Current concepts in the management of periodontitis

Periodontitis

Periodontitis is a chronic multifactorial inflammatory disease associated with the accumulation of dental plaque (which will be referred to as dental biofilm/biofilm), and characterised by progressive destruction of the teeth-supporting apparatus, including the periodontal ligament and alveolar bone1, 2. The disease involves complex dynamic interactions among specific bacterial pathogens, destructive host immune responses, and environmental factors such as smoking (Figure 1)1, 3. The common features of periodontitis include gingival inflammation, clinical attachment loss, radiographic evidence of alveolar bone loss, sites with deep probing depths, mobility, bleeding upon probing and pathologic migration2, 4, 5.

image

Periodontitis is multifactorial in nature and results from the presence of pathogenic bacteria, the host inflammatory and immune responses and other identified environmental and systemic risk factors.

Prevalence and Significance

According to data from the National Health and Nutrition Examination Survey 2009–2014, 42% of adults in the United States had periodontitis, with 7.8% having severe periodontitis6. This survey confirmed a high prevalence of periodontitis in the United States affecting almost 50% of the adult population (30 years old or older)6. Globally, approximately 11% of the world population may have severe periodontitis, affecting 743 million individuals (Figure 2)7-13. Furthermore, a robust literature has identified potential associations between periodontitis and certain non-communicable chronic diseases14. In addition, the loss of periodontal support was associated with a significant reduction in masticatory performance15. Thus, periodontitis and its clinical ramifications, including tooth loss, may have a substantially negative effect on oral health related quality of life (OHRQoL), while successful management may improve patients' OHRQoL15, 16.

image Global prevalence of severe periodontitis7-9 in comparison to diabetes10, hypertension11, depression12 and asthma13. Aetiology Dental biofilm

For a susceptible host, microbial infection in subgingival dental biofilm by periodontal pathogens, in particular a group of specific Gram-negative anaerobic species referred to as the red complex, results in chronic inflammation17, 18. These red-complex bacteria include Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, which are predominantly found in deep periodontal pockets of patients with periodontitis (Table 1)17-24. Lipopolysaccharide along with other virulence factors from these periodontal pathogens stimulate the host macrophages, and other inflammatory and constituent cells, leading to the production of a range of pro-inflammatory cytokines such as tumour necrosis factor (TNF)-α, interleukin (IL)-1β and prostaglandin E2 (PGE2). The presence of these pro-inflammatory cytokines and virulence factors stimulates the production of matrix metalloproteinases (MMPs) by macrophages, fibroblasts, junctional epithelial cells, and neutrophils3, 25. The resulting MMPs then mediate the destruction of collagen fibres in periodontal tissues, especially periodontal ligaments3. In addition, the pro-inflammatory cytokines induce the expression of receptor activator of nuclear factor κB ligand (RANK-L) on the osteoblasts and T helper cells. The resulting RANK-L on the osteoblasts and the T helper cells then interacts with receptor activator of nuclear factor κB (RANK) on osteoclast precursors, which results in the genesis of osteoclasts and their maturation. The mature osteoclasts mediate alveolar bone destruction26, 27.

Table 1. Red complex bacteria and their characteristics Pathogens Characteristics19 Virulence factors Major functions Porphyromonas gingivalis

Gram negative

Non-motile

Anaerobic

Pleomorphic rod (coccal to short)

Capsule Antiphagocytic20 Fimbriae Cellular adhesion20 Outer membrane proteins Contain LPS, eliciting the host pro-inflammatory response and the production of pro-inflammatory cytokines21 Gingipains Possibly linked to Alzheimer’s disease22 Tannerella forsythia

Gram negative

Non-motile

Anaerobic

Pleomorphic rod (spindle shaped)

Various proteinases Degrade host proteins, providing essential amino acids, peptides and heme for the growth of Tannerella forsythia23 Degrade periodontal tissues23 Activate host degradative enzymes23 Modify host cell proteins to expose cryptotopes for bacterial colonization23 Cleave components in host innate (cytokines, complement factors) & adaptive immune system (immunoglobulins), thus paralyzing host immunity23 Active components involved in clotting and fibrinolysis23 Surface lipoproteins Induces host cellular apoptosis23 Treponema denticola

