Fernando Suarez - Periodontics_ The Complete Summary-Quintessence Publishing (2021) pages 11 - 21.pdf

2 EXAMINATION AND DIAGNOSIS Shan-Huey Yu, dds, ms A thorough and comprehensive clinical and radiographic examination DEFINITIONS AND is the critical first step for establishing a proper periodontal diagno- TERMINOLOGY sis before a treatment plan can be develop...

2 EXAMINATION AND DIAGNOSIS Shan-Huey Yu, dds, ms A thorough and comprehensive clinical and radiographic examination DEFINITIONS AND is the critical first step for establishing a proper periodontal diagno- TERMINOLOGY sis before a treatment plan can be developed. The objective of this Clinical attachment level: The chapter is to review the main components of a periodontal examination distance from the cementoenamel and interpretation of these parameters to aid in developing a periodontal junction (CEJ) to the tip of a peri- diagnosis. The second part of this chapter is an overview of the different clas- odontal probe during periodontal diagnostic probing. The health of the sifications for periodontal diseases and conditions that have been proposed attachment apparatus can affect the and developed over the years. measurement.1 Furcation: The anatomical area of a multirooted tooth where the roots Clinical Examination diverge.1 Furcation involvement: Pathologic To determine a proper periodontal diagnosis, clinicians should perform a resorption of bone within a furcation. periodontal examination that includes but is not limited to the following The degree of interradicular bony parameters2,3: destruction of a multirooted tooth. It is characterized by factors such as root Probing depth (PD) trunk length, root concavities, and the extent of root separation.2 Gingival recession Clinical attachment level (CAL) Recession: The migration of the Width of keratinized gingiva (KG) and attached gingiva (AG) marginal soft tissue to a point apical to the CEJ of a tooth or the platform of a Signs of gingival inflammation (ie, bleeding on probing [BOP], suppura- dental implant.1 tion, gingival color and texture) Tooth mobility Degree of furcation involvement Extent, distribution, and pattern of radiographic bone loss Patient’s medical and dental history3 PROBING DEPTH The measurement of PDs is considered to be one of the most important parameters of the periodontal examination because it provides an overall assessment of the periodontal pockets, which are usually considered as a critical sign for the establishment of a diagnosis. In addition, pockets 11  2 | EXAMINATION AND DIAGNOSIS BOX 2-1 Common types of periodontal probes and utilized for different indications. Box 2-1 summarizes the common types of conventional probes used in the Williams probe clinic and their characteristics and indications.4 The graduations on this probe are 1-, 2-, 3-, 5-, Conventional probes are easily operated and inexpen- 7-, 8-, 9-, and 10-mm. The 4- and 6-mm markings sive; therefore, these are the most commonly used probe are absent to improve visibility and avoid confu- system in dental clinics. However, conventional probes sion in reading the markings. also present with several disadvantages4: Merritt B probe The graduations and markings on this probe are The pressure applied cannot be standardized. the same as Williams probe. Assistants are often needed to transfer measurements Goldman-Fox probe This probe has a flattened tip. The graduations to a periodontal chart. and markings on this probe are the same as Operator variability and errors can affect the readings Williams probe; however, the flat tip end might of the markings. preclude easy access into tight or narrow pockets. In order to overcome these disadvantages of conven- UNC 15 probe tional probes, new generations of probes have been devel- The graduations on this probe are 1-, 2-, 3-, 4-, 5-, 6-, 7-, 8-, 9-, 10-, 11-, 12-, 13-, 14-, and 15-mm. oped. These include but are not limited to the following4: This probe is color-coded at every millimeter demarcation, and it is suitable for deeper pock- Constant-pressure probes: Designed to be pressure ets (ie, > 10 mm). sensitive, therefore allowing for standardization of the Marquis color-coded probe force applied during PD measurements. The graduations on this probe are 3-, 6-, 9-, and Computer-assisted/automated probes: This generation 12-mm. Color markings are darker at 3–6 mm of probes was developed based on constant-pressure and 9–12 mm. The main disadvantage of this probe is its accuracy; the measurements are probes. Added features include automated detection of usually estimated between color markings. the measurement and computer-assisted data capture Michigan O probe into a storage system. This minimizes possible errors The graduations on this probe are 3-, 6-, and from probe reading and data recording. 