Periodontitis/ˌpɛrioʊdɒnˈtaɪtɪs/ or pyorrhea/ˌpaɪəˈriə/ 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. Specialists in the treatment of periodontitis are periodontists; their field is known as "periodontology" or "periodontics".
The word "periodontitis" (Greek: περιοδοντίτις) comes from the Greek peri, "around", odous (GENodontos), "tooth", and the suffix -itis, in medical terminology "inflammation". 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; in English this term can describe, as in Greek, any discharge of pus, i.e. it's not restricted to these diseases of the teeth.
The 1999 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases, of which 2-6 are termed destructive periodontal disease because the damage is essentially irreversible. The seven categories are as follows:
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.
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:
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.
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:
Mild: 1–2 mm (0.039–0.079 in) of attachment loss
Moderate: 3–4 mm (0.12–0.16 in) of attachment loss
Severe: ≥ 5 mm (0.20 in) of attachment loss
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:
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
Spitting out blood after brushing teeth
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)
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.
The primary etiology (cause) of gingivitis is poor or ineffective oral hygiene, which leads to the accumulation of a mycotic and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes. Diabetics must be meticulous with their homecare to control periodontal disease. 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, and may interfere with or adversely affect its treatment.
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.
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 amoebaEntamoeba gingivalis and active periodontal disease then called pyorrhea. 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. 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. 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. This antiparasitic control technique was proposed as an effective therapy to overcome periodontitis. 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.
Daily oral hygiene measures to prevent periodontal disease include:
Brushing properly on a regular basis (at least twice daily), with the patient attempting to direct the toothbrush bristles underneath the gum-line, helps disrupt the bacterial-mycotic growth and formation of subgingival plaque.
Flossing daily and using interdental brushes (if the space between teeth is large enough), as well as cleaning behind the last tooth, the third molar, in each quarter
Using an antiseptic mouthwash: Chlorhexidine gluconate-based mouthwash in combination with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment loss due to periodontitis.
Using periodontal trays to maintain dentist-prescribed medications at the source of the disease: The use of trays allows the medication to stay in place long enough to penetrate the biofilms where the micro-organism are found.
Regular dental check-ups and professional teeth cleaning as required: Dental check-ups serve to monitor the person's oral hygiene methods and levels of attachment around teeth, identify any early signs of periodontitis, and monitor response to treatment.
Microscopic evaluation of biofilm may serve as a guide to regain commensal health flora.
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.
Contributing causes may be high alcohol consumption or a diet low in antioxidants.
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.
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.
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). 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.
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.
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.
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.
Additionally, periodontitis can be treated in a noninvasive manner by means of Doxycycline, an FDA-approved, orally administered drug that has been shown to reduce bone loss. Its mechanism of action in part involves inhibition of matrix metalloproteinases (such as collagenase), which degrade the extracellular matrix under inflammatory conditions. This ultimately can lead to reduction of aveolar bone loss in patients with periodontal disease (as well as patients without periodontitis).
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 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, 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.
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.
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.
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. 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.
Javed, Fawad; Näsström, Karin; Benchimol, Daniel; Altamash, Mohammad; Klinge, Björn; Engström, Per-Erik (2005). "Comparison of periodontal and socioeconomic status between subjects with type 2 diabetes mellitus and non-diabetic controls". Journal of Periodontology78 (11): 2112–9. doi:10.1902/jop.2007.070186. PMID17970677.
Kinane, Denis; and Bouchard, Phillippe on behalf of group E of the European Workshop on Periodontology; Group E of European Workshop on Periodontology (2008). "Periodontal diseases and health: Consensus Report of the Sixth European Workshop on Periodontology". Journal of Clinical Periodontology35 (s8, Special Issue: The 6th European Workshop on Periodontology Contemporary Periodontics): 333–7. doi:10.1111/j.1600-051X.2008.01278.x. PMID18724860.
Kingman, Albert; Albandar, Jasim M. (2008). "Methodological aspects of epidemiological studies of periodontal diseases". Periodontology 200029 (1): 11–30. doi:10.1034/j.1600-0757.2002.290102.x.
