Comparison Of The Clinical Features Of Chronic And Aggressive Periodontitis

Ó 2010 John Wiley & Sons A/S

Periodontology 2000, Vol. 53, 2010, 12–27
Printed in Singapore. All rights reserved

PERIODONTOLOGY 2000

Comparison of the clinical
features of chronic and
aggressive periodontitis
G A R Y C. A R M I T A G E & M A R Y P. C U L L I N A N

Historical perspective
In the late 1800s, what is now known as chronic
periodontitis was clinically characterized asa slowly
progressive destruction of the periodontium due to
the accumulation of Ôlime depositsÕ on the teeth (21),
or Ôcalcic inflammation of the peridental membraneÕ
secondary to deposits of ÔsalivaryÕ and ⁄ or ÔserumalÕ
calculus (13). The calcified deposits were considered
to be mechanical irritants that led to gingival recession and a generalized or even pattern of bone loss
(13, 21).Throughout most of the 20th century, this
form of periodontitis has been considered an
inflammatory disease associated with local irritants
and the formation of dental plaque (biofilms) on
tooth surfaces (4). This concept prevails today.
What is now known as Ôgeneralized aggressive
periodontitisÕ was not clearly described until the latter part of the 20th century. However, G.V. Black used
theterms Ôphagedenic pericementitisÕ and Ôchronic
suppurative pericementitisÕ to describe patients who
suffered from a rapid destruction of alveolar bone
(14). In the past three decades, authors have used a
variety of terms for cases in which there is generalized severe periodontal destruction in young
patients, including Ôgeneralized juvenileÕ (16, 94),
Ôrapidly progressiveÕ (46, 64), or simplyÔsevereÕ
periodontitis (18). In most respects, the disease
clinically resembles chronic periodontitis except the
affected individuals are much younger and the rate of
progression is assumed to be rapid since there is
extensive periodontal damage in a young person.
Current views regarding the major characteristics
of localized aggressive periodontitis have been considerably influenced byhistorical perspectives of the
disease. In a series of papers from 1920 to 1928,

12

Bernard Gottlieb of the University of Vienna School
of Medicine described an unusual form of periodontal disease that primarily affected some or all of
the permanent incisors and first molars of young
individuals (29–33). Based on certain histological
observations such as thin cementum on extracted
teeth fromaffected sites, he believed that the disease
was due to defective deposition of cementum or
ÔcementopathiaÕ (32–34). Gottlieb applied the principles of classical pathology as they were practiced in
the 1920s, which stated that all human non-neoplastic diseases could be classified as either inflammatory or non-inflammatory (4). Since his adolescent
patients did not exhibit the intense gingivalinflammation ordinarily seen in other patients (i.e. adults)
with periodontitis, he believed that the disease was a
non-inflammatory or degenerative condition. It was
claimed that initial stages of the disease were not
associated with local irritants such as dental plaque
or calculus, and therefore the disease was subsequently referred to as Ôdiffuse atrophy of the alveolar
boneÕ orÔperiodontosisÕ (34, 63). According to this
hypothesis, the alveolar bone degenerated and the
teeth drifted apart or migrated without the formation
of periodontal pockets (90). Since it was thought that
continuous deposition of cementum was required in
order to prevent the apical migration of epithelium
along the root surface, pockets formed at sites that
were supposedly afflicted with cementopathia. As asecondary phenomenon, once a pocket formed, it
became susceptible to colonization by oral bacteria
and was Ô…a potential trap for accumulating deposits
from salivaÕ (63). In the final stage of the disease,
bacterial toxins and other irritants eventually caused
some inflammation, which contributed to additional
loss of bone and connective tissue attachment to the

Comparison of the...