Gram negative

Motile

Anaerobic

Cork-screw shaped or spiraled

Motility & chemotaxis Enable the bacterium to rapidly colonize new sites, penetrate deep periodontal pockets, and penetrate epithelial layers24 Outer sheath proteins (Dentilisin, major sheath proteins, lipoproteins) Impair neutrophil chemotaxis and phagocytosis24 Interact synergistically with other periodontal pathogens including Porphyromonas gingivalis and Tannerella forsythia at several levels24 Bind to and coat their surface with soluble host proteins, thus avoiding and delaying host recognition24 Metabolic end products Cytotoxic to various host cells24 Toxin-antitoxin system, and transposases Contribute to biofilm formation and persistence24 Resist to various environmental assaults such as antibiotics24 Allows transfer of virulence genes through horizontal gene transfer within biofilm24 Natural History/Progression

Periodontitis was previously believed to progress at a constant rate until treatment or tooth loss28. For instance, individuals with so-called rapidly progressing periodontitis exhibited an annual rate of interproximal attachment loss of between 0.1 and 1.0 mm, while individuals with moderately progressing periodontitis exhibited a loss of between 0.05 and 0.5 mm29. Individuals with minimal to no progression exhibited an annual loss rate of between 0.05 and 0.09 mm29. Currently, based on longitudinal observations from human and animal studies, periodontitis is now believed to progress by recurrent acute episodes instead28, 30. During their lifetime, patients with periodontitis exhibit a cycle of bursts of destruction at individual sites over short periods of time, followed by longer periods of remission28, 31.

Diagnosis

A patient's medical history should be obtained prior to periodontal assessment. This will provide identification of any systemic or environmental risk factors for periodontitis, such as diabetes and smoking. A comprehensive periodontal evaluation includes several clinical parameters: biofilm index, periodontal probing depth, presence of bleeding on probing, gingival recession, mucogingival deformity, furcation involvement, tooth mobility, and occlusal trauma. A comprehensive radiographic evaluation is a part of the initial periodontal evaluation to determine the extent of horizontal and vertical alveolar bone loss. According to the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions2, a new periodontitis classification categorises the disease based on a multi-dimensional staging and grading system. Staging is determined by the severity of the disease at initial presentation and the complexity of disease management (Table 2)2. Furthermore, grading is used as an indicator of the rate of periodontitis progression, which is determined by the history as well as the presence of risk factors for periodontitis (Table 3)2.

Table 2. The stages of periodontitis Periodontal stage Stage I Stage II Stage III Stage IV Severity Interdental CAL at site of greatest loss 1 to 2 mm 3 to 4 mm ≥5 mm ≥5 mm Radiographic bone loss Coronal third (<15%) Coronal third (15% to 33%) Extending to middle or apical third of the root Extending to middle or apical third of the root Tooth loss No tooth loss due to periodontitis Tooth loss due to periodontitis of ≤4 teeth Tooth loss due to periodontitis of ≥5 teeth Complexity Local Maximum probing depth ≤4 mm. Mostly horizontal bone loss Maximum probing depth ≤5 mm. Mostly horizontal bone loss

In addition to stage II complexity:

Probing depth ≥6 mm Vertical bone loss ≥3 mm Furcation involvement Class II or III Moderate ridge defect

In addition to stage III complexity:

Need for complete rehabilitation due to:

