Introducing Periodontal Health and Plaque Induced Gingival Diseases and Conditions 2024-2025 PDF

Dental Clinical Practice 2 Introducing Periodontal Health and Plaque Induced Gingival Diseases and Conditions DR. ABIER ABDULSATTAR MOHAMMED  LEARNING OBJECTIVES 1. Explain 2017- Classification for Periodontal and Peri-implant Diseases and Conditions. 2. De...

Dental Clinical Practice 2 Introducing Periodontal Health and Plaque Induced Gingival Diseases and Conditions DR. ABIER ABDULSATTAR MOHAMMED  LEARNING OBJECTIVES 1. Explain 2017- Classification for Periodontal and Peri-implant Diseases and Conditions. 2. Describe Periodontal Health. 3. Apply the classification in the diagnosis of plaque induced gingival conditions and diseases. 4. List the Systemic etiological factors of plaque induced gingival diseases. Abier A.S. Mohammed 2  Classification systems are necessary to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. 3  PERIODONTIUM Periodontium is composed of : 1. Gingiva 2. Periodontal ligament 3. Cementum Attachment Apparatus 4. Alveolar bone 4 PERIODONTAL DISEASES CLASSIFICATION https://www.cda-adc.ca/jcda/vol-66/issue-11/594.pdf  The 1999 classification of periodontal diseases was based on their extent (generalized versus localized); severity (slight, moderate, or severe); rate of progression (aggressive versus chronic); and localization (i.e., contained within the gingiva, as in gingivitis, or further involving alveolar bone, as in periodontitis) that are briefly mentioned for historical purposes and continuity. Since then, periodontology has seen major advances over the last two decades. Therefore, in 2017, the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) convened periodontal experts from around the world to develop updated definitions for periodontal health, gingival disease, periodontitis, periodontal manifestations of systemic diseases, and peri-implant diseases. 6 On October 30–November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held, and a new classification was agreed upon and has been accepted by the American Academy of Periodontology (AAP). I. Gingival Diseases A. Dental plaque-induced gingival diseases B. Non-plaque-induced gingival lesions II. Chronic Periodontitis III. Aggressive Periodontitis IV. Periodontitis as a Manifestation of Systemic Diseases V. Necrotizing Periodontal Diseases VI. Abscesses of the Periodontium VII. Periodontitis Associated With Endodontic Lesions VIII. Developmental or Acquired Deformities and Conditions 2 0 1 7 C L A S S I F I C AT I O N O F P E R I O D O N TA L A N D P E R I - I M P L A N T D I S E A S E S A N D CO N D I T I O N S The workshop was co-sponsored by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) and included expert participants from all over the world. planning for the conference, which was held in Chicago on November 9 to 11, 2017, began in early 2015. The authors were charged with updating the 1999 classification of periodontal diseases and conditions and developing a similar scheme for peri-implant diseases and conditions. The intent of the workshop was to base classification on the strongest available scientific evidence, lower-level evidence and expert opinion were inevitably used whenever sufficient research data were unavailable. The scope of this workshop was to align and update the classification scheme to the current understanding of periodontal and peri-implant diseases and conditions.  PERIODONTAL HEALTH,GINGIVAL DISEASES AND CONDITIONS  PERIODONTAL HEALTH, GINGIVAL DISEASES AND CONDITIONS Gingivitis: Gingival Disease: Periodontal health Dental Biofilm- Non-Dental and Gingival Health Induced Biofilm-Induced  1. PERIODONTAL HEALTH AND GINGIVAL HEALTH “Health is a state of complete physical, mental and social well- being and not merely the absence of disease or infirmity.”(WHO,March,2018) Periodontal health should be defined as a state free from inflammatory periodontal disease that allows an individual to function normally and not suffer any consequences (mental or physical) as a result of past disease. State free from inflammatory periodontal disease. This, in turn, means that absence of inflammation associated with gingivitis or periodontitis, as assessed clinically, is a prerequisite for defining periodontal health. Pristine Clinical Health Clinically Healthy  PERIODONTAL HEALTH AND GINGIVAL HEALTH Clinical Gingival Health on Reduced a Periodontium Clinical Gingival Health on an Intact Periodontium Stable Periodontitis Patient Non-Periodontitis Patient  PERIODONTAL HEALTH AND TREATMENTS TARGETS FOR A DISEASED OR REDUCED PERIODONTIUM It is proposed that there are 4 levels of periodontal health, depending upon whether the periodontium has normal attachment and bone level or reduced support, as well as the ability to control modifying factors and relative treatment outcomes. These 4 categories include: 1) Pristine periodontal health, defined as a total absence of clinical inflammation periodontium with normal support (no attachment or bone loss). Pristine periodontal health is not likely to be observed clinically. 