8-mm and are color-coded. This probe might 3D probes: This instrument aims to develop a method not be suitable for deeper pockets (ie, > 8 mm), to record the PD in a serial matter instead of linear and the measurements are also estimated measurements. between color markings. Noninvasive probes: Probing into periodontal pockets CPITN probe can often be uncomfortable and/or painful to patients. The graduations on this probe are 3.5-, 5.5-, 8.5-, and 11.5-mm. Markings are a darker color This probe system is still under development, and it at 3.5–5.5 mm and 8.5–11.5 mm. This probe is aims to identify the periodontal pocket and attach- particularly useful for screening and monitoring ment level without the need to physically penetrate patients or for epidemiologic research. the tissues. UNC, University of North Carolina; CPITN, community periodontal index of treatment needs. The usage of these newer probe systems is still very limited due to various considerations such as cost (more are also the major habitats for periodontal pathogens.3 expensive), less tactile sensitivity, and less accessibility Currently, the most widely used instrument to obtain PDs for most dentists. To date, the conventional periodontal in clinical practice is the conventional or manual probe. probe is still the most popular system that is used in dental In 1936, periodontist Charles H. M. Williams created the offices when a periodontal examination is performed.4 first periodontal probe, and his invention—the Williams It is very important to bear in mind that, when measur- periodontal probe—has been the prototype or benchmark ing PDs with a conventional probe, there are a number for all manual probes.4 Different types of conventional of factors that can affect these measurements and their periodontal probes have been developed over the years accuracy. The variables are summarized in Table 2-1.5–14 12  Clinical Examination TABLE 2-1 Variables affecting probing measurements Reproducibility Operators’ experience and skills would affect the inter- and intraexaminer reproducibility. Probing force Probing force affects how deep the periodontal probes penetrate into the pocket and the connective tissue; greater probing force usually results in deeper PDs.5 It has been recommended that 30 g (0.3 N) of probing force be used during periodontal examination to allow the probe tip to remain within the junctional epithelium.6,7 Probing forces up to 50 g (0.5 N) would penetrate deeper, and the probe tip could reach closer to the alveolar bone.6,7 Probe angulation Mean PDs could be 1 mm greater with midproximal compared to line-angle measurements.8 Gingiva inflammation Periodontal probes tend to penetrate deeper into the gingival tissue when inflammation is present9–14: Healthy dentition Apical one-third of junctional epithelium Gingivitis Apical one-third of junctional epithelium Periodontitis Coronal one-third of connective tissue Posttreatment periodontitis Apical one-third of junctional epithelium Site and local anatomy Crown contours, defective restorations and margins, tipped or rotated teeth, osseous ledges, and subgingival calculus can all affect probing accuracy. Type of probe Different types of conventional probes, pressure-sensitive probes, and computer-assisted data recording probes could yield different measurements. Natural dentition versus Probing at an implant site usually results in deeper depths compared with probing at a natural dental implants tooth9–14: Healthy implant Apical one-third of junctional epithelium to coronal one-third of connective tissue Peri-implant mucositis Apical two-thirds of connective tissue Peri-implantitis Apical one-third of connective tissue and close proximity to bone Posttreatment Apical two-thirds of connective tissue peri-implantitis It is also of relevance to differentiate between the terms CLINICAL ATTACHMENT LEVEL “pocket depth” and “probing depth.” The measurement obtained with a probe into the gingiva includes not only The definition of CAL is the distance from the cemen- the depth of the gingival sulcus or periodontal pocket, toenamel junction (CEJ) to the tip of a periodontal probe but also an additional distance that represents varying during diagnostic periodontal probing.1 The amount of degrees of adjacent tissue penetration.15 Therefore, the gingival recession is needed to calculate the CAL. Reces- objective when a periodontal probe is inserted into