Diagnosis of Periodontal Diseases*
This position paper on the diagnosis of periodontal diseases was prepared by the Research, Science and Therapy Committee of the American Academy of Periodontology. It is intended for the information of the dental profession and other interested parties. The purpose of the paper is to provide the reader with a general overviewof the important issues related to the diagnosis of periodontal diseases. It is not intended as a comprehensive review of the subject. J Periodontol 2003;74:1237-1247.
laque-induced periodontal diseases are mixed infections associated with relatively specific groups of indigenous oral bacteria.1-6 Susceptibility to these diseases is highly variable and depends on host responses toperiodontal pathogens.7-11 Although bacteria cause plaque-induced inﬂammatory periodontal diseases, progression and clinical characteristics of these diseases are inﬂuenced by both acquired and genetic factors that can modify susceptibility to infection.12-15
TRADITIONAL APPROACH TO DIAGNOSIS Despite our increased understanding of the etiology and pathogenesis of periodontal infections, the diagnosisand classiﬁcation of these diseases is still based almost entirely on traditional clinical assessments.16,17 To arrive at a periodontal diagnosis, the dentist must rely upon such factors as: 1) presence or absence of clinical signs of inflammation (e.g., bleeding upon probing); 2) probing depths; 3) extent and pattern of loss of clinical attachment and bone; 4) patient’s medical and dentalhistories; and 5) presence or absence of miscellaneous signs and symptoms, including pain, ulceration, and amount of observable plaque and calculus.18-20 Plaque-induced periodontal diseases have traditionally been divided into two general categories based on whether attachment loss has occurred: gingivitis and periodontitis. Gingivitis is the presence of gingival inflammation without loss of connectivetissue attachment.16 Periodontitis can be deﬁned as the presence of gingival inflammation at sites where there has been a pathological detachment of collagen ﬁbers from cementum and the junctional epithelium has migrated apically. In addition, inﬂammatory events
* This paper was developed under the direction of the Research, Science and Therapy Committee and approved by the Board of Trustees of theAmerican Academy of Periodontology in May 2003.
associated with connective tissue attachment loss also lead to the resorption of coronal portions of toothsupporting alveolar bone.16 This simple separation of plaque-induced periodontal diseases into two categories is not as clearcut as it first appears. For example, if sites that have been successfully treated for periodontitis develop somegingival inflammation at a later date, do those sites have recurrent periodontitis or gingivitis superimposed on a reduced but stable periodontium? There are currently no data to definitively answer this question. However, since not all sites with gingivitis necessarily develop loss of attachment and bone,17 it is reasonable to assume that gingivitis can occur on a reduced periodontium in whichongoing attachment loss is not occurring. A similar problem exists when the term “periodontitis” is assigned to sites with attachment loss and periodontal pockets in which ongoing periodontal destruction is not occurring. Demonstration of the progression of periodontitis requires documentation of additional attachment loss occurring between at least two time points. Since this is not always possible,especially when a patient is examined for the ﬁrst time, most clinicians assign the diagnosis of “periodontitis” to inﬂamed sites that also have loss of attachment and bone. This is a prudent practice since such sites may be either currently progressing or are at an increased risk for further periodontal destruction. Therefore, demonstration of progressive attachment loss is not generally...