Chronic periodontitis

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Chronic periodontitis is one of the seven categories of periodontitis as defined by the American Academy of Periodontology 1999 classification system. Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that is caused by the accumulation of profuse amounts of dental plaque. Periodontitis initially begins as gingivitis and can progress onto chronic and subsequent aggressive periodontitis according to the 1999 classification.

Contents

Diagnosing chronic periodontitis is important in its early stages to prevent severe and irreversible damage to the protective and supportive structures of the tooth. However, due to chronic periodontitis being a painless progressing disease, few patients will seek dental care in the early stages. Mild to moderate chronic periodontitis can be managed by proper mechanical removal of the biofilm and calculus subgingivally. Full and effective oral hygiene and regular 3 monthly periodontal checkups are important for maintaining the stability of the disease.

Chronic periodontitis is prevalent in adults and seniors worldwide. In the US around 35% of adults (30–90 years) are affected. [1] The cumulative effects of alveolar bone loss, attachment loss and pocket formation is more apparent with an increase in age. Age is related to the incidence of periodontal destruction: "...in 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]

There are a variety of periodontal risk factors which can affect the prevalence, rate, extent and severity of the disease progression. Major risk factors include smoking, lack of oral hygiene with inadequate plaque biofilm control.

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, anxiety and depression. Care should be taken however, when diagnosing a patient who smokes as smoking can alter some of the results of an examination. In smokers, the gingiva are pale and fibrous and tend to bleed less while being probed due to the effect of nicotine on the vasculature by vasoconstricting them. Thus, a lowered response is produced and this explains why incorrect data can be gained. There is also an increase in supragingival calculus alongside visible nicotine staining. The anterior dentition occasionally have recession and maxillary anterior and palatal surfaces are more adversely affected.

Pathophysiology

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.

Plaque hypothesis

At least two mechanisms of the microbiology of periodontitis have been described: the specific plaque hypothesis and the non-specific plaque hypothesis. Consensus is that neither view is entirely correct, but via a middle path, that damage is due to a shift in the relative populations of more and less dangerous bacteria in the plaque. This is called the ecological 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]

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:

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 as well as supragingival calculus due to the bacteria migrating apically and the combined effect of the host response system of the body.

Diagnosis

1999 classification

Chronic periodontitis is one of the seven destructive periodontal diseases as listed in the 1999 classification. [5] Not every case of gingivitis will progress onto chronic periodontitis, but all chronic periodontitis results from gingivitis. Therefore it is important to control the first step; gingival inflammation.

A difficulty which arises with diagnosing chronic periodontitis patients is due to the slow and painless progression of the disease. [6] The most effective and timely diagnosis would be during the mild to moderate stage. However, usually when presenting complaints do arise the effects of mobility and alveolar bone loss have become severe.

A full mouth examination and recording is required to document and track periodontal disease including:

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. True pocket formation of 4 mm or more are specifically related to chronic periodontitis. 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.

Evidence of alveolar bone loss is also required to differentiate between true bone loss and not attributions of gingival oedema. Usually, a horizontal pattern of bone loss would be found however, vertical (infrabony) bone loss may also be present on specific sites. A Basic Periodontal Examination (BPE) or Periodontal Screening and Recording (PSR) should give a score of 3 or 4. A correct diagnosis is vital to allow the formation of a specific treatment plan for the patient and to arrest the disease progression.

Chronic periodontitis can be further classified into:

  1. Extent (can be either localised affecting < 30% of sites; or generalised if > 30% of sites are affected)
  2. Severity (slight = 1–2 mm CAL; moderate = 3–4 mm CAL; severe ≥5 mm CAL)

2017 classification

Chronic periodontitis is not included within the newer 2017 World Workshop classification. The 2017 classification of Periodontal Diseases and Conditions includes: [7]

Periodontitis:

  1. Necrotizing periodontal diseases
  2. Periodontitis
  3. Periodontitis as a manifestation of systemic disease

Therefore, in accordance to the 2017 classification, a diagnosis would be achieved through the patient assessment individually on the basis of:

Table 1. Periodontitis status
StableRemissionUnstable
Bleeding on Probing<10%≥10%-
Periodontal Pocket Depth≤4mm≤4mm≥5mm
Bleeding on Probing at 4mm sites✗✗✓

Treatment

There is professional agreement among dentists that smoking cessation and good oral hygiene are key to effective treatment and positive outcomes for patients. Similarly, any plaque retentive factors which exist and are modifiable should be corrected, such as overhangs on restorations.