the sion by definition is the migration of the gingiva to a point space between the tooth and the gingiva is to measure apical to the CEJ,1 and it is often described as the distance the probing depth instead of the anatomical structure between CEJ and the free gingival margin. Recession can of the pocket depth, which can only be accomplished be recorded as a positive (+) or negative (–) measurement. histologically.2 Listgarten also emphasized the use of the Recession is recorded as “+” when CEJ is visible and the correct terminology “probing depth” when describing free gingival margin is below the CEJ. However, when periodontal probing in the literature.15 there is gingival enlargement, recession is recorded as a negative “–” measurement (Fig 2-1). CAL can then be 13  2 | EXAMINATION AND DIAGNOSIS 3mm 0 3 6 9 12 PD = 6 mm PD = 6 mm PD = 6 mm PD = 6 mm Rec = –6 mm Rec = –3 mm Rec = 0 mm Rec = +3 mm CAL = 0 mm CAL = 3 mm CAL = 6 mm CAL = 9 mm Fig 2-1 Representation of different situations with 6 mm PD and different attachment levels. Rec, recession. Gingival sulcus ATTACHED GINGIVA AND KERATINIZED GINGIVA The amount of AG and the width of KG are also important Free or marginal gingiva clinical parameters to record during a comprehensive periodontal evaluation. AG extends from the free gingival marginal groove to the mucogingival junction (MGJ), and Marginal groove it is the portion of the gingiva bonded to the tooth and the alveolar bone through gingival fibers1 (Fig 2-2). On the other hand, KG includes free (marginal) gingiva and the AG. Around teeth, healthy and uninflamed gingival Attached gingiva tissue usually encompass a band of AG, which is crucial to defend against pathogens.2 Lang and Löe performed a clinical study evaluating Mucogingival the inflammation status by examining gingival exudate junction of teeth with or without 2 mm of KG.16 The results from this investigation indicated that most teeth with < 2 mm Alveolar mucosa of KG presented with clinical inflammation and vary- ing amounts of exudate while surfaces with ≥ 2 mm of KG were healthy, and most of these surfaces showed no Fig 2-2 Gingival landmarks. exudate.16 Therefore, it was concluded that 2 mm of KG and 1 mm of AG are needed to maintain periodontal stability.16 Nevertheless, evidence from another study demonstrated that when good plaque control is achieved through adequate home care, the presence of AG/KG is calculated by adding PD and recession (making sure to not an essential prerequisite for the maintenance of peri- include “+” or “–”). In Fig 2-1, all four case scenarios odontal health and attachment.17 Overall, it is generally measured 6 mm PD; however, when recession is taken into accepted that the presence of a collar of KG and AG is account to determine the CAL, it is clear that the degree of beneficial for the long-term stability of the periodon- periodontal destruction of these four cases is very differ- tium, and even more important when oral hygiene is ent. Therefore, compared with PD, the level of CAL can not optimal. The MGJ and the width of KG can be deter- provide a better overall estimate of the periodontium, and mined using the methods demonstrated in Fig 2-3 and it usually correlates better with radiographic bone loss.3 Box 2-2.2,16 14  Clinical Examination BLEEDING ON PROBING BOP is another important parameter to record during periodontal examination, and it indicates evidence of gingival inflammation. A prospective study by Lang and colleagues evaluated the prognostic value of sites with BOP and the risk for periodontal breakdown of at least 2 mm of attachment loss during periodontal maintenance therapy.18 The results showed that only a 30% probability of future attachment loss may be predicted for sites repeat- edly positive for BOP (Table 2-2).18 Further calculations Fig 2-3 Visual examination of the MGJ. The arrow indicates confirmed that frequent BOP for prediction of future the junction between the KG and the mucosa. KG presents as a coral pink color, while mucosa is redder. attachment loss yields a specificity of 88%, and the contin- uous absence of BOP has a positive predictive value of 98%.19 Therefore, it is of paramount importance to under- BOX 2-2 Methods to determine the location of MGJ and stand that BOP alone does not represent a good positive the width of KG3,16 predictor for disease progression7; instead, studies have shown that absence of BOP is a more reliable parameter Visual to indicate periodontal stability.19 BOP is also sensitive to Examine for color difference. AG/KG of healthy the forces applied with the probe2,19; therefore, Lang et