You are on page 1of 2

SECTION III: ETIOLOGY OF PERIODONTAL DISEASES

CHAPTER 5
Periodontal Pathogenesis
Philip M. Preshaw

CHAPTER OUTLINE
Histopathology of Periodontal Linking Pathogenesis to Clinical Immune Responses in Periodontal
Disease Signs of Disease Pathogenesis
Inflammatory Responses in the Resolution of Inflammation Concept of Host Susceptibility
Periodontium

Understanding periodontal pathogenesis is key to improving man- its too enthusiastic supporters into the status of an accepted fact.”28
agement strategies for this common, complex disease. The first The end of the focal infection era was signaled by an editorial in
challenge is to understand exactly what is meant by the term patho- the Journal of the American Medical Association in 1952, which
genesis. According to Merriam Webster ’s Collegiate Dictionary, stated that “many patients with diseases presumably caused by foci
the word pathogenesis is defined as “the origination and develop- of infection have not been relieved of their symptoms by removal
ment of a disease.” Essentially, this refers to the step-by-step pro- of the foci, many patients with these same systemic diseases have
cesses that lead to the development of a disease and that result in no evident focus of infection, foci of infection are as common in
a series of changes in the structure and function of, in this case, apparently healthy persons as in those with disease.”165
the periodontium. In broad terms, the pathogenesis of a disease Advances in the management of periodontitis have been driven
is the mechanism by which a causative factor or factors causes by improved knowledge of the epidemiology, causation, and patho-
the disease. The word itself is derived from the Greek roots genesis of the disease.195 During the 1970s, the role of plaque as
pathos (meaning “suffering”) and genesis (meaning “generation or the sole causative factor for periodontitis was unquestioned. In
creation”). those days, nonsurgical treatment was in its infancy, and most
Our knowledge of periodontal pathogenesis has evolved over treatment options involved surgery (e.g., gingivectomy for the
the years. It is important to be aware of this, because treatment treatment of shallower pockets, access flap surgery for the treat-
philosophies have similarly changed in parallel with our improving ment of deeper sites). When looking back, it becomes clear that
understanding of the disease processes. For example, during the the treatment strategies used during a given time period are entirely
late 1800s, Willoughby D. Miller (an eminent dental researcher dependent on the prevailing understanding of pathogenesis at
who established the important causal role of oral bacteria for dental that particular point in time. It is therefore very likely that the
caries) asserted that “during the last few years the conviction has management options that we take for granted now will change
grown continually stronger, among physicians as well as dentists, again in the future. This is to be welcomed, because a progressive
that the human mouth, as a gathering-place and incubator of diverse clinical discipline such as periodontology that is well founded
pathogenic germs, performs a significant role in the production of in science and with patient benefit as its primary value should
varied disorders of the body, and that if many diseases whose origin strive to improve therapeutic strategies in the light of continued
is enveloped in mystery could be traced to their source, they would discovery.
be found to have originated in the oral cavity.”116 This marked the Periodontal disease results from a complex interplay between
beginning of an era of dental treatment strategies that aimed to treat the subgingival biofilm and the host immune–inflammatory events
systemic diseases by eliminating the so-called “foci of infection” that develop in the gingival and periodontal tissues in response to
in the mouth. As a result, many patients underwent unnecessary the challenge presented by the bacteria. It is generally accepted that
dental clearances to manage their systemic diseases. gingivitis precedes periodontitis, but it is clear that not all cases of
By the 1930s, such approaches were beginning to be questioned gingivitis progress to periodontitis. With gingivitis, the inflamma-
as evidenced by a clinical study of 200 patients with rheumatoid tory lesion is confined to the gingiva; however, with periodontitis,
arthritis of whom 92 had their tonsils removed as treatment for the the inflammatory processes extend to additionally affect the peri-
arthritis (even though only about 15% gave any history of tonsillitis odontal ligament and the alveolar bone. The net result of these
or sore throat) and of whom 52 had some or all of their teeth inflammatory changes is the breakdown of the fibers of the peri-
removed.28 Of the 92 who had their tonsils removed, there was no odontal ligament, resulting in clinical loss of attachment together
impact on the arthritis in 86 patients (although 2 got worse); of the with resorption of the alveolar bone.
52 who had teeth removed, there was no benefit in 47 cases (and During the 1970s and 1980s, bacterial plaque was generally
3 reported a worsening of their arthritis after the extractions). The considered to be preeminent as the cause of periodontitis. At that
authors wrote that “focal infection is a splendid example of a time, it was accepted that poor oral hygiene resulted in increased
plausible medical theory which is in danger of being converted by plaque accumulation, which in turn resulted in periodontal disease.