2) Clinical periodontal health, characterized by an absence or minimal levels of clinical inflammation in a periodontium with normal support; 3) Periodontal disease stability in a reduced periodontium, defined as a state in which periodontitis has been successfully treated through control of local and systemic factors, resulting in minimal BoP/Bleeding on Probing, optimal improvements in PPD/Periodontal Pocket depth and attachment levels, and a lack of progressive destruction. The principal signs of successful periodontal treatment would be as detailed above with regard to BoP, PPD, and clinical attachment levels. In addition, control of modifying factors such as reduction of daily cigarette smoking and good control of diabetes are achieved. In many respects, attainment of periodontal disease stability can be considered a prognostic definition. 4) Periodontal disease remission/control in a reduced periodontium; defined as a period in the course of disease during which treatment has resulted in reduction (although not total resolution) of inflammation and some improvement in PPD and attachment levels, but not optimal control of local or systemic contributing factors. This may be a reasonable treatment outcome for individuals with uncontrollable modifying factors. Indeed, for many chronic inflammatory medical conditions (eg, diabetes, cardiovascular disease, etc.) Ideally, restoration to periodontal stability should be a major treatment goal while remission/control should be a clear target, based on available evidence. It should be recognized that successfully treated and stable periodontitis patients remain at increased risk of recurrent progression of periodontitis. In non-periodontitis patients, there is no current evidence for increased risk of periodontitis. A case of gingival health on a reduced periodontium in a stable periodontitis patient must be distinguished from a case of periodontal health in a reduced periodontium in a non-periodontitis patient (recession, crown lengthening), because there is a difference in risk for periodontal disease progression. Gingivitis at a site level (gingivitis site) is completely different from defining a gingivitis case (GC) & a one gingivitis site does not equate to a GC. What is the biology of clinical gingival health? Clinical gingival health is generally associated with an inflammatory infiltrate and a host response consistent with homeostasis. 18 2. GINGIVITIS: DENTAL BIOFILM-INDUCED Plaque-induced gingivitis is an inflammatory response of the gingival tissues resulting from bacterial plaque accumulation located at and below the gingival margin Gingivitis can be classified as; 1. Gingivitis on an intact periodontium 2. Gingivitis on a reduced periodontium in a non-periodontitis patient (e.g., recession, crown lengthening) 3. Gingival inflammation on a reduced periodontium in a successfully treated periodontitis patient (Note that recurrent periodontitis cannot be ruled out in this case) 20  G I N G I VA L D I S EA S ES D E N TA L B I O F I L M - I N D U C E D G I N G I V I T I S Gingivitis that is associated with retained dental biofilm (plaque) is the most common form of gingival disease. As compared to periodontal health, patients with gingivitis present with signs of inflammation such as swelling, bleeding, and/or redness in the gingiva. The gingivitis patients may feel pain or soreness from the inflamed gingiva. Gingivitis can be categorized as localized or generalized based on the percentage of Bleeding on Probing ”BOP” sites. Localized gingivitis is defined as 10% to 30% BOP sites and generalized gingivitis is defined as greater than 30% BOP sites 21 CLASSIFICATION OF PLAQUE-INDUCED GINGIVITIS AND MODIFYING FACTORS Associated With Mediated By Systemic or Local Drug-Influenced Gingival Enlargement Bacterial Biofilm Alone Factor i. Systemic Risk Factors / Modifying Factors: ii. Local Risk Factors/Predisposing factors: a. Smoking. a. Dental plaque biofilm retention factors (e.g., b. Hyperglycemia. prominent restoration margins) c. Nutritional factors ( Malnutrition). b. Oral Dryness( Hyposalivation) d. Sex Steroid Hormones( puberty, Menstrual cycle,Pregnancy, Oral contraceptives). e. Hematological Conditions (Leukemia).  G I N G I VA L D I S E A S E S M E D I AT E D B Y S YS T E M I C FAC TO R S Several systemic risk factors (i.e., modifying factors) may contribute to gingivitis by exacerbating the gingival inflammatory response to dental biofilm. This altered response appears to result from the effects of systemic conditions on the host’s cellular and immunologic functions, but microbial biofilm is still the primary etiologic factor. These systemic factors include: (a) smoking; (b) hyperglycemia; (c) nutritional factors; (d) pharmacological agents (prescription, non-prescription, and recreational); (e) sex steroid hormones (puberty , menstrual cycle, pregnancy , oral contraceptives); (f) hematological conditions. 