al gingiva usually presents a coral pink coloration, suggested a probing force of 25 g (0.25 N) when recording while mucosa is darker and redder (see Fig 2-3). BOP, as heavier pressures (> 25 g) might traumatize the Schiller’s iodine test gingival tissue and provoke bleeding.19 In conclusion, the Oral mucosa can be stained with an iodine solu- presence of BOP has low sensitivity and high specificity tion because of the glycogen distribution, while KG is iodine-negative.16 with respect to the development of additional attachment Roll technique loss. For clinicians to monitor patients’ periodontal stabil- Oral mucosa is movable while AG/KG is bonded ity over time in daily practice, the absence of BOP at 25 g to tooth surface and bone. A clear demarcation is a reliable indicator for periodontal stability with a nega- (MGJ) would appear when rolling from movable tive predictive value of 98%.7,18,19 mucosa to AG/KG. FURCATION INVOLVEMENT The furcation is the anatomical area of a multirooted TABLE 2-2 Positive predictive values for loss of tooth from where the roots diverge and form bifurcation attachment of ≥ 2 mm in 2 years in sites that bled on (two-rooted tooth) or trifurcation (three-rooted tooth).2 probing 0, 1, 2, 3, or 4 times out of 4 maintenance visits18 Furcation involvement or furcation invasion describes the Sites with loss of BOP incidence pathologic resorption of bone within a furcation area1,2,20 attachment > 2 mm (Fig 2-4). The Nabers furcation probe is widely used 4/4 30% and suited for detection and examination of furcation involvement.2,20 The extent and configuration of furcation 3/4 14% involvement can be characterized by anatomical factors 2/4 6% including but not limited to presence of cervical enamel 1/4 3% projections, enamel pearls, root trunk distance, tooth surface concavities, and the extent of root separation. The 0/4 1.5% following summarizes the furcation entrances of multi- rooted teeth to aid in detection of furcation involvement20: 15  2 | EXAMINATION AND DIAGNOSIS Degree I Degree II Degree III Fig 2-4 Furcation entrance on a mandibular first molar. Fig 2-5 Different degrees of furcation involvement. Maxillary premolar: Grade II: Loss of interradicular bone and pocket forma- – Furcation involvement can be detected from the tion of varying depths into the furcation area but not mesial or distal surface; the entrance is located at completely through to the opposite side of the tooth. the apical third of the root and/or approximately 8 Grade III: Through-and-through lesion. mm below the CEJ. Grade IV: Same as Grade III with through-and-through Maxillary molars: lesion with gingival recession, rendering the furcation – Buccal entrance: Centered mesiodistally. area clearly visible on clinical examination. – Mesial entrance: Two-thirds of the buccolingual width toward the palatal aspect, easier to approach Hamp et al (1975) proposed three levels of furcation from mesiopalatal aspect. involvement22 (Fig 2-5): – Distal entrance: Furcation entrance is centered buccolingually and can be examined from either Degree I: Horizontal loss of periodontal tissue support the buccal or palatal aspect. < 3 mm. Mandibular molars: Degree II: Horizontal loss > 3 mm, but not passing the – Buccal entrance: Centered mesiodistally at the buccal total width of the furcation. surface. Degree III: Horizontal through-and-through – Lingual entrance: Centered mesiodistally at the destruction. lingual surface. Vertical destruction The amount of furcation involvement of a multirooted Tarnow and Fletcher (1985) proposed the following classi- tooth can be registered depending on the horizontal and fication based on the vertical bone loss around furcations. vertical amount of bony destruction into the furcation It is encouraged to supplement each category of horizontal area.20–22 Many systems have been proposed for classifying destruction with a subclass based on the vertical bone furcation involvement.2 Hamp’s classification is one of resorption.23 the most commonly used for furcation destruction.22 A brief review of three systems is presented in the following Subclass A: 0 to 3 mm probeable depth. sections.2,20–23 Subclass B: 4 to 6 mm probeable depth. Subclass C: ≥ 7 mm probeable depth. Horizontal destruction Glickman (1958) divided furcation involvement into 4 MOBILITY grades21: The definition of tooth mobility is the movement of a tooth Grade I: Pocket formation into the flute but intact inter- in its socket resulting from an applied force.1 Increase radicular bone. Incipient lesion. in tooth mobility is often a sign of periodontal break- down and/or presence