Masticatory dysfunction Secondary occlusal trauma (tooth mobility degree ≥2) Severe ridge defect Bite collapse, drifting, flaring Less than 20 remaining teeth (10 opposing pairs) Extent and distribution Add to stage as descriptor For each stage, describe extent as localised (<30% of teeth involved), generalised, or molar/incisor pattern The stage of periodontitis is initially determined based on clinical attachment loss (CAL). If CAL is not available, then radiographic bone loss can be used. A history of tooth loss due to periodontitis may modify the stage. In the presence of any complexity factor, the stage may shift to a higher tier. For example, the presence of class II or III furcation involvement would shift to either stage III or IV regardless of CAL, radiographic bone loss, or tooth loss due to periodontitis. The extent and distribution is primarily determined by the percentage of teeth involved2. The table was reprinted with the permission of the Journal of Periodontology.2 Table 3. The grades of periodontitis Periodontitis grade Grade A: Slow rate of progression Grade B: Moderate rate of progression Grade C: Rapid rate of progression Primary criteria Direct evidence of progression Longitudinal data (radiographic bone loss or CAL) Evidence of no loss over 5 years <2 mm over 5 years ≥2 mm over 5 years Indirect evidence of progression % bone loss/ age <0.25 0.25 to 1.0 ≥ 1.0 Case phenotype Heavy biofilm deposits with low levels of destruction Destruction commensurate with biofilm deposits Destruction exceeds expectation given biofilm deposits; specific clinical patterns suggestive of periods of rapid progression and/or early onset disease (e.g. molar/ incisor pattern; lack of expected response to standard bacterial control therapies) Grade modifiers Risk factors Smoking Non-smoker Smoker <10 cigarettes/day Smoker ≥10 cigarettes/day Diabetes Normoglycaemic/ no diagnosis of diabetes HbA1c <7.0% in patients with diabetes HbA1c ≥7.0% in patients with diabetes Grade is primarily determined by the direct evidence of progression. If not available, then the indirect evidence of progression can be used. In the presence of risk factors for periodontitis, the grade can shift to a higher tier2. The table was reprinted with the permission of the Journal of Periodontology.2. CAL, clinical attachment loss; HbA1c, haemoglobin A1c. Risk Factors Smoking

Smoking is the most important environmental risk factor for periodontitis. Compared to non-smokers or past smokers, smokers exhibited a significantly higher prevalence of red-complex periodontal pathogens in their subgingival biofilm32-34. Furthermore, a potential negative effect of smoking on host immune cells, especially neutrophils, was reported, making their host more susceptible to periodontitis35-37. Consistent with these findings, light and heavy smokers are at a greater risk for developing alveolar bone loss with an odds ratio of 3.25 and 7.28, respectively, compared to non-smokers. Similarly, light and heavy smokers are at a greater risk for developing periodontal attachment loss with an odds ratio 2.05 and 4.07, respectively, compared to non-smokers38. Furthermore, smoking has a negative impact on the outcome of active periodontal therapy as well as long-term maintenance periodontal therapy39, 40. Thus, patients should be continuously reminded of the importance of smoking cessation for successful management of periodontitis41.

Diabetes

Patients with uncontrolled diabetes are at a greater risk for developing periodontitis as compared to systemically healthy patients or patients with well-controlled diabetes42, 43. Plausible biological mechanisms underlying this association have been scientifically validated43. The association is partly due to alterations in the immune system of patients with uncontrolled diabetes, which result in impaired neutrophil function or hyper-responsive macrophages producing pro-inflammatory cytokines43. Furthermore, patients with uncontrolled diabetes exhibit alterations in connective tissue metabolism, which modulates the resorptive and formative process in the periodontium43. The alterations in connective tissue metabolism are due to higher levels of advanced glycation end products (AGEs) and interaction with their receptors, receptors for AGE (RAGEs), in patients with uncontrolled diabetes compared to systemically healthy patients or patients with well-controlled diabetes43-47. The interaction between AGEs and RAGEs results in the marked elevation of gingival crevicular fluid levels of IL-1β, TNF-α and PGE2 in patients with uncontrolled diabetes43, 45, 47. These pro-inflammatory cytokines then contribute to the inflammatory response that characterises periodontitis43, 45, 47. Lastly, macrovascular (i.e. atherosclerosis) and microvascular changes (i.e. thickening of the basement membrane) in patients with uncontrolled diabetes may result in the abnormal growth of vessels, impaired regeneration of vessels, and abnormal homeostatic transport across the basement membrane in the periodontium43.