Treatment can involve both non-surgical and surgical therapies. The typical initial treatment known to be effective is scaling and root planing (SRP) to mechanically debride the depths of the periodontal pocket and disrupt the biofilm present. This is done using a powered ultrasonic or sonic scaler and/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". [8] It is important for patients to be reviewed within 8–12 weeks to assess the treatment response.

Full mouth disinfection protocols are favoured by some clinicians. There is no evidence that full mouth disinfection or full mouth scaling protocols improve the outcome when compared to standard mechanical scaling and root planing. [9]

Open flap debridement

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." [10]

Guided tissue regeneration

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." [11]

Enamel matrix derivative

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." [12]

However, studies have shown that regardless of the conventional periodontal treatments, 20-30% of chronic periodontitis patients do not respond favorably to their treatment. [1] There are many factors which account for these including: ineffective removal of calculus, defective restorations, impaired immune response as a result of a systemic condition, poor plaque control, smoking, etc.

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." [13]

There is currently low-quality evidence suggesting if adjunctive systemic antimicrobials are beneficial for the non-surgical treatment of periodontitis. [14] It is not sure whether some antibiotics are better than others when used alongside scaling and root planning).  

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." [15]

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

Hydrogen peroxide is a naturally occurring antimicrobial that can be delivered directly to the gingival sulcus or periodontal pocket using a custom formed medical device called a Perio Tray. [Title = Custom Tray Application of Peroxide Gel as an Adjunct to Scaling and Root Planing in the Treatment of Periodontitis: A Randomized, Controlled Three-Month Clinical Trial J Clin Dent 2012;23:48–56.]

Hydrogen peroxide gel was demonstrated to be effective in controlling the bacteria biofilm [Subgingival Delivery of Oral Debriding Agents: A Proof of Concept J Clin Dent 2011;22:149–158] The research shows that a direct application of hydrogen peroxide gel killed virtually all of the bacterial biofilm, was directly and mathematically delivered up to 9mm into periodontal pockets.

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." [16]

Systemic Factors

Chronic periodontitis is an inflammatory immune response against the presence of bacteria present. Recent research has suggested that epithelial lining ulceration in chronic periodontal pockets are due to systemic bacterial dissemination and widespread bacterial inflammatory markers present in the host. Two of the most widely investigated systemic diseases associated with chronic periodontitis is diabetes mellitus and cardiovascular disease. [17]

Diabetes Mellitus

Both type 1 and type 2 diabetes have shown a link with the treatment and progression of chronic periodontitis. Chronic periodontitis is more severe in patients that have diabetes than those without, confirming a significant association. With type 2 diabetes patients being shown to have 3.8 times more bone loss and 2.8 times more clinical attachment loss than non-diabetic individuals. With patients with poorly controlled diabetes having a higher risk of alveolar bone loss. [18] Chronic periodontitis can also be a metabolic stressor influencing diabetes control, influencing insulin resistance or becoming a source of inflammatory marker secretion which may strengthen the amount of advanced glycation end product (AGE) mediated cytokine response. [19] Monocytic hyperresponsiveness to bacterial antigen is a biological mechanism that links periodontal disease and diabetes. Increased production of proinflammatory cytokines and mediators cause tissue destruction, attachment loss as well as bone loss causing delayed wound healing. [20]