23  Plaque-induced gingivitis exacerbated by sex steroid hormones Evidence has accrued to show that tissue responses within the periodontium are modulated by androgens, estrogens, and progestins at one time or another in a person's life. Elevations in sex steroid hormones may mediate inflammatory response in gingiva. The following conditions may modify plaque-induced gingivitis 24  Puberty The incidence and severity of gingivitis in adolescents are influenced by a variety of factors, including dental biofilm levels, dental caries, mouth breathing, crowding of teeth. Although puberty-associated gingivitis has many of the clinical features of plaque- induced gingivitis, it is the propensity to develop frank signs of gingival inflammation in the presence of relatively small amounts of plaque during the circumpubertal period that are key to distinguishing this condition 25 FIG. 5.3 A 13-year-old female with hormone-exaggerated marginal and papillary inflammation, with 1- to 4-mm probing depths yet minimal clinical attachment loss. (A) Facial view. (B) Lingual view. 26  Menstrual cycle During the menstrual cycle, significant and observable inflammatory changes in the gingiva most women with menstrual cycle–associated gingival inflammation will present with clinically non-detectable sign Most clinical studies have shown there are only modest inflammatory changes that may be observable during ovulation More specifically, gingival crevicular fluid flow has been shown to increase by at least 20% during ovulation in over 75% of women tested 27  Pregnancy During pregnancy, the prevalence and severity of gingivitis has been reported to be elevated and frequently unrelated to the amount of biofilm present. Bleeding on probing or bleeding with toothbrushing is also increased, and gingival crevicular fluid flow is elevated in pregnant women. Pregnancy may also be associated with the formation of pregnancy-associated pyogenic granulomas. FIG. 5.4 (A) Clinical image of pyogenic granuloma in a 27-year- old pregnant female. (B) Histologic image depicts dense inflammatory infiltrate and prominent vessels. 28  Oral contraceptives Oral contraceptive agents were once associated with gingival inflammation and gingival enlargements In the early studies, the increased gingival inflammation or enlargement was reversed when oral contraceptive use was discontinued, or the dosages reduced. it is known that current formulations of oral contraceptive do not induce the clinical changes in gingiva that were reported with high-dose contraceptive 29  Hyperglycemia Gingivitis is a consistent feature found in children with poorly controlled type 1 diabetes mellitus, and the level of glycemic control may be more important in determining the severity of gingival inflammation than the quality of plaque control In adults with diabetes mellitus, it is much more difficult to detect the effects of this endocrine disease on gingival diseases, and only limited evidence is available studies have evaluated gingival inflammation in association with attachment loss. 30  Leukemia Oral manifestations have been described primarily in acute leukemia and consist of cervical lymphadenopathy, petechiae, and mucosal ulcers as well as gingival inflammation and enlargement. In blood dyscrasias (e.g., leukemia), the reduced number of immunocompetent lymphocytes in the periodontal tissues is associated with increased edema, erythema, and bleeding of the gingiva. Gingival enlargement caused by the excessive infiltration of malignant blood cells is often associated with the swollen and spongy gingival tissues Signs of inflammation in the gingiva include swollen, glazed, and spongy tissues which are red to deep purple in appearance. Gingival bleeding is a common sign in patients with leukemia and is the initial oral sign and/or symptom Gingival enlargement has also been reported, initially beginning at the interdental papilla followed by the marginal and attached gingiva 31  Smoking Epidemiologic studies have revealed that smoking is one of the major lifestyle- related environmental risk factors for periodontal diseases. Although plaque accumulation and disease progression are exacerbated in smokers, smokers have fewer clinical signs and symptoms of gingival inflammation, and therefore smoking can mask an underlying gingivitis..The chemical components of cigarette can affect systemic immune response and induce microvascular vasoconstriction as well as fibrosis in gingiva. The vasoconstriction may reduce BOP which influences clinical diagnosis of gingivitis. 32  Malnutrition Gingival diseases modified by malnutrition have received attention because of clinical descriptions of bright red, swollen, and bleeding gingiva associated with severe ascorbic acid (vitamin C) deficiency or scurvy. The one nutritional deficiency that has well-documented effects on the periodontium involves depletion of plasma ascorbic acid (i.e., vitamin C). Even though scurvy is unusual in areas with an adequate food supply, certain populations on restricted diets (e.g., infants from low socioeconomic families, the institutionalized elderly, and alcoholics) are at risk of developing this condition. 33 34  REFERENCES 1. ChappleILC,MealeyBL,etal.Periodonta lhealth and gingival diseases and conditions on an intact and a reduced periodontium: consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84. 2. Caton et al. A new classification scheme for periodontal and peri-implant diseases and conditions – Introduction and key changes from the 1999 classification J Periodontol. 2018;89(Suppl 1):S1–S8 3. Murakami_et_al-2018-Journal_of_Periodontology. 4. Newman, M. G., Klokkevold, P. R., Elangovan, S., & Kapila, Y. (2023). Newman and Carranza's Clinical Periodontolog y and Implantolog y (14th ed.). Elsevier - OHCE. “Periodontal Disease Classification Update. Xviii” 35