Clinically, patients with type 2 diabetes exhibited an increased risk of periodontitis with an odds ratio of 2.81 for clinical attachment loss and an odds ratio of 3.43 for alveolar bone loss33. Patients with diabetes exhibit a greater percentage of teeth having at least one site with a probing depth of 5 mm or more, a greater percentage of sites with bleeding on probing, and a greater number of missing teeth compared to non-diabetic patients48. Moreover, patients with uncontrolled diabetes may not respond as favourably to periodontal therapy as do patients with periodontitis but milder diabetes43. Thus, patients' glycaemic status should be continuously monitored, and haemoglobin A1c (HbA1c) levels should be documented. Ideally, the HbA1c level should be <7.0%2. For patients with poorly managed diabetes, inter-professional practice is essential.

Contributing Factors Overhanging/over-contoured restorations

Overhanging or over-contoured restorations may promote dental biofilm retention, initiating a local periodontal lesion49, 50. Thus, a restoration with overhang or excessive contour should be eliminated during the course of periodontal therapy to create an environment that allows biofilm removal (Figure 3).

image

Management of a restoration with excessive contour. (a) Pre-operative radiograph; over-contoured restoration was present on the distal aspect of the mandibular right second molar, causing biofilm and food accumulation in the area. As a result, the distal aspect of the mandibular right second molar exhibited 6–7 mm probing depths. (b) Post-operative radiograph; the restoration was modified in order to improve the distal contour of the mandibular right second molar.

Open interproximal contacts

Open interproximal contacts may promote biofilm retention due to chronic food impaction51. Thus, during the course of treatment, open interproximal contacts should be corrected.

Occlusal trauma

Though occlusal trauma is not considered a risk factor for alveolar bone loss or development of periodontal disease, when occlusal trauma is present, periodontitis may exhibit a greater rate of progression52, 53. Thus, resolution of occlusal trauma should be considered during periodontal therapy (Figure 4). For example, fremitus on centric occlusion or excursive movement should be eliminated in periodontally compromised teeth. Teeth presenting with excessive or increasing mobility as a result of occlusal trauma may be splinted54.

image

A mandibular right central incisor with severe alveolar bone loss and secondary occlusal trauma. (a) Pre-operative radiograph; the mandibular right central incisor exhibited a severe vertical bone loss. Clinically, the tooth exhibited excessive mobility as a result of occlusal trauma. (b) One year post-operative radiograph; after initial periodontal therapy with occlusal adjustment and splinting, radiographic evidence of increased height of alveolar bone was noted for the mandibular incisors. No surgical treatment was performed.

Mucogingival deformity

The presence of 2 mm or more of attached gingiva is considered necessary to maintain gingival health55. A significantly higher gingival index was noted for teeth with <2 mm of attached gingiva compared to those with at least 2 mm of attached gingiva55. Thus, all mucogingival deformities should be recorded during a comprehensive periodontal evaluation and, if indicated, treated during the phase of surgical periodontal therapy.

Anatomical factors

The presence of certain anatomical factors such as a cemental tear56, narrow furcation entrance57, enamel pearl58, 59, root concavity57, cervical enamel projection60, and positioning of the tooth61, 62 may increase the risk of local periodontal attachment loss (Figure 5). Thus, these factors should be considered during diagnosis and treatment.

image

A mandibular right second molar with a distal cemental tear. Right mandibular second molar exhibited cemental tear on its distal surface. This was associated with an infrabony defect as well as a deep periodontal pocket (9 mm).