Cardiovascular Disease

Chronic periodontitis is a marker for cardiovascular disease (CVD). [21] Mechanisms associated with cardiovascular risk are that chronic periodontitis increases inflammatory mediator levels and this may contribute to the onset of CVD, while treatment of chronic periodontitis reduces systemic levels of inflammatory mediators. [22] Certain bacteria found in the periodontal pockets have also been associated to cause atheromatous plaques. [23] Treatment protocol for chronic periodontitis with CVD does not need to be modified as normal periodontal treatment techniques are seen to be effective in CVD patients with additional supportive therapy. [24]

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.". [25] However, health outcomes of periodontal therapy are not directly comparable with those from implants or bridgework. [26]

Research

Management

For adults without severe periodontitis and who get routine dental care, regular scale and polish treatment does not make any difference to gingivitis, probing depths or other oral health-related problems. It seems that there is also no difference in plaque levels. [27]

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." [28]

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." [29]

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)". [30]

Related Research Articles

<span class="mw-page-title-main">Periodontal disease</span> Medical condition

Periodontal disease, also known as gum disease, is a set of inflammatory conditions affecting the tissues surrounding the teeth. In its early stage, called gingivitis, the gums become swollen and red and may bleed. It is considered the main cause of tooth loss for adults worldwide. In its more serious form, called periodontitis, the gums can pull away from the tooth, bone can be lost, and the teeth may loosen or fall out. Bad breath may also occur.

<span class="mw-page-title-main">Calculus (dental)</span> Form of hardened dental plaque

In dentistry, calculus or tartar is a form of hardened dental plaque. It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation. This leads to calculus buildup, which compromises the health of the gingiva (gums). Calculus can form both along the gumline, where it is referred to as supragingival, and within the narrow sulcus that exists between the teeth and the gingiva, where it is referred to as subgingival.

Periodontology or periodontics is the specialty of dentistry that studies supporting structures of teeth, as well as diseases and conditions that affect them. The supporting tissues are known as the periodontium, which includes the gingiva (gums), alveolar bone, cementum, and the periodontal ligament. A periodontist is a dentist that specializes in the prevention, diagnosis and treatment of periodontal disease and in the placement of dental implants.

<span class="mw-page-title-main">Gingival sulcus</span> Space between tooth and gums

The gingival sulcus is an area of potential space between a tooth and the surrounding gingival tissue and is lined by sulcular epithelium. The depth of the sulcus is bounded by two entities: apically by the gingival fibers of the connective tissue attachment and coronally by the free gingival margin. A healthy sulcular depth is three millimeters or less, which is readily self-cleansable with a properly used toothbrush or the supplemental use of other oral hygiene aids.

<span class="mw-page-title-main">Gingival and periodontal pocket</span>

Gingival and periodontal pockets are dental terms indicating the presence of an abnormal depth of the gingival sulcus near the point at which the gingival tissue contacts the tooth.

Bleeding on probing (BoP) which is also known as bleeding gums or gingival bleeding is a term used by dentists and dental hygienists when referring to bleeding that is induced by gentle manipulation of the tissue at the depth of the gingival sulcus, or interface between the gingiva and a tooth. BoP is a sign of periodontal inflammation and indicates some sort of destruction and erosion to the lining of the sulcus or the ulceration of sulcular epithelium. The blood comes from lamina propria after the ulceration of the lining. BoP seems to be correlated with Periodontal Inflamed Surface Area (PISA).

<span class="mw-page-title-main">Scaling and root planing</span> Dental procedure

Scaling and root planing, also known as conventional periodontal therapy, non-surgical periodontal therapy or deep cleaning, is a procedure involving removal of dental plaque and calculus and then smoothing, or planing, of the (exposed) surfaces of the roots, removing cementum or dentine that is impregnated with calculus, toxins, or microorganisms, the agents that cause inflammation. It is a part of non-surgical periodontal therapy. This helps to establish a periodontium that is in remission of periodontal disease. Periodontal scalers and periodontal curettes are some of the tools involved.