of excessive occlusal forces.1 Tooth 16  Radiographic Interpretation mobility is detected by using the ends of two instruments clinical attachment variations are greater than radio- (eg, mirror handle) on either side of the tooth and alter- graphic changes.26 nately applying forces.2 The most commonly used clinical Radiographic changes are detectable by simple visual index for tooth mobility is the Miller Index; using this inspection when approximately 30% to 50% of the bone index, mobility can be scored as the following2,24: mineral has been lost.27 Class 0: Normal (physiologic) movement when force The presence or absence of the crestal lamina dura is applied. It has been defined as movement up to 0.2 is another common interpretation of radiographs for mm horizontally and 0.02 mm axially. diagnosing periodontitis. Rams et al28 observed that Class I: First distinguishable sign of movement greater the presence of intact crestal lamina dura is positively than “normal” or “physiologic.” correlated to periodontal stability over a 2-year follow Class II: Movement of the crown up to 1 mm in any up period. However, no significant relationship could be direction (buccolingual or mesiodistal). found between future periodontal breakdown and lack of Class III: Movement of the crown more than 1 mm crestal lamina dura.28 A recent publication by Rams et al in any direction (buccolingual or mesiodistal) and/or also reported similar findings and concluded that patients vertical depression (apicocoronal) or rotation of the with angular bony morphology and PD greater than 5 crown in its socket. mm poses a significant risk of periodontitis progression after treatment. However, if intact crestal lamina dura is present, despite the bony morphology, clinical stability Radiographic Interpretation for at least 24 months can be anticipated.29 Also, molar furcation involvement can sometimes be observed on Clinical periodontal examination provides information radiographs. Hardekopf et al were the first to describe the with regard to PDs, recession defects, AG/KG, and more; radiographic features of maxillary molars with furcation however, it cannot reveal the status of the alveolar bone. destruction: a triangular radiographic shadow, commonly The alveolar bone is another critical aspect to take into known as “furcation arrow,” can be noted over the mesial consideration to accurately diagnose different periodon- and distal proximal areas of maxillary molars.30 The clin- tal diseases and conditions.2 Dental radiographs are the ical reliability of the presence of furcation arrow can be most commonly used noninvasive method of examining subjective and also greatly dependent on the degree of alveolar bone levels. Other valuable information that can destruction. For instance, when furcation arrows are pres- be obtained through radiographic examination includes ent on radiographs, these can only predict actual furcation subgingival calculus deposition, root length and form, invasion 70% of the time. On the other hand, when there crown-to-root ratio, presence of periapical lesions, peri- is true furcation involvement, a furcation arrow is seen odontal ligament space, root proximity, and the destruc- in less than 40% of the sites.31 It has been reported that tion of alveolar bone.2,7 the presence of furcation arrow for diagnosing furcation Clinicians should keep in mind the following limita- involvement on maxillary molars has a low sensitivity tions of conventional dental radiography when interpret- (38.7%) and high specificity (92.2%).31 When mandibular ing radiographs during the examination phase3,7,25: molars suffer from furcation involvement, radiolucency can be noted at the area where roots start to separate. Radiographs do not show periodontal pockets.25 In recent years, the utilization of CBCT has been Radiographs cannot distinguish between posttreatment rapidly increasing in popularity. CBCT has become an periodontitis and active periodontitis.25 integral tool for researchers and clinicians, mostly applied Radiographs do not show buccal and lingual aspects to the implant field. As such, the use of CBCT imaging of tooth and alveolar bone.25 for the diagnosis of periodontitis has also been studied. Radiographs cannot detect tooth mobility.25 However, in 2017, the American Academy of Periodon- Radiographs can provide evidence of past destruction tology reported that even though its use may be beneficial to the periodontium, but they cannot identify sites with in selective cases, there is limited evidence to support the active or ongoing periodontal inflammation.7 use of CBCT for