Periodontal Disease
Disease
of the periodontal tissues constitutes the chief reason, more prevalent even
than dental caries, for the loss of teeth. It is almost universally present
among adults. Epidemiologic studies have shown an association between the
development of coronary artery disease and the presence of periodontal disease.
This is presumed to be independent of the close association between tobacco
smoking and each of these conditions.
Periodontitis manifests as a chronic
inflammation resulting from endogenous plaque bacteria, which arise from a
worsening gingivitis culminating in the loss of dentition. A marginal
periodontitis is usually the sequel to long-standing marginal gingivitis
and generally includes all the signs of marginal gingivitis plus alveolar crestal
bone and adjacent peridental membrane resorption. The formation of a
periodontal pocket, a pathologic alteration of the gingival attachment, is
pathognomonic for this condition. Periodontal disease is defined by pocket
depth and loss of attachment. The epithelial lining of the gingival crevice is
ulcerated, and the peridental membrane fibers are destroyed, generating an
inflammatory cell infiltrate in the corium which may produce a purulent
discharge. The epithelial attach- ment is displaced and takes successively
deeper positions as the pocket increases. Beginning with notching of the
alveolar crest, bone resorption continues, with destruction of the cribriform
plate (lamina dura). Under the influence of occlusal trauma, the pocket
penetrates toward the apex of the root; such pocket formation is seen in
radiographic images as “vertical” in type, indi- cating advanced periodontal
disease, compared with the simpler “horizontal” resorption. The local factors
that contribute to the development of these pockets include deposition of
plaque and calculi from saliva; food debris, which creates an environment for
incubation of bacteria and a resulting microbiofilm in the mouth; poor oral
hygiene; and mouth breathing. Tobacco is the most significant risk factor
associated with the development of periodontal disease. Patients with diabetes
mellitus, HIV infection, or cancer or who have undergone radia- tion therapy to
the head and neck region are also at increased risk for periodontal disease.
Medications that reduce salivary production can also contribute to the
development of this condition. Some individuals are genetically susceptible to
the development of periodontal disease; when they also have other high-risk
factors, there is a greater likelihood of the development of severe periodontal
disease.
Eighty-five percent of patients with
periodontitis have mild disease, and less than 5% have aggressive
periodontitis. Rapidly progressive chronic periodontitis can develop in young
children, resulting in bone and possibly tooth loss by early adulthood. Aggressive
periodontitis in healthy adolescents is typically a result of colonization by
Aggregatibacter actinomycetemcomitans. A less common form of aggressive
periodontitis affects the deciduous teeth, resulting in acute proliferative
gingivitis with rapid alveolar destruction, which resolves before the eruption
of the permanent teeth.
HIV infection is associated with a
particularly virulent form of rapidly progressive periodontitis (see Plate
2-53).
Occlusal trauma, most often as a result of grinding (bruxism),
clenching, or similar habits producing repetitive and excessive contacts of tooth
on tooth, can result in an augmentation of lateral stresses on a tooth.
The malpositioned, nonfunctional contacts result in dental abrasions on the
surfaces and a widening of the periodontal membrane within the infrabony
pockets, leading to tooth mobility.
A missing tooth permits an open
contact, with food impaction causing an interproximal pocket, typically
associated with caries on the distal tooth surface. The stress of occlusion on
such a tooth may further accelerate the formation of a pocket on the mesial
surface.
Migration of teeth, a late symptom in periodontitis, is a consequence
of open contacts, wedging of food particles, extrusion of teeth through the
pressure of granulation tissues, and other traumatic relationships in the deranged
occlusion. Mobility of the teeth becomes marked as bone resorption increases
the ratio of dental parts supported by bone to those not supported. The gingiva
in this phase of periodontitis is typically soft and spongy and is duskier in
color than normal, and there is retraction of the margin and abundant
accretions of calculus.
Regardless of disease severity, the
initial phase of treatment requires removal of plaque and calculus deposits
through professional scaling and root planing, followed by proper oral hygiene.
