CHAPTER 23
Chronic Periodontitis
H. Dommisch and M. Kebschull
CHAPTER OUTLINE
Clinical Features
Risk Factors for Disease
Chronic periodontitis is the most prevalent form of periodontitis,
and it generally demonstrates the characteristics of a slowly pro-
gressing inflammatory disease. However, systemic and environ-
mental factors (e.g., diabetes mellitus, smoking) may modify the
hosts immune response to the dental biofilm so that periodontal
destruction becomes more progressive. Although chronic peri-
odontitis is most frequently observed in adults, it can occur in
children and adolescents in response to chronic plaque and calculus
accumulation.
Chronic periodontitis has been defined as an infectious disease
resulting in inflammation within the supporting tissues of the teeth,
progressive attachment loss, and bone loss.18 This definition out-
lines the major clinical and etiologic characteristics of the disease:
(1) microbial biofilm formation (dental plaque); (2) periodontal
inflammation (e.g., gingival swelling, bleeding on probing); and
(3) attachment as well as alveolar bone loss.
In addition to the local immune response caused by the dental
biofilm, periodontitis may also be associated with a number of
systemic disorders and defined syndromes. In most cases, patients
with systemic diseases that lead to impaired host immunity may
also show periodontal destruction. Therefore, periodontitis is a
disease that is not only limited to the area of the oral cavity; it is
also associated with severe systemic diseases (e.g., cardiovascular
disorders, diabetes mellitus).40
This chapter discusses clinical features that have been described
for chronic periodontitis. In addition, the diseases etiology is sum-
marized with the use of categories that explain the known factors
(i.e., microbiologic, immunologic, and genetic) involved in the
pathology of chronic periodontitis.
Clinical Features
General Characteristics
Characteristic clinical findings in patients with untreated chronic
periodontitis include the following (see also the case presentation
in Figures 23-1 through 23-6):
Supragingival and subgingival plaque and calculus
Gingival swelling, redness, and loss of gingival stippling
Altered gingival margins (e.g., rolled, flattened, cratered papil-
lae, recessions)
Pocket formation
Bleeding on probing
Attachment loss (angular or horizontally)
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Bone loss
Root furcation involvement (exposure)
Increased tooth mobility
Change in tooth position
Tooth loss
Chronic periodontitis can be clinically revealed with periodon-
tal screening and recording, which results in a periodontal screen-
ing index rating. The condition is diagnosed via the assessment of
the clinical attachment level and the detection of inflammatory
changes in the marginal gingiva (see Figure 23-1). Measurements
of periodontal pocket depth in combination with the location of the
marginal gingiva allow for conclusions to be drawn regarding the
loss of clinical attachment (see Figures 23-2 and 23-6). Dental
radiographs display the extent of bone loss, which is indicated by
the distance between the cementoenamel junction and the alveolar
bone crest (see Figure 23-3). The distinction between aggressive
and chronic periodontitis is sometimes difficult, because the clini-
cal features may be similar at the time of the first examination. At
later time points during treatment, aggressive and chronic peri-
odontitis may be differentiated by the rate of disease progression
over time, the familial nature of aggressive disease, the diseases
resistance to periodontal anti-infective therapy, and the presence of
local factors.
Disease Distribution
Chronic periodontitis is considered a site-specific disease. Local
inflammation, pocket formation, attachment loss, and bone loss are
the consequences of direct exposure to the subgingival plaque
(biofilm). As a result of this local effect, pocket formation and
attachment as well as bone loss may occur on one surface of a
tooth, whereas other surfaces maintain normal attachment levels.
As a result of the site-specific nature, the number of teeth with
clinical attachment loss classifies chronic periodontitis into the
following types:
Localized chronic periodontitis: less than 30% of the sites
show attachment and bone loss
Generalized chronic periodontitis: 30% or more of the sites
show attachment and bone loss
During chronic periodontitis, the local inflammatory response
may lead to different patterns of bone loss, including vertical
(angular) and horizontal bone destruction. Although vertical bone
loss is associated with intrabony pocket formation, horizontal
Text continued on p. 314
309
310 PART 1 Biologic Basis of Periodontology

A B C

D E
Figure 23-1 Clinical features of generalized chronic periodontitis in a 49-year-old, medically healthy, male patient. The patient reported a
smoking habit of 15 cigarettes per day. At the first visit, the periodontal photostatus displays untreated chronic periodontitis with abundant
dental plaque and calculus deposits, gingival redness and swelling, and an alteration of the gingival texture (i.e., loss of gingival stippling).
The patient noticed multiple recessions. In this case, recessions were the result of a loss of clinical attachment and alveolar bone. A, Right
lateral view. B, Frontal view. C, Left lateral view. D, Maxillary view. E, Mandibular view. (Reprinted from Kebschull and Dommisch, Thieme,
2012.)

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 CHAPTER 23 Chronic Periodontitis 311

Figure 23-2 Documentation of the periodontal attachment level in the same patient as shown in Figure 23-1 at the time of the first visit.
The red line displays the gingival margin as it reflects the recessions. Clinical attachment loss is illustrated by the filled (blue) area on the
root surfaces. The deepest periodontal pocket was measured at 9mm. Class I (green) and Class II (yellow) furcation involvements were
documented. Bleeding with periodontal probing (i.e., gingival inflammation) is reflected by red dots. As a result of the patients history of
smoking, the bleeding on probing score was relatively low, although the patient presented advanced attachment loss. Tooth mobility is
indicated by the green line (tooth #19). (Reprinted from Kebschull and Dommisch, Thieme, 2012.)