the different types of bony defects, and Clinical attachment loss always precedes visual radio- there are no guidelines for its application to periodontal graphic changes by approximately 6 to 8 months, and treatment planning.32 17  2 | EXAMINATION AND DIAGNOSIS BOX 2-3 Classification proposed in 1989 World Workshop notable proinflammatory cytokines that has been exten- in Clinical Periodontics37 sively studied in the periodontal field.34,35 Periodontal pathogens that have been extensively studied and proved I. Adult periodontitis (> 35 y) to be closely linked to the development of periodontitis II. Early-onset periodontitis (≤ 35 y) include Porphyromonas gingivalis, Treponema denticola, A. Prepubertal periodontitis (< 13 y) 1. Generalized Tannerella forsythia, Aggregatibacter actinomycetemcomi- 2. Localized tans, Fusobacterium nucleatum, and more.2,36 Research in B. Juvenile periodontitis (13 to 26 y) the field of advanced examination and biomarkers is still 1. Generalized ongoing, and the results have indicated a promising future 2. Localized for early detection of periodontitis. However, these exam- C. Rapid progressive periodontitis (25 to inations are still not routinely utilized, due at least in part to 35 y) III. Periodontitis associated with systemic the additional costs and disassociation to treatment options diseases (ie, the test results would not alter the treatment plan).34 IV. Necrotizing ulcerative periodontitis V. Refractory periodontitis Classifications of Periodontal Diseases and Conditions Classification systems are essential to properly study the Advanced and Emerging diagnosis, etiology, pathogenesis, and treatment of the Examination different diseases. As such, the field of periodontology has witnessed the creation and continued update of differ- Periodontitis is a multifactorial disease involving the ent classification systems since the early 1940s. The first combination of dysbiosis of oral bacteria and an over- World Workshop in Periodontics37 was held in Ann Arbor, reacted immune response from the host.33 One of the Michigan, on June 6 to 9, 1966, and the most recent World disadvantages of the clinical periodontal evaluation is Workshop took place in Chicago on November 9 to 11, that these examinations only record destruction that 2017, with the related publications released in June 2018.38 has already occurred, such as the bone loss pattern and Understanding the development and the variations among periodontal pockets. Therefore, patients would greatly the different classifications is critical for comprehending benefit from techniques that detect the development of the literature published in different eras. periodontal inflammation before tissue breakdown occurs and prevent further complications such as bone loss, tooth 1989 WORLD WORKSHOP IN CLINICAL mobility, and ultimately tooth loss. The major rationale to PERIODONTICS develop advanced methods for examination is to detect disease activity at a subclinical level in order to provide One of the first major and comprehensive classifications early diagnosis and create a treatment plan tailored to of periodontitis emerged from the World Workshop each individual.34 in 1989.37 On this date, the World Workshop in Clini- Researchers and scientists have been investigating possi- cal Periodontics gathered scientists and researchers to ble periodontitis-related biomarkers that could be used develop a classification for periodontal diseases. There to distinguish between healthy and diseased patients.34 were essentially five different classifications, which are These biomarkers can be collected from saliva, which listed in Box 2-3.37 can demonstrate overall periodontal health at a subject Under the 1989 classification system, age of onset and level, or gingival crevicular fluid, which is site specific.34 distribution of lesions were taken into consideration for For instance, proportions of specific periodontal patho- classifying adult periodontitis and early onset periodon- gens, pro- and anti-inflammatory cytokines, and tissue- titis as well as the subforms of early-onset periodontitis degradation products have all been studied to differenti- that included prepubertal periodontitis (generalized/ ate between healthy and periodontitis subjects. Among localized), juvenile periodontitis (generalized/ localized), all biomarkers, interleukin-1 (IL-1) is one of the most and rapidly progressive periodontitis.37 18  Classifications of Periodontal Diseases and Conditions 1999 INTERNATIONAL WORKSHOP FOR A classification scheme to the current understanding of CLASSIFICATION OF PERIODONTAL