Treatment Initial cause-related therapy Home care review

Achieving adequate home care is an essential component of prevention of periodontal disease, successful periodontal therapy and long-term retention of the dentition63-65. Clinicians should educate patients about the importance of effectively removing dental biofilm at home, especially prior to proceeding with active periodontal therapy (Figure 6) 66. The importance of adequate home care should be reinforced frequently during the initial and subsequent phases of periodontal treatment.

image

Effect of home care on reducing periodontal inflammation. Improved home care/biofilm removal should be demonstrated prior to beginning active periodontal therapy. Patient presented with generalised gingival marginal erythema as well as oedema in the maxillary arch. Moderate deposits of dental biofilm were noted at the gingival margin. As a result of home care, after 9 weeks, significant resolution of gingival erythema and oedema were noted. Minimally visible dental biofilm was present, indicating effective home care. Scaling and root planing was then initiated, specifically aimed at the removal of supragingival and subgingival calculus. After completing initial cause-related therapy and achieving a stable periodontium, the maxillary left lateral incisor was extracted due to its linguoversion and endodontic pathology. (a) Initial. (b) After 9 weeks of home care. (c) Periodontal re-evaluation: 6 weeks after completing initial cause-related therapy (i.e. home care, scaling and root planing; no periodontal surgery was performed).

Scaling and root planing

After adequate home care or biofilm control is achieved, scaling and root planing should be performed at the sites with periodontal probing depths of 5 mm or greater. This phase of treatment should be delivered in conjunction with correction of local contributing factors, extraction of hopeless teeth and treatment of active carious lesions. During scaling and root planing, adequate local anaesthesia should be administered prior to initiating the procedure to ensure patient comfort. Automated instruments, such as piezoelectric or ultrasonic scalers, may be used in combination with manual instruments67. For areas where access is difficult, automated instruments may be superior to curettes for removal of subgingival biofilm and calculus68. Occlusal adjustment should be considered to relieve fremitus, severe mobility, or excessive central and lateral excursive contact54. Clinically, a periodontal explorer such as Old Dominion University explorer 11/12 should be used to check for removal of subgingival calculus. Furthermore, post-operative intraoral radiographs may be helpful to assess removal of subgingival calculus visible on pre-operative intraoral radiographs. For patients with severe periodontitis, adjunctive use of systemic antibiotics may be considered69, 70. Recent randomised clinical trials71, 72 as well as systematic reviews and meta-analysis73-75 reported a significant improvement in the outcome of scaling and root planing when antibiotics were used systemically as an adjunctive therapy. For example, in a recent systematic review of a total of 28 double-blinded randomised controlled trials investigating the benefit of systemic antibiotics as an adjunctive therapy to scaling and root planing in the treatment of moderate to severe periodontitis76, meta-analysis reported a statistically significant additional full-mouth probing depth mean reduction of 0.448 mm and a clinical attachment gain of 0.389 mm at 6-month follow-up in the antibiotic versus the placebo control groups, which appeared to persist at 12-month follow-up (i.e. pocket probing reduction of 0.485 mm and clinical attachment level gain of 0.285 mm)76. These improvements were further supported by reductions in bleeding on probing and in frequency of residual periodontal pockets, and increases in periodontal pocket closure76. The most significant benefit was observed with amoxicillin and metronidazole76. Considering the limited evidence to support the superiority of any specific dosage regimen, clinicians should consider using the highest dosage for the shortest duration of time to reduce the risk of antibiotic resistance73. For a localised site with a deep periodontal probing depth, administration of a locally delivered antibiotic (i.e. minocycline microspheres77-80) or an antimicrobial (i.e. chlorhexidine chip81, 82) may be considered. Benefit of host modulation therapy was also reported in several studies83, 84. When administered at sub-antimicrobial dosages, doxycycline inhibits MMPs in the gingival tissues without a microbial effect83, 84. The significant adjunctive effect of sub-antimicrobial dosage doxycycline in addition to scaling and root planing was found in treating patients with periodontitis83. Furthermore, the adjunctive use of omega-3 fatty acids and 81 mg acetylsalicylic acid with scaling and root planing in patients with periodontitis resulted in a significant reduction of probing depths and a significant clinical attachment gain compared to scaling and root planing alone85,

留言 (0)

沒有登入
gif