A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi-dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history-based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic-periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.

A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi-dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history-based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic-periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.

The purpose of this review was to assess the scientific and clinical bases for the proposed classification of periodontitis. The clinical and histopathological signs and the etiology of periodontitis were described. Cross-sectional studies were analyzed to determine when onset of periodontitis most frequently occurs in adults. In addition, the progression rates of periodontitis have been assessed from longitudinal studies. No clinical, histopathological, or microbiological features could be identified that would characterize different disease entities of chronic periodontitis. The prevalence, extent, and severity of periodontitis were found to increase continually with higher age and there was no age when onset of disease would most likely occur. The rate of periodontitis progression varies largely between patients and there is no natural threshold for distinguishing various rates of disease progression. The incidence of periodontitis unresponsive to treatment depends on pretreatment progression rate, extent and severity of disease, tooth type, smoking, high levels of putative periodontal pathogens, a deficient immune response, and the type of therapy provided. There is no scientific basis for the classification "adult periodontitis" and "refractory adult periodontitis." Extensive clinical examinations are required for the diagnosis of "rapidly progressive adult periodontitis." It appears unrealistic that these examinations can be performed routinely in clinical practice. Therefore, the classification proposed by the Organizing Committee to define adult, rapidly progressive, and refractory periodontitis as specific disease entities was replaced with a simplified classification of periodontitis based on the scientific data available.

One in four patients and one in six implants have peri-implantitis after 11 years. The data suggest that periodontal and diabetes status of the patient may be useful for predicting implant outcomes.

With respect to clinical outcome measures, the available data do not indicate a difference between ultrasonic/sonic and manual debridement in the treatment of chronic periodontitis for single-rooted teeth; however, the evidence for this is not very strong. In addition, ultrasonic/sonic subgingival debridement requires less time than hand instrumentation. Further research is needed to assess the efficacy of machine-driven debridement on multirooted teeth and clinical outcome variables having tangible benefit to the patients should be used.

The novel low abrasive air-polishing powder is superior to curettes in removing subgingival plaque from pockets of 3-5 mm depth in supportive periodontal therapy and offers greater patient comfort.

Using a multivariate approach, a prognostic model was developed that may be of value for clinical decision making.

Self-performed plaque removal using manual or powered toothbrushes and interdental cleaning devices is improved in subjects that have received oral hygiene instructions. Personal oral hygiene coupled with regular professional supragingival debridement may further improve the level of plaque control but still fails to achieve a completely plaque-free dentition. Both patient-performed and professional supragingival plaque removal has an effect on subgingival microbiota that is limited to the marginal 3 mm of the periodontal pocket. At sites with 4 mm or more of probing depth, only subgingival scaling leads to a significant reduction of the bacterial load. The subgingival microflora can be further reduced by pocket elimination surgery. Due to the sequence of bacterial recolonization that occurs following mechanical debridement, the level of periodontal pathogens such as B. forsythus, P. gingivalis and T. denticola may be reduced for several months. Mechanical debridement also influences the patient's immune system response, resulting in antibody titers and avidity against periodontal pathogens. As a basis for the restoration and maintenance of periodontal health, repeated subgingival debridement, as performed in supportive periodontal therapy, can reduce the number and proportions of periodontopathogenic bacteria in subgingival plaque. However, intensive subgingival scaling and root planing should be avoided in sites that probe less than 3 mm, as this is likely to traumatize the periodontium and cause attachment loss.