76
CHAPTER 5 Periodontal Pathogenesis 77

However, this model failed to take into account observations such and causing tissue damage. Our current understanding of suscep-
as the fact that there are many individuals with poor oral hygiene tibility to periodontitis suggests that individuals who are more
who do not develop advanced periodontal disease and, conversely, susceptible to the disease mount an excessive or dysregulated
that there are unfortunate individuals who, despite good oral immune–inflammatory response for a given bacterial challenge,
hygiene and compliance with periodontal treatment protocols, con- which leads to increased tissue breakdown as compared with those
tinue to experience progressive periodontal breakdown and who individuals who have a more normal inflammatory response.
would be considered to have aggressive periodontitis. These find-
ings were confirmed by the work of Löe and colleagues, who Clinically Healthy Gingival Tissues
studied Sri Lankan tea laborers who had no access to dental care Clinically healthy gingival tissues (e.g., those observed in patients
and who could be divided into three main categories: (1) individu- with excellent oral hygiene and no visible plaque deposits who
als (≈8% of the population studied) who had a rapid progression typically have received regular and meticulous professional clean-
of periodontal disease; (2) those (≈81%) who had a moderate pro- ing) are pink in appearance, not swollen, not inflamed, and firmly
gression of such disease; and (3) those (≈11%) who demonstrated attached to the underlying tooth and bone, with minimal bleeding
no progression of periodontal disease beyond gingivitis.107 All on probing. The dentogingival junction is a unique anatomic
patients in this population displayed abundant plaque and calculus feature that functions to attach the gingiva to the tooth. It comprises
deposits. The causative role of plaque bacteria is clear in that the an epithelial portion and a connective tissue portion, both of which
bacteria initiate and perpetuate the inflammatory responses that are of fundamental importance for periodontal pathogenesis. The
develop in the gingival tissues. However, the major determinant of epithelial portion can be divided into three distinct epithelial struc-
susceptibility to disease is the nature of the immune–inflammatory tures: the gingival epithelium, the sulcular epithelium, and the
responses themselves. It is paradoxical that these defensive pro- junctional epithelium (Figure 5-1). These epithelial structures are
cesses, which are protective by intent (i.e., to prevent the ingress in continuity with each other, but they have distinct structures and
of the bacteria and their products into the tissues), result in the functions as indicated in Box 5-1.
majority of tissue damage that leads to the clinical manifestations The junctional epithelium is a particularly unique epithelial
of disease. structure, because the surface cells are specialized for the purpose
Periodontal disease is therefore a unique clinical entity. It is of attachment to the tooth.11 Therefore, unlike other epithelial
not an infection in the classic sense of the word. With most infec- tissues elsewhere in the body, there is no opportunity for the
tions, a single infective organism causes the disease (e.g., human sloughing of cells from the surface. Instead, cells at the basal layer
immunodeficiency virus/acquired immunodeficiency syndrome,
syphilis, tuberculosis), and the identification of that organism pro-
vides the basis for the diagnosis. With periodontal disease, a large
number of species are identifiable in the periodontal pocket, and
many more are as yet unknown because they have not been cul-
tured. It is impossible to conclude that a single species or even a
group of species causes periodontal disease. Many of the species
that are considered important in periodontal pathogenesis may
simply reside in deep pockets because the pocket is a favorable
environment in which they can survive (i.e., it is warm, moist, and
anaerobic, with a ready supply of nutrients). Many of the unique
features of periodontitis are derived from the anatomy of the peri-
odontium, in which a hard, nonshedding surface (the tooth) is
partly embedded within the body (within connective tissue),
crosses an epithelial surface, and is partly exposed to the outside
world (within the confines of the mouth). The bacteria that colo-
nize this surface are effectively outside of the body (although they
are in the subgingival crevice), yet the inflammatory response that
develops is located within the body. These factors add complexity
to our understanding of the role of the biofilm and the immune–
inflammatory responses that are part of periodontal tissue
breakdown.

Histopathology of Periodontal Disease


To better understand periodontal pathogenesis, it is important to
have an appreciation of the histologic appearance of clinically
healthy tissues as well as of inflamed gingival and periodontal
tissues. It is important to note that, even in gingival tissues that Figure 5-1 Histologic appearance of healthy gingiva. A photomi-
clinically would be considered to be noninflamed and healthy, there crograph of a demineralized tooth with the gingival tissues in situ
is always evidence of inflammatory responses occurring if they are (hematoxylin and eosin staining, low magnification). Ameloce-
mental junction (A). Enamel space (ES). Gingival health is charac-
examined microscopically. This is normal given that there is a
terized by the organization of the epithelium into distinct zones;
chronic low-grade challenge presented by the subgingival plaque junctional epithelium (A and B), sulcular epithelium (B and C), free
bacteria. The low-grade inflammatory response that results is not gingiva (C and D), and attached gingiva (D and E). The gingival
detectable macroscopically at the clinical level, but it is an essential connective tissue is composed of densely packed, organized, and
protective mechanism for combating the microbial challenge and interlacing collagen bundles. There are a few scattered inflamma-
for preventing bacteria and their products from infiltrating tissues tory cells but no significant inflammatory cell infiltrate.