Periodontal Disease and Overall Health: A Clinician's Guide

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CHAPTER 2 Overview of Periodontal Disease:CHAPTER 2 Causes, Pathogenesis, and Characteristics 9active inflammatory cells producing highlevels of cytokines and enzymes causingrapid, aggressive destruction of periodontaltissues. Aggressive periodontitis can be furthercharacterized as localized and generalizedforms. The localized form usuallyaffects first molar and incisor sites. The generalizedform usually involves at least threeteeth other than first molars and incisors.Periodontitis as a Manifestationof Systemic DiseasesSystemic conditions such as diabetesare associated with this form of periodontitis.16 Several hematologic and genetic disordershave also been associated with the developmentof periodontitis such as acquired,familial, and cyclic neutropenias, leukemias,Down’s syndrome, certain types of Ehlers-Danlos syndrome, Papillon-Lefevre syndrome,Cohen syndrome, and hypophospha -tasia. The mechanisms by which all of thesedisorders affect the health of the periodontiumare not fully understood and continue tobe investigated by many basic and clinical researchers.It is speculated that these diseasescan alter host defense mechanisms and upregulateinflammatory responses, resultingin progressive periodontal destruction.Necrotizing Periodontal DiseasesThese lesions are most commonly observedin individuals with systemic conditions,such as human immunodeficiency virusinfection, malnutrition, and immunosuppression.Necrotizing periodontal diseasesare further divided into two forms: necrotizingulcerative gingivitis (NUG) and necrotizingulcerative periodontitis (NUP). Thesetwo diseases have the same etiology andclinical signs, except NUP involves clinicalattachment and alveolar bone loss. 17Abscesses of the PeriodontiumPeriodontal abscess is a localized purulentinfection of the periodontal tissues. 18Periodontal abscesses usually develop inperiodontitis patients who may have fooddebris lodged in a pocket, or deep depositsof calculus where drainage from a pocketbecomes blocked. Iatrogenic abscess formationcan be precipitated after inadequate scalingand root planing, leading to a tighteningof the coronal epithelial cuff with continuedsubgingival calculus driving inflammation.Abscesses can also occur in healthy periodontaltissues due to the presence of foreignobjects lodged in the gingival crevice, suchas a toothbrush bristle or a popcorn kernelbeing tightly packed into the interproximalspaces or between the tooth and the tissues.A pericoronal abscess is an infection of thegingiva around a partially erupted tooth leadingto pericoronitis. A small flap of tissuemay cover a partially erupted tooth surface,serving as a nidus for food and debris to accumulateand become trapped beneath thetissue flap. Patients usually find it very difficultto keep these areas clean, and can developinflammation and infection. In addition,trauma due to constant contact betweenthe tissue flap and a tooth in the opposingarch can also lead to a pericoronal abscess.The areas most commonly affected are associatedwith mandibular third molars. Pain,swelling, redness, and suppuration are associatedwith periodontal abscess. Treatmentmay include incision and drainage, use ofantibiotics, and removal of the offendingsource.EPIDEMIOLOGY ANDRISK FACTORSEpidemiology of GingivitisGingivitis can occur in early childhood,becomes more prevalent during teenageyears, and decreases in older individuals. 19 In1986-1987, the National Institute of DentalResearch conducted a nationwide survey oforal health in US school children 20 andreported that approximately 60% of chil -dren 14 to 17 years of age were found to
10 Periodontal Disease and Overall Health: A Clinician's Guidehave gingivitis. In 1960–1962, the first USnational survey of periodontal disease inadults reported that 85% of men and 79% ofwomen have some degree of gingivitis. 21 Inthe most recent National Health and NutritionExamination Survey (NHANES III)conducted from 1988 to 1994, 22 more than50% of adults had gingivitis on an average ofthree or four teeth, while 63% of 13- to 17-year-old teenagers had gingival bleeding.Both surveys assessed gingival bleeding bya gingival sweep method. 21,22Epidemiology of PeriodontitisBasic clinical measurements for perio -dontitis are gingival bleeding on probing,clinical attachment loss, and pocket depthsaccompanied by radiographic bone loss.These types of clinical measurements maybe somewhat subjective. As our knowledgeof the pathogenesis of periodontitis improves,new diagnostic markers for the diseasemay emerge to help better diagnose it.Inflammatory cytokines, enzymes, and bonebreakdown products released into gingivalcrevicular fluid reflect the host response tothe bacterial challenge. These biochemicalmarkers may be good candidates for newdiagnostic or prognostic markers of disease.A number of cytokines have been asso ciatedwith active disease, including prostaglandinE2 (PGE2), tumor necrosis factor-alpha(TNF-α), interleukin-1 beta (IL-1β), andothers. 23,24 Enzymes such as matrix metalloproteinases(MMPs) and breakdown productssuch as the collagen telopeptide havebeen studied as well. To date, these biochemicalmarkers in gingival crevicularfluid are still being investigated. It will behelpful to both clinicians and researchersif one or more of these markers can be developedas a more objective chairside tool tomeasure active periodontitis. The devel -opment of these markers will also helpto facilitate screening for periodontaldiseases by medical professionals or evenself- assessment by patients, thereby promptingreferrals to the dental office for clinicalassessment.The national data suggest that the milderforms of periodontitis are close to uni -versal. 25 The more severe forms are lessprevalent. According to a review of the literatureby Brown and Löe 26 focused on anumber of epidemiologic studies resultingfrom a 1981 national probability survey, theprevalence of CP is about 36% for the adultUS population as assessed by pocket depthmeasurements. The prevalence of periodontitisincreases with age; 29% in those aged 19to 44 had CP; this rate increased to 50% forpeople 45 years or older. In general, moderateperiodontitis occurred in 28% of all peoplewhile 8% had advanced disease. However,the prevalence of moderate and severeperiodontitis increased to 44% in the populationolder than 45. Based on the presenceof periodontal pockets ≥ 4 mm, it was determinedthat 30% of the population hasperiodontitis on an average of three or fourteeth. Severe pockets of ≥ 6 mm were foundin less than 5% of the population. 22 Theprevalence of aggressive periodontitis waslow with less than 1%. 27 More recently,NHANES III (1988–1994) reported theprevalence of periodontitis for adults 30 to90 years old. 28 Attachment loss and probingdepths were assessed at two sites per tooth.When assessed by the level of attachmentloss, 53% of the population was found tohave ≥ 3 mm attachment loss. The prevalenceof attachment loss increased with age,from approximately 35% for the 30-yearoldparticipants to 89% for the 80-year-oldparticipants. When assessed by probingdepth, approximately 64% of the populationhad probing depths of ≥ 3 mm. The prevalenceof periodontitis increases with age andwas found to be more prevalent in malesthan females, and in African-Americans andMexican-Americans than in non-HispanicCaucasians.
Page 5: ivCONTRIBUTORSSrividya Kidambi, MDA
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