803.
  16. ↑ Elter, John R.; Champagne, Catherine M.E.; Beck, James D.; Offenbacher, Steven (2004). "Relationship of Periodontal Disease and Tooth Loss to Prevalence of Coronary Heart Disease". Journal of Periodontology 75 (6): 782–790. doi:10.1902/jop.2004.75.6.782. PMID 15295942.
  17. ↑ Humphrey, Linda L.; Fu, Rongwei; Buckley, David I.; Freeman, Michele; Helfand, Mark (2008). "Periodontal Disease and Coronary Heart Disease Incidence: A Systematic Review and Meta-analysis". Journal of General Internal Medicine 23 (12): 2079–2086. doi:10.1007/s11606-008-0787-. PMC 2596495. PMID 18807098.
  18. ↑ 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. doi:10.1136/jnnp.2009.174029. PMC 3073380. PMID 19419981.
  19. ↑ Kaye, Elizabeth Krall; Valencia, Aileen; Baba, Nivine; Spiro III, Avron; Dietrich, Thomas; Garcia, Raul I. (2010). "Tooth Loss and Periodontal Disease Predict Poor Cognitive Function in Older Men". Journal of the American Geriatrics Society 58 (4): 713–718. doi:10.1111/j.1532-5415.2010.02788.x. PMID 20398152.
  20. ↑ Zadik Y, Bechor R, Galor S, Levin L (May 2010). "Periodontal disease might be associated even with impaired fasting glucose". Br Dent J 208 (10): e20. doi:10.1038/sj.bdj.2010.291. PMID 20339371.
  21. ↑ Soskolne WA, Klinger A (December 2001). "The relationship between periodontal diseases and diabetes: an overview". Ann Periodontol 6 (1): 91–8. doi:10.1902/annals.2001.6.1.91. PMID 11887477.
  22. ↑ Zadik Y, Bechor R, Galor S, Justo D, Heruti RJ (April 2009). "Erectile dysfunction might be associated with chronic periodontal disease: two ends of the cardiovascular spectrum". J Sex Med 6 (4): 1111–6. doi:10.1111/j.1743-6109.2008.01141.x. PMID 19170861.
  23. ↑ Crich, Aubrey (1932). "Blastomycosis of the gingiva and jaw". Can Med Assoc J. 26 (6): 662–5. PMC 402380. PMID 20318753.
  24. ↑ 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.
  25. ↑ Matsuo, Toshihiko; Nakagawa, Hideki; Matsuo, Nobuhiko; Matsuo, Nobuhiko (1995). "Endogenous Aspergillus endophthalmitis associated with periodontitis". Ophthalmologica 209 (2): 109–11. doi:10.1159/000310592. PMID 7746643.
  26. ↑ Migliari, Dante A.; Sugaya, Norberto N.; Mimura, Maria A.; Cucé, Luiz Carlos (1998). "Periodontal aspects of the juvenile form of paracoccidioidomycosis". Revista do Instituto de Medicina Tropical de São Paulo 40 (1). doi:10.1590/S0036-46651998000100004. ISSN 0036-4665.
  27. ↑ Lalla, Evanthia; Cheng, Bin; Lal, Shantanu; Kaplan, Selma; Softness, Barney; Greenberg, Ellen; Goland, Robin S.; Lamster, Ira B. (2007). "Diabetes mellitus promotes periodontal destruction in children". Journal of Clinical Periodontology 34 (4): 294–8. doi:10.1111/j.1600-051X.2007.01054.x. PMID 17378885.
  28. ↑ http://drstevenlandin.com/faq-gumdisprev.html
  29. ↑ Obeid, Patrick; Bercy, P. (2000). "Effects of smoking on periodontal health: A review". Advances in Therapy 17 (5): 230–7. doi:10.1007/BF02853162. PMID 11186143.
  30. ↑ Tomar, Scott L.; Asma, Samira (2000). "Smoking-Attributable Periodontitis in the United States: Findings From NHANES III". Journal of Periodontology 71 (5): 743–751. doi:10.1902/jop.2000.71.5.743. PMID 10872955.
  31. ↑ Ryder, Mark I. (2007). "The influence of smoking on host responses in periodontal infections". Periodontology 2000 43 (1): 267–277. doi:10.1111/j.1600-0757.2006.00163.x. PMID 17214844.
  32. ↑ Pauletto, Nathalie C.; Liede, Kirsti; Nieminen, Anja; Larjava, Hannu; Uitto, Veli-Jukka (2000). "Effect of Cigarette Smoking on Oral Elastase Activity in Adult Periodontitis Patients". Journal of Periodontology 71 (1): 58–62. doi:10.1902/jop.2000.71.1.58. PMID 10695939.
  33. ↑ Persson, Lena; Bergström, Jan; Gustafsson, Anders (2003). "Effect of Tobacco Smoking on Neutrophil Activity Following Periodontal Surgery". Journal of Periodontology 74 (10): 1475–82. doi:10.1902/jop.2003.74.10.1475. PMID 14653394.
  34. ↑ Bergström, Jan; Boström, Lennart (2001). "Tobacco smoking and periodontal hemorrhagic responsiveness". Journal of Clinical Periodontology 28 (7): 680–5. doi:10.1034/j.1600-051x.2001.028007680.x. PMID 11422590.
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  65. ↑ Muller-Esnault, Susan, DVM. "Periodontal Disease in the Dog and Cat" (2009). http://www.critterology.com/articles/periodontal-disease-dog-and-cat

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