CHAPTER 31 Chronic Periodontitis

7/30/2019 CHAPTER 31 Chronic Periodontitis

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CHAPTER 31 Chronic Periodontitis

M. John Novak and Karen F. Novak

Periodintitis kronis dahulunya dikenal sebagai periodontitis dewasa atau periodontitiskronis dewasa merupakan penyakit yang sudah umum dari periodontitis.

Chronic periodontitis, formerly known as “adult periodontitis” or “chronic adultperiodontitis,” is the most prevalent form of periodontitis. It is generally considered tobe a slowly progressing disease.However, in the presence of systemic or environmental factors that may modify thehost response to plaque accumulation, such as diabetes, smoking, or stress, diseaseprogression may become more aggressive. Although chronic periodontitis is mostfrequently observed in adults, it can occur in children and adolescents in response tochronic plaque and calculus accumulation. This observation underlies the recentname change from “adult” periodontitis, which suggests that chronic, plaque-induced

periodontitis is only observed in adults, to a more universal description of “chronic”periodontitis, which can occur at any age (see Chapter 7).Chronic periodontitis has beeed as “an infectious disease resulting in inflammationwithin the supporting tissues of the teeth, progressive attachment loss, and boneloss.”2 This definition outlines the major clinical and etiologic characteristics of thedisease: (1) microbial plaque formation, (2) periodontal inflammation, and (3) loss of attachment and alveolar bone. Periodontal pocket formation is usually a sequela of the disease process unless gingival recession accompanies attachment loss, inwhich case pocket depths may remain shallow, even in the presence of ongoingattachment loss and bone loss.

CLINICAL FEATURES

General CharacteristicsCharacteristic clinical findings in patients with untreated chronic periodontitis mayincludesupragingival and subgingival plaque accumulation (frequently associated withcalculus formation),gingival inflammation, pocket formation, loss of periodontal attachment, loss of alveolar bone, andoccasional suppuration (Figure 31-1). In patients with poor oral hygiene, the gingivatypically maybe slightly to moderately swollen and exhibits alterations in color ranging from pale

red to magenta.Loss of gingival stippling and changes in the surface topography may include bluntedor rolledgingival margins and flattened or cratered papillae.In many patients, especially those who perform regular home care measures, thechanges in color,



contour, and consistency frequently associated with gingival inflammation may notbe visible oninspection, and inflammation may be detected only as bleeding of the gingiva in

response toexamination of the periodontal pocket with a periodontal probe (Figures 31-2, A, and31-3, A).Gingival bleeding, either spontaneous or in response to probing, is common, andinflammationrelatedexudates of crevicular fluid and suppuration from the pocket also may be found. Insomecases, probably as a result of long-standing, low-grade inflammation, thickened,fibrotic marginaltissues may obscure the underlying inflammatory changes. Pocket depths arevariable, and both

horizontal and vertical bone loss can be found. Tooth mobility often appears inadvanced cases withextensive attachment loss and bone loss.

Clinical features of chronic periodontitis in 45-year-old patient with poor oral homecare and noprevious dental treatment. Abundant plaque and calculus are associated withredness, swelling,and edema of the gingival margin. Gingival recession is evident, resulting from lossof attachment and alveolar bone. Spontaneous bleeding is present, and there is visible

exudate of gingival crevicular fluid. Gingival stippling has been lost Chronic periodontitis can beclinically diagnosed by the detection of chronic inflammatory changesin the marginal gingiva, presence of periodontal pockets, and loss of clinicalattachment. It isdiagnosed radiographically by evidence of bone loss. These findings may be similar to those seeninaggressive disease. A differential diagnosis is based on the age of the patient, rateof diseaseprogression over time, familial nature of aggressive disease, and relative absence of local factors in

aggressive disease compared with the presence of abundant plaque and calculus inchronic



periodontitis.

Disease SeverityThe severity of destruction of the periodontium that occurs as a result of chronicperiodontitis isgenerally considered a function of time. With increasing age, attachment loss and

bone loss becomemore prevalent and more severe because of an accumulation of destruction (seeChapter 8). Diseaseseverity may be described as being slight (mild), moderate, or severe (see Chapter 7). These termsmay be used to describe the disease severity of the entire mouth or part of themouth (e.g., quadrant,sextant) or the disease status of an individual tooth, as follows.Slight (mild) periodontitis: Periodontal destruction is generally considered slightwhen no morethan 1 to 2 mm of clinical attachment loss has occurred.

Moderate periodontitis: Periodontal destruction is generally considered moderatewhen 3 to 4 mm



of clinical attachment loss has occurred.Severe periodontitis: Periodontal destruction is considered severe when 5 mm or more of clinicalattachment loss has occurred.

SymptomsPatients may first become aware that they have chronic periodontitis when theynotice that their gums bleed when brushing or eating; that spacesoccur between their teeth as aresult of toothmovement; or that teeth havebecome loose. Because chronic periodontitis is usuallypainless,however, patients may be totally unaware that they have the disease and maybeless likely to seektreatment and accept treatment recommendations. In addition, a negative response

to questions suchas, “Are you in pain?” is not sufficient to eliminate suspicion of periodontitis.Occasionally, painmay be present in the absence of caries caused by exposed roots that are sensitiveto heat, cold, or both. Areas of localized dull pain, sometimes radiating deep into the jaw, have beenassociated withperiodontitis. The presence of areas of food impaction may add to the patient’sdiscomfort. Gingivaltenderness or “itchiness” may also be found.



Add Although chronic periodontitis requires an infection to initiate the host response andsubsequentinflammatory reaction, the specific bacteria causing the infection in an individual areunknown.

Several different microorganisms apparently are capable of initiating the hostresponse, and acertain combination of species is probably required to overwhelm the host andinitiate tissue loss(attachment loss and bone loss). This provides the basis for periodontal therapy inwhich periodic monitoring, removal of plaque, and management of risk factors are aimed at keeping the hostbacteriarelationship tipped in favor of the host response and control of the disease process.Chronic periodontitis is generally slowly progressive, with some patients havingincreased

susceptibility to bone loss and pocketing. Some patients who have a genetic profilethataccentuates interleukin-1 production have a 2.9-times increased risk of tooth loss,and if thesepatients are also smokers, their risk increases to 7.7 times. Diabetes is another factor that oftenleads to severe and extensive periodontal destruction. Also, a specific group of microorganisms isseen in the subgingival biofilm of patients with ongoing bone loss associated withchronicperiodontitis, including Porphyromonas gingivalis, Tannerella forsythia, andTreponemadenticola.The identification and characterization of these other and pathogenicmicroorganisms and their association with attachment and bone loss have led to the specific plaque hypothesisfor thedevelopment of chronic periodontitis. This hypothesis implies that although a generalincreaseoccurs in the proportion of gram-negative micro-organisms in the subgingival plaquein

periodontitis, it is the presence of increased proportions of members of the redcomplex, and perhapsother microorganisms, that precipitates attachment and bone loss. The mechanismsby which thisoccurs have not been clearly delineated, but these bacteria may impart a local effecton the cells of the inflammatory response and the cells and tissues of the host, resulting in a local,site-specificdisease process. The interactions between pathogenic bacteria and the host andtheir potential effectson disease progression are discussed in detail in Chapter 13.





Radiopaque horizontal line across the roots. This line demarcates the portion of therootwhere the labial or lingual bony plate has been partially or completely destroyed from

the remainingbone-supported portion (Figure 36-26).



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CHAPTER 31 Chronic Periodontitis