Lucarini, Guendalina; Zizzi, Antonio; Aspriello, Simone Domenico; Ferrante, Luigi; Tosco, Eugenio; Lo Muzio, Lorenzo; Foglini, Paolo; Mattioli-Belmonte, Monica; Di Primio, Roberto; Piemontese, Matteo; Mattioli-Belmonte, Monica et al. (2009). "Involvement of vascular endothelial growth factor, CD44 and CD133 in periodontal disease and diabetes: an immunohistochemical study". Journal of Clinical Periodontology36 (1): 3–10. doi:10.1111/j.1600-051X.2008.01338.x. PMID19017033.
Williams, Ray C.; Offenbacher, Steven (2000). "Periodontal medicine: the emergence of a new branch of periodontology". Periodontology 200023 (1): 9–12. doi:10.1034/j.1600-0757.2000.2230101.x.
^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 Periodontology36 (6): 458–467. doi:10.1111/j.1600-051X.2009.01408.x. PMID19508246.
^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 Res83 (2): 156–160. doi:10.1177/154405910408300214. PMID14742655.
^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 Periodontology34 (11): 931–7. doi:10.1111/j.1600-051X.2007.01133.x. PMID17877746.
^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 Periodontology35 (4): 277–290. doi:10.1111/j.1600-051X.2007.01173.x. PMID18294231.
^D'Aiuto, Francesco; Ready, Derren; Tonetti, Maurizio S. (2004). "Periodontal disease and C-reactive protein-associated cardiovascular risk". Journal of Periodontal Research39 (4): 236–241. doi:10.1111/j.1600-0765.2004.00731.x. PMID15206916.
^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 Society58 (4): 713–718. doi:10.1111/j.1532-5415.2010.02788.x. PMID20398152.
^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 Med6 (4): 1111–6. doi:10.1111/j.1743-6109.2008.01141.x. PMID19170861.
^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. PMID18608938.
^Kofoid CA, Hinshaw HC, Johnstone HG. Animal parasites of the mouth and their relation to dental disease. Journal of the American Dental Association 1929 Aug;1436-1455.
^Keyes PH, Rogosa M, RamsTH, Sarfatti DE. Diagnosis of Creviculoradicular Infections : Disease-Associated Bacterial Patterns in Periodontal Lesions. Host-Parasite Interactions in Periodontal Diseases. Genco and Mergenhagen 1982. ISBN 0-914826-37-9
^Lyons T, Sholten T, Palmer JC. Oral amoebiasis: a new approach for the general practitioner in the diagnosis and treatment of periodontal disease. Oral Health 1980 Oct; 70(10) : 39-41,108,110.
^Lyons T, Sholten T, Palmer JC, Stanfield E. Oral amoebiasis: alternatives in oral disease. Ontario dentist 1982 Feb;59(2):16-20.
^Lyons T, Sholten T, Palmer JC, Stanfield E. Oral amebiasis: the role of Entamoeba gingivalis in periodontal disease. Quintessence Int. 1983 Dec;14(12): 1245-8.
^Trim RD, Skinner MA, Farone MB, Dubois JD, Newsome AL. Use of PCR to detect Entamoeba gingivalis in diseased gingival pockets and demonstrate its absence in healthy gingival sites. Parasitol Res. 2011 Sep;109(3):857-64.
^Bonner M. To Kiss or Not To Kiss. A Cure for Gum Disease. Editions Amyris 2013. EAN: 978-28755-2016-6
^Bonner M, Amard V, Amiot P, Ihler S, Marty M, Rochet JP, Verdy M. Antiparasitic treatment of periodontitis and peri-implantitis: 12-months multicentric follow-up. AOS Journal no 261 February 2013 (in French).
^Bonner M. To Kiss or Not to Kiss. A cure for gum disease. Amyris Editions, 2013 EAN : 978-28755-2016-6
^Stambaugh RV, Dragoo M, Smith DM, Carasali L (1981). "The limits of subgingival scaling". Int J Periodontics Restorative Dent1 (5): 30–41. PMID7047434.
^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. doi:10.1902/jop.19126.96.36.199. PMID340634.
^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. doi:10.1902/jop.19188.8.131.52. PMID288899.
^Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK (February 1996). "Long-term evaluation of periodontal therapy: II. Incidence of sites breaking down". J. Periodontol.67 (2): 103–8. doi:10.1902/jop.19184.108.40.206. PMID8667129.
^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 Periodontol22 (9): 674–8. doi:10.1111/j.1600-051X.1995.tb00825.x. PMID7593696.