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.

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. 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."

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.

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

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

Signs and symptoms In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following: Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g. apples) (though this may occur even in gingivitis, where there is no attachment loss) Gum swelling that reoccurs 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) Drifting of incisors

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. 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. 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. 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:

Pocket Depth (PD) Clinical Attachment Loss (CAL) Bleeding On Probing (BOP) Plaque index/score Furcation involvement Suppuration Mobility Radiographs

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:

Extent (can be either localised affecting < 30% of sites; or generalised if > 30% of sites are affected) 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:

Periodontitis:

Necrotizing periodontal diseases Periodontitis 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:

Type Distribution: localised (up to 30% of teeth) or generalised (more than 30% of teeth) and the molar/incisor pattern Stage and grading Stages: I (early/mild) with <15% or <2mm interproximal bone loss, II (moderate) with coronal third of root bone loss, III (severe) with mid third of root bone loss, IV (very severe) with apical third of root bone loss Grading: A (slow) with <0.5% bone loss/age, B (moderate) with 0.5-1.0% bone loss/age, C (rapid) with >1.0% bone loss/age Status: stable, remission or unstable (see Table 1) Risk factors, which include systemic diseases such as diabetes or extrinsic factors such as smoking.

+Table 1. Periodontitis statusStableRemissionUnstableBleeding on Probing<10%≥10% -Periodontal Pocket Depth≤4mm≤4mm≥5mmBleeding 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". 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.

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."

Guided tissue regeneration