Gingivectomy is a dental procedure in which a dentist or oral surgeon cuts away part of the gums in the mouth.

Laser-assisted new attachment procedure (LANAP) is a surgical therapy for the treatment of periodontitis, intended to work through regeneration rather than resection. This therapy and the laser used to perform it have been in use since 1994. It was developed by Robert H. Gregg II and Delwin McCarthy.

Guided bone regeneration (GBR) and guided tissue regeneration (GTR) are dental surgical procedures that use barrier membranes to direct the growth of new bone and gingival tissue at sites with insufficient volumes or dimensions of bone or gingiva for proper function, esthetics or prosthetic restoration. Guided bone regeneration typically refers to ridge augmentation or bone regenerative procedures; guided tissue regeneration typically refers to regeneration of periodontal attachment.

<span class="mw-page-title-main">Gingivitis</span> Inflammation of the gums

Gingivitis is a non-destructive disease that causes inflammation of the gums; ulitis is an alternative term. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms that are attached to tooth surfaces, termed plaque-induced gingivitis. Most forms of gingivitis are plaque-induced.

<span class="mw-page-title-main">Debridement (dental)</span> Removal of plaque and calculus from teeth

In dentistry, debridement refers to the removal by dental cleaning of accumulations of plaque and calculus (tartar) in order to maintain dental health. Debridement may be performed using ultrasonic instruments, which fracture the calculus, thereby facilitating its removal, as well as hand tools, including periodontal scaler and curettes, or through the use of chemicals such as hydrogen peroxide.

<span class="mw-page-title-main">Furcation defect</span>

In dentistry, a furcation defect is bone loss, usually a result of periodontal disease, affecting the base of the root trunk of a tooth where two or more roots meet. The extent and configuration of the defect are factors in both diagnosis and treatment planning.

Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis as defined by the 1999 classification system:

  1. Localized aggressive periodontitis (LAP)
  2. Generalized aggressive periodontitis (GAP)
<span class="mw-page-title-main">Peri-implantitis</span> Inflammatory disease

Peri-implantitis is a destructive inflammatory process affecting the soft and hard tissues surrounding dental implants. The soft tissues become inflamed whereas the alveolar bone, which surrounds the implant for the purposes of retention, is lost over time.

In dentistry, numerous types of classification schemes have been developed to describe the teeth and gum tissue in a way that categorizes various defects. All of these classification schemes combine to provide the periodontal diagnosis of the aforementioned tissues in their various states of health and disease.

Peri-implant mucositis is defined as an inflammatory lesion of the peri-implant mucosa in the absence of continuing marginal bone loss.

Host modulatory therapy is an emerging treatment concept in the management of periodontitis that aims to reduce tissue destruction and stabilise or even regenerate the periodontium by modifying the host response. Historically treatment of periodontitis has been focused on reducing the bacterial challenge. However the outcomes of the conventional treatment procedures like scaling and root planning (SRP) are not always stable or predictable. Periodontal disease is seen as a balance between (1) a persisting bacterial challenge and the proinflammatory destructive events in the tissue and (2) resolution of inflammation and downregulation of destructive processes. The goal is to maximize treatment response by reducing inflammation and inhibiting destructive processes in the tissues which will result in enhanced periodontal stability after conventional periodontal treatments like SRP.

Periodontal surgery is a form of dental surgery that prevents or corrects anatomical, traumatic, developmental, or plaque-induced defects in the bone, gingiva, or alveolar mucosa. The objectives of this surgery include accessibility of instruments to root surface, elimination of inflammation, creation of an oral environment for plaque control, periodontal diseases control, oral hygiene maintenance, maintain proper embrasure space, address gingiva-alveolar mucosa problems, and esthetic improvement. The surgical procedures include crown lengthening, frenectomy, and mucogingival flap surgery.

