Bacteria ¡Nöuce the Disease Process Antigens Lipopolysaccharides Host
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Bacteria ¡nöuce the disease process Antigens Lipopolysaccharides Host response: monocytes/macrophages, etc Cylokines(IL-1,TNF-o Recruiied cells: fibroblasts. endothelial and epithelial cells, etc PGE, Matrix metallcproleinases Bone Loss of résorption connective tissue The International Journal of Periodontics & Restorative Dentis.tr' y 337 Changing Periodontal Paradigms: Therapeutic Innplications Gary Greenstein, DDS, MS* Periodontal diseases are the result of Ira Lamster, DDS. MMSc** infectionsoftheperiodontJum.^They should be considered infections because there is a bacterial etiology Many paradigms concerning the epidemiology, pathogeoesis, and systemic and a subsequent immune response. impact oí penodontai diseases have been modified. For example, bacterial A microbial challenge often results in hioñims are essential to induce penodontitis, but their mere presence is not suffi- a subclinical infection because the cient to mitiate disease. Jt is also now recognized that the host response to these host response prevents the bacterial b/ofiims causes most of the destruction of the periodontal tissues. Code terminants challenge from reaching the thresh- that influence the clinical severity of the disease process (ficiude enw'ranmentai, old necessary to cause symptoms.^ genetic, and acquired factors. In general, the prevalence of advanced periodonti- However, when subgingival bacteria tfs and the incidence of disease progression are tower thar) previously believed. overwhelm the host response, tissue However, pen'odontitis remains the rnost common chronic illness, in addition, the destruction occurs; this is termed finding that acquired systemic diseases may predispose individuals to periodonti- pedodonta! disease. During the last tis, and conversely that periodontitis may be a risk factor for certain systemic dis- eases, fias expanded the scope of periodon tics. These changed paradigms and decade, numerous paradigms their consequences with regard to selecting therapies are discussed in this review regarding periodontal diseases have article. (Int J Periodontics Restorative Dent 2000;20:337-357.) been modified, including preva- lence, incidence of disease progres- sion, etiology, pathogenic mecha- nisms, predisposing factors, and impact on the systemic health of the patient. This article addresses these modified concepts and explores their therapeutic implications. 'Clinical Professor, Department of Period ontology. University of Prevalence of gingivitis Medicine and Dentistry New Jersey, Newark. New Jersey. and adult periodontitis 'Assistant Dean, Columbia School of Dentistry, New York, New York. Reprint requests: Dr Gary Greenstein, 900 West Main Street, Freehold, Epidemiologie surveys have found New Jersey 07728. that gingivitis without accompanying Volume 20, Number 4, 2000 338 ^^^^™ InriHpnrp of diipasp pmqrpisinn in patiptitc with pprinrlnntitis' ^ % of patients No. of No. of Evaluation Disease activity deteriorating % of sites Study patients sites period ¡mo) threshold (mm) in > 1 site deteriorating Grbjc et al^° 75 11,466 6 2.5 41.3 0.99 Deas et al-' 21 2,094 9 2.0 90.0 6.1 Persson and Page^^ 25 200 24 2.0 40.0 10.7 Halazonetisetal^^ 55 24,720 5-12 1.75 42.0 5.0 Jeffcoatand Reddy^" 30 — 6 0.4 77.0 29.0 periodontitis affects 50% of adults studies often record measurements Incidence of disease over 18 years old and involves an at the line angles of the teeth, but progression average of 6 or more teeth per pa- the mid-proximal areas tend to dis- tient.^ Furthermore, most inflamed play deeper probing depths'^'"; The incidence of disease progres- sites do not progress to periodonti- and the use of survey teeth routinely sion will also be influenced by the tis,''"' This was documented in stud- misrepresents the prevalence of dis- standard that is selected to define ies that longitudinally monitored eased sites.'^" In addition, the stan- disease progression. The data pre- patients with gingivitis'* and in inves- dard used to define periodontitis sented in Table 1 suggest that a tigations that assessed the preva- dramatically impacts on the data. small number of sites in a limited lence of attachment loss in untreated For example, when Brown et aP^ sel- number of individuals manifests dis- populations,^'* and it was supported ected a 5-mm loss of clinical attach- ease progression during a defined by animal studies.' However, Löe^ ment at one or more sites as a period."'