periodontal and peri-implant diseases and conditions. DISEASES AND CONDITIONS Therefore, in addition to updating the 1999 classification of periodontal diseases and conditions, this was also the The 1989 classification raised problems in several areas39: first world consensus to develop a classification scheme for peri-implant diseases and conditions.38 Considerable overlap in disease categories A brief classification scheme for the 2017 world work- Absence of a gingival disease component shop is presented in Box 2-5,38 and major changes to the Inappropriate emphasis on age of onset of disease and 1999 classification include the following40: rates of progression Inadequate or unclear classification criteria The 2017 workshop characterized periodontal health and gingival inflammation in a reduced periodontium Therefore, the next landmark classification was the after completion of successful treatment of a patient 1999 International Workshop for a Classification of with periodontitis. Periodontal Diseases and Conditions, which addressed The workshop agreed that, consistent with current some of the problems in the previous classification. The knowledge on pathophysiology, three forms of peri- major changes in the classification system for periodontal odontitis can be identified: diseases included (Box 2-4)39: – Necrotizing periodontitis – Periodontitis as a manifestation of systemic disease Addition of a section on gingival diseases – Periodontitis Replacement of “Adult periodontitis” with “Chronic The forms of the disease previously recognized as periodontitis” “chronic” or “aggressive” are now grouped under a Replacement of “Early-onset periodontitis” with single category, “periodontitis.” “Aggressive periodontitis” A new classification framework for periodontitis was Elimination of a separate disease category for Refrac- established and further characterized based on a multi- tory periodontitis dimensional staging and grading system that can be Clarification of the designation “Periodontitis as a adapted over time as new evidence emerges. manifestation of systemic diseases” – Goals of staging a periodontitis patient40: Replacement of “Necrotizing ulcerative periodontitis” Classify severity and extent of an individual based with “Necrotizing periodontal diseases” on currently measurable extent of destroyed and Addition of “Periodontal abscesses” category damaged tissue attributable to periodontitis. Addition of “Periodontic-endodontic lesions” category Assess specific factors that may determine Addition of “Developmental or acquired deformities complexity of controlling current disease and and conditions” category managing long-term function and esthetics of the patient’s dentition. – Goals of grading a periodontitis patient40: 2017 WORLD WORKSHOP ON THE Estimate future risk of periodontitis progres- CLASSIFICATION OF PERIODONTAL AND PERI-IMPLANT DISEASES AND sion and responsiveness to standard therapeu- CONDITIONS tic principles, to guide intensity of therapy and monitoring. In order to update the 1999 classification of periodontal Estimate potential health impact of periodonti- diseases and conditions,39 an organizing committee from tis on systemic disease and the reverse, to guide the American Academy of Periodontology (AAP) and the systemic monitoring and cotherapy with medical European Federation of Periodontology (EFP) commis- colleagues. sioned the world workshop that was held in Chicago on A new classification scheme for dental implants was November 9 to 11, 2017.38 The world workshop included developed by the workshop, including the follow- expert participants in the field of periodontology and ing: peri-implant health, peri-implant mucositis, implant dentistry from around the world. The scope of peri-implantitis, and peri-implant soft and hard tissue the 2017 world workshop was to align and update the deficiencies. 19  2 | EXAMINATION AND DIAGNOSIS BOX 2-4 Summary of 1999 International Workshop for a Classification of Periodontal Diseases and Conditions39 I. Gingival diseases V. Necrotizing periodontal diseases A. Dental plaque–induced gingival diseases A. Necrotizing ulcerative gingivitis (NUG) 1. Gingivitis associated with dental plaque B. Necrotizing ulcerative periodontitis (NUP) only VI. Abscesses of the periodontium 2. Gingival diseases modified by systemic A. Gingival abscess factors B. Periodontal abscess 3. Gingival diseases modified by C. Pericoronal abscess medications VII. Periodontitis associated with endodontic 4. Gingival diseases modified by lesions malnutrition A. Combined periodontic-endodontic lesions B. Non-plaque-induced gingival