References

  1. 1 2 Shaddox LM, Walker CB (2010-08-11). "Treating chronic periodontitis: current status, challenges, and future directions". Clinical, Cosmetic and Investigational Dentistry. 2: 79–91. doi: 10.2147/CCIDE.S7712 . PMC   3645457 . PMID   23662085.
  2. ↑ Heitz-Mayfield LJ, Schätzle M, Löe H, Bürgin W, Anerud A, Boysen H, Lang NP (October 2003). "Clinical course of chronic periodontitis. II. Incidence, characteristics and time of occurrence of the initial periodontal lesion". Journal of Clinical Periodontology. 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". Infection and Immunity. 42 (2): 510–5. doi:10.1128/IAI.42.2.510-515.1983. PMC   264458 . PMID   6642641.
  4. 1 2 Loesche WJ, Grossman NS (October 2001). "Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment". Clinical Microbiology Reviews. 14 (4): 727–52, table of contents. doi:10.1128/CMR.14.4.727-752.2001. PMC   89001 . PMID   11585783.
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  6. ↑ Ramachandra SS, Gupta VV, Mehta DS, Gundavarapu KC, Luigi N. Differential Diagnosis between Chronic versus Aggressive Periodontitis and Staging of Aggressive Periodontitis: A Cross-sectional Study. Contemp Clin Dent. 2017 Oct-Dec;8(4):594-603.
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  12. ↑ Esposito M, Grusovin MG, Papanikolaou N, Coulthard P, Worthington HV (October 2009). Esposito M (ed.). "Enamel matrix derivative (Emdogain(R)) for periodontal tissue regeneration in intrabony defects". The Cochrane Database of Systematic Reviews. 2009 (4): CD003875. doi:10.1002/14651858.CD003875.pub3. PMC   6786880 . PMID   19821315.
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  17. ↑ Shaddox LM, Walker CB (2010-08-11). "Treating chronic periodontitis: current status, challenges, and future directions". Clinical, Cosmetic and Investigational Dentistry. 2: 79–91. doi: 10.2147/CCIDE.S7712 . PMC   3645457 . PMID   23662085.
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  25. ↑ Pretzl B, Wiedemann D, Cosgarea R, Kaltschmitt J, Kim TS, Staehle HJ, Eickholz P (August 2009). "Effort and costs of tooth preservation in supportive periodontal treatment in a German population". Journal of Clinical Periodontology. 36 (8): 669–76. doi:10.1111/j.1600-051X.2009.01409.x. PMID   19566541.
  26. ↑ Pennington M, Vernazza C, Heasman P (August 2009). "Making the leap from cost analysis to cost-effectiveness". Journal of Clinical Periodontology. 36 (8): 667–8. doi:10.1111/j.1600-051X.2009.01424.x. PMID   19566540.
  27. ↑ Lamont T, Worthington HV, Clarkson JE, Beirne PV (27 December 2018). "Routine scale and polish for periodontal health in adults". Cochrane Database Syst Rev. 2020 (4): CD004625. doi:10.1002/14651858.CD004625.pub5. PMC   6516960 . PMID   30590875.
  28. ↑ 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". Journal of Periodontology. 79 (11): 2021–8. doi: 10.1902/jop.2008.080197 . PMID   18980508.
  29. ↑ Michalowicz BS, Hodges JS, Novak MJ, Buchanan W, DiAngelis AJ, Papapanou PN, et al. (April 2009). "Change in periodontitis during pregnancy and the risk of pre-term birth and low birthweight". Journal of Clinical Periodontology. 36 (4): 308–14. doi:10.1111/j.1600-051X.2009.01385.x. PMC   2741139 . PMID   19426177.
  30. ↑ Tezal M, Sullivan MA, Hyland A, Marshall JR, Stoler D, Reid ME, et al. (September 2009). "Chronic periodontitis and the incidence of head and neck squamous cell carcinoma". Cancer Epidemiology, Biomarkers & Prevention. 18 (9): 2406–12. doi: 10.1158/1055-9965.EPI-09-0334 . PMID   19745222.
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