^°"^'' The following results concluded that gingivitis is often threshold to characterize periodon- can be deduced from the data; 0) associated with and precedes peri- titis, 12% ofthe study population less than 50% of individuals with odontitis. Therefore, elimination of had advanced periodontal disease. periodontitis manifested disease inflammation remains a critical ob- However, if a 3-mm standard was activity within 1 year; 0 around 5% jective of periodontal treatment be- employed (equivalent to 25% ofthe to 10% of diseased sites demon- cause the absence of inflammation is length of a maxillary molar root), strated deterioration within 1 to 2 a negative predictor of future clinical then 42% ofthe subjects had peri- years; and (3) approximately 20% of attachment loss,'''" odontitis; depending on the estab- the patients accounted for 60% of all The prevalence of moderate lished threshold used to define peri- sites that progressed. periodontitis in the adult population odontitis. the data change. Despite The finding that a small number is approximately 30%,^ and severe the impression that the prevalence of of individuals provides the majority of periodontitis afflicts approximately advanced periodontitis has de- sites demonstrating disease pro- 10% ofthe population. "-I s Unfor- creased during the past several de- gression supports the concept that tunately, these data underestimate cades, it still affects over 30 million all individuals are not equally sus- the occurrence of periodontitis for Americans and remains the most ceptible to periodontitis. Support for the following reasons: epidemiologic common chronic disease. this conclusion is provided by the The International Journal of Periodontics & Resiorative Dentistry 339 study of Loe et al,* which monitored untreated patients in Sri Lanka during ••••• •gñgjfl Models of disease progression a 15-year period. This study assessed Model Mechanism a homogeneous population that did Continuous modeP' Slow, steady, progressive disease process not practice oral hygiene and had Episodic burst theory^*-" Irregular periods of exacerbation and remission no dental care, thereby providing an Synchronous burst Periods of exacerbation and remission during a unusual opportunity to monitor the theory^^ defined period Epidemiologie model^* Consistent with continuous disease aging process natural history of periodontal dis- that depends only on the duration of the process ease. They noted that 9% of the indi- Brownian motion or Random periodsof sharp bursts and/or remission can viduals developed severe periodon- stochastic model^^ occur, but underlying disease activity remains constant titis, 81% displayed moderate bone Random walking modeP' When observed at regular intervals, modei is similar to Brownian motion model loss, and 11% had gingivitis. These Fracturai modeP Multifactorial model,simulates disease advancing with data underscorethe need to identify age in bursts and remissions susceptible individuals and provide appropriate therapy. Patterns of disease progression Several models of disease progres- sion have been proposed to explain temporal patterns of tissue destruc- tion fiable 2).^"" Historically, it was believed that periodontitis resulted ithin a patient share a common experiencing bursts of disease pro- in a slow, continuous, and progres- ^^"^^ Studies that employed gression,^* Similarly, others note that sive deterioration of the periodon- large thresholds to identify disease a linear pattern is the most common tium.^^ However, this did not ac- progression may have spuriously model of tissue breakdown,-^'' One count for patterns of destnjction that supported the burst theory. For in- explanation isthat discrete episodes developed quickly, or for observed stance, in one study when both 0,4- of disease progression occur, but periods of remission. Subsequent mm and 2.4-mm standards for dis- these microbursts cannot be de- clinical studies suggested that dis- ease progression were used, the tected by clinicians. Therefore, over ease progression occurs as episodic number of sites deteriorating dur- time, the cumulative result appears bursts of activity with periods of re- ing a ó-month period was 29% and as a linear change. On the other mission.^*'^' Other models of dis- 2%, respectively.^^ Different thresh- hand, it is possible that large incre- ease progression listed in Table 2 olds not only resulted in altering the ments of attachment loss can hap- suggest that episodes of disease number of deteriorating sites, but it pen before destruction is contained progression may be superimposed was dear that rejection of small alter- by the host response. The various on linear changes.^^^° ations was misleading with respect models described in Table 2 explain Several authors question the sta- to identifying patterns of clinical at- a variety of clinical and radiographie tistical procedures used to support tachment loss. In that investigation, findings. Nevertheless, several pat- the episodic burst theory because use of the 0.4-mm threshold resulted terns of disease progression may disease progression at sites was