lesions VIII. Developmental or acquired deformities and 1. Gingival diseases of specific bacterial conditions origin A. Localized tooth-related factors that modify 2. Gingival diseases of viral origin or predispose to plaque-induced gingival 3. Gingival diseases of fungal origin diseases/periodontitis 4. Gingival lesions of genetic origin 1. Tooth anatomical factors 5. Gingival manifestations of systemic 2. Dental restorations/appliances conditions 3. Root fractures 6. Traumatic lesions (factitious, iatrogenic, 4. Cervical root resorption and cemental accidental) tears 7. Foreign body reactions B. Mucogingival deformities and conditions 8. Not otherwise specified (NOS) around teeth II. Chronic periodontitis 1. Gingival/soft tissue recession A. Localized (≤ 30% of sites involved) 2. Lack of keratinized gingiva B. Generalized (> 30% of sites involved) 3. Decreased vestibular depth III. Aggressive periodontitis 4. Aberrant frenum/muscle position A. Localized (≤ 30% of sites involved) 5. Gingival excess B. Generalized (> 30% of sites involved) C. Mucogingival deformities and conditions IV. Periodontitis as a manifestation of systemic on edentulous ridges diseases 1. Vertical and/or horizontal ridge A. Associated with hematologic disorders deficiency 1. Acquired neutropenia 2. Lack of gingiva/keratinized tissue 2. Leukemias 3. Gingival/soft tissue enlargement 3. Other 4. Aberrant frenum/muscle position B. Associated with genetic disorders 5. Decreased vestibular depth 1. Familial and cyclic neutropenia 6. Abnormal color 2. Down syndrome D. Occlusal trauma 3. Leukocyte adhesion deficiency 1. Primary occlusal trauma syndromes 2. Secondary occlusal trauma 4. Papillon–Lefèvre syndrome 5. Chediak-Higashi syndrome 6. Histiocytosis syndromes 7. Glycogen storage disease 8. Infantile genetic agranulocytosis 9. Cohen syndrome 10. Ehlers-Danlos syndrome (Types IV and VIII) 11. Hypophosphatasia 12. Other C. Not otherwise specified (NOS) D. Necrotizing ulcerative periodontitis (NUP) 20  Classifications of Periodontal Diseases and Conditions BOX 2-5 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions38 I. Periodontal health, gingival diseases/conditions 3. G rades: Evidence of risk of rapid A. Periodontal health and gingival health progression, anticipated treatment 1. Clinical gingival health on an intact i. Grade A: Slow rate of progression periodontium ii. Grade B: Moderate rate of 2. Clinical gingival health on a reduced progression periodontium iii. Grade C: Rapid rate of progression i. Stable periodontitis patient III. Periodontal manifestation of systemic diseases ii. Non-periodontitis patient and developmental and acquired conditions B. Gingivitis: Dental biofilm–induced A. Systemic diseases or conditions affecting 1. Associated with dental biofilm alone the periodontal supporting tissues 2. Meditated by systemic or local risk B. Other periodontal conditions factors 1. Periodontal abscesses 3. Drug-influenced gingival enlargement 2. Endodontic-periodontic lesions C. Gingival diseases: Non-dental- C. Mucogingival deformities and conditions biofilm-induced around teeth 1. Genetic/developmental disorders 1. Gingival biotype 2. Specific infections 2. Gingival/soft tissue recession 3. Inflammatory and immune conditions 3. Lack of gingiva 4. Reactive processes 4. Decreased vestibular depth 5. Neoplasms 5. Aberrant frenum/muscle position 6. Endocrine, nutritional, and metabolic 6. Gingival excess diseases 7. Abnormal color 7. Traumatic lesions 8. Condition of the exposed root surface 8. Gingiva pigmentation D. Traumatic occlusal forces II. Forms of periodontitis 1. Primary occlusal trauma A. Necrotizing periodontal diseases 2. Secondary occlusal trauma 1. Necrotizing gingivitis 3. Orthodontic forces 2. Necrotizing periodontitis E. Prosthesis- and tooth-related factors that 3. Necrotizing stomatitis modify or predispose to plaque-induced B. Periodontitis as manifestation of systemic gingival diseases/periodontitis diseases 1. Localized tooth-related factors C. Periodontitis 2. Localized dental prosthesis–related 1. Stages: Based on severity and factors complexity of management IV. Peri-implant diseases and conditions i. Stage I: Initial periodontitis A. Peri-implant health ii. Stage II: Moderate periodontitis B. Peri-implant mucositis iii. Stage III: Severe periodontitis with C. Peri-implantitis potential for additional tooth loss D. Peri-implant soft and hard tissue iv. Stage IV: Severe periodontitis with deficiencies potential for loss of the dentition 2. Extent and distribution: Localized (< 30% teeth); generalized (≥ 30% teeth); molar-incisor distribution 21