ADA.org: Future of Dentistry Full Report

FUTURE OFDENTISTRY

periodontitis is gingival inflammation with loss of
alveolar bone and periodontal ligament. In some
patients inflammatory gingivitis can exist for many
years, with only limited amounts of marginal bone
loss over decades. In other individuals, gingivitis pro-
gresses to periodontitis. At present, the specific events
that lead to the transition of gingivitis to periodonti-
tis are not defined, but are likely to involve a qualita-
tive or quantitative shift in the bacterial infection,
with activation of inflammatory cascades and pro-
duction of mediators with catabolic effects.
The currently accepted model for progression of
periodontitis consists of periods of disease activity
and inactivity. The amount of loss measured on a
tooth site is variable and can be dependent on many
factors including identifiable risk factors as well as
the sensitivity of the technique used for measuring
change (Armitage, 1996).
Approximately one dozen species of bacteria, pri-
mary Gram-negative anaerobic organisms, have
been associated with chronic periodontitis:
Actinobacillus actinomycetemcomitans, Actinomyces
naeslundii, Bacteroides forsythus, Campylobacter
rectus, Eikenella corrodens, Eubacterium species,
Fusobacterium nucleatum, Peptostreptococcus
micros, Prevotella intermedia, Porphyromonas gin-
givalis, Selenomonas sputigena, Streptococcus inter-
medius andTreponema species.
Among the host inflammatory mediators that have
been proposed as important to the pathogenesis of peri-
odontitis are the arachidonic acid metabolite
prostaglandin E 2 , enzymes known as matrix metallo-
proteinases (collagenases and other connective tissue-
degrading enzymes) and the cytokines interleukin (IL)-
1, IL-6 and tumor necrosis factor-a(TNF-a) (Schwartz
et al, 1997). The prevalence of moderately severe to
severe periodontitis is remarkably consistent in different
populations throughout the world ranging from 8-12%
(Papapanou, 1996). The prevalence of early-onset
forms of periodontitis ranges between 0.1% and 0.5%
in the United States (Löe and Brown, 1991).

Risk Assessment and Diagnosis

Periodontitis is a multifactorial disease. A num-
ber of risk factors for periodontitis have been iden-
tified, including cigarette smoking, type 1 and type
2 diabetes, increased age, existing periodontitis,
male gender, low socioeconomic status, limited
access to dental care, as well as the periodontal
pathogens Porphyromonas gingivalis and

Bacteroides forsythus, and an exuberant inflamma-

tory response as evidenced by increased production

of inflammatory mediators.

The most important environmental risk factor for

periodontitis is cigarette smoking. This finding has

emerged within the last ten to fifteen years. A recent

report by Tomar and Asma calculated that 41.9% of

all cases of periodontitis were attributable to current

use of cigarettes, and 10.9% of cases were attribut-

able to former smoking (Tomar and Asma, 2000).

Greater extent and severity of periodontitis have been

associated with both type 1 and type 2 diabetes. Recent

studies have begun to define the molecular mechanisms

that account for this association. The binding of

advanced glycation endproducts in the periodontium to

their receptor on macrophages, endothelial cells, and

other structural cells can induce a hyperinflammatory

state. Increased production of proinflammatory cyto-

kines (IL-6, TNF-a) can then contribute to tissue dam-

age (Lalla et al, 1998; and Mealey, 2000).

Today the diagnosis of periodontal disease relies

on clinical and standard radiographic techniques

and parameters:

u Probing attachment level and bleeding following

probing;

u Radiographic analysis of the height of alveolar

bone with periapical or bitewing exposures;

u Subtraction radiograph to determine if loss (or

gain) of alveolar bone has occurred during a defined

interval (limited to research environmentsbecause the

software and hardware necessary for the subtraction

are not commercially available); and,

u Digital radiography.

Diagnostic tests have been developed that identi-

fy specific microbial pathogens by use of culture

DNA probes or specific cell surface antigens

(Zambon et al, 1995). The host response can be

assessed by analysis of gingival crevicular fluid, sali-

va, or blood. These methods have not been widely

accepted as a routine part of patient management

(Lamster, 1997; and Kaufman and Lamster, 2000).

Treatment and Prevention

Treatment of periodontal diseases focuses on

reducing and removing plaque and calculus accu-

Dental and Craniofacial Research