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312 PART 1 Biologic Basis of Periodontology

Figure 23-3 Collage of a total of 11 radiographs showing the radiographic periodontal status at the time of diagnosis. Compare this with
Figures 23-1 and 23-2. Note the generalized horizontal and localized angular and vertical bone loss on the mesial and distal sites of the
molars. The radiographs show deep subgingival restorations (teeth #2 and #19), overhanging margins of restorations (teeth #14 and #15),
a carious lesion (tooth #14), and insufficient root canal treatment (tooth #18). (Reprinted from Kebschull and Dommisch, Thieme, 2012.)

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 CHAPTER 23 Chronic Periodontitis 313

A B

C D

E F
Figure 23-4 After the anti-infective therapy and periodontal reevaluation, resective periodontal surgery was performed for the patient
introduced in Figures 23-1, 23-2, and 23-3. The surgical method involved an apically repositioned flap. A, Intrasulcular incisions at the
buccal sites. Notice the Class I furcation involvement on tooth #14. B, Paramarginal incision at the palatal sites, with the excision of a distal
wedge. C and D, Suturing with the use of 5-0 Prolene; buccal and palatal views, respectively. E, Occlusal view after suturing. F, Occlusal
view 1 week after surgery. Tooth #14 received endodontic therapy and crown restoration before periodontal surgery. (Reprinted from Kebschull
and Dommisch, Thieme, 2012.)

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314 PART 1 Biologic Basis of Periodontology

B
Figure 23-5 After the anti-infective therapy and periodontal reevaluation, resective periodontal surgery was performed for the patient
introduced in Figures 23-1 through 23-4. The surgical method involved an apically repositioned flap. A, Intrasulcular incisions at the buccal
sites. Note the Class I furcation involvement on tooth #19 and the horizontal bone loss affecting teeth #18, #19, and #20. B, Suturing with
the use of 5-0 Prolene; buccal view. (Reprinted from Kebschull and Dommisch, Thieme, 2012.)

bone loss is usually associated with suprabony (supra-alveolar)
pockets.
Disease Severity
The severity of periodontal destruction that occurs as a result of
chronic periodontitis is generally considered a function of time in
combination with systemic disorders that impair or enhance host
immune responses. With increasing age, attachment loss and bone
loss become more prevalent and more severe as a result of an
accumulation of destruction. Disease severity may be described as
mild, moderate, or severe (see Chapter 4):
Mild chronic periodontitis: when no more than 1mm to 2mm
of clinical attachment loss has occurred
Moderate chronic periodontitis: when 3mm to 4mm of
clinical attachment loss has occurred
Severe periodontitis: when 5mm or more of clinical attach-
ment loss has occurred
Symptoms
Chronic periodontitis is commonly a slowly progressive disease
that does not cause the affected individual to feel pain. Therefore,
most patients are unaware that they have developed a chronic
disease that is also associated with other systemic diseases (e.g.,
cardiovascular disease). For the majority of the patients, gingival
bleeding during oral hygiene procedures or eating may be the first
self-reported sign of disease occurrence. As a result of gingival
recession, patients may notice black triangles between the teeth or
tooth sensibility in response to temperature changes (i.e., cold and
heat). In patients with advanced attachment and bone loss, tooth
mobility, tooth movement, and, in rare occasions, tooth loss may
be reported. In those individuals with advanced disease progres-
sion, areas of localized dull pain or pain sensations that radiate to
other areas of the mouth or head may occur. The presence of areas
of food impaction may add to the patients discomfort. Gingival
tenderness or itchiness may also be found.
Disease Progression
Patients appear to have the same susceptibility to plaque-induced
chronic periodontitis throughout their lives. The rate of disease
progression is usually slow, but it may be modified by systemic,
environmental, and behavioral factors. The onset of chronic peri-
odontitis can occur at any time, and the first signs may be detected
during adolescence in the presence of chronic plaque and calculus
accumulation. Because of its slow rate of progression, however,
chronic periodontitis usually becomes clinically significant when a
patient reaches his or her mid-30s or later.
Chronic periodontitis does not progress at an equal rate in all
affected sites throughout the mouth. Some involved areas may
remain static for long periods,33 whereas others may progress more
rapidly. More rapidly progressive lesions occur most frequently in
interproximal areas,32,34 and they may also be associated with areas
of greater plaque accumulation and inaccessibility to plaque-
control measures (e.g., furcation areas, overhanging margins of
restorations, sites of malposed teeth, areas of food impaction).
Further factors that influence disease progression may be of
systemic origin. Patients with poorly adjusted diabetes mellitus
show a significantly higher risk of developing a severe progression
of chronic periodontitis.43,61

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 CHAPTER 23 Chronic Periodontitis 315

Figure 23-6 Documentation of the periodontal attachment level in the same patient introduced in Figures 23-1 through 23-5 after active
periodontal therapy was completed and the supportive periodontal therapy was initiated. The red line displays the gingival margin as it
reflects recessions after therapy. Clinical attachment loss is illustrated by the filled (blue) area on the root surfaces. The deepest periodontal
pocket was measured at 4mm. (Reprinted from Kebschull and Dommisch, Thieme, 2012.)

Several models have been proposed to describe the rate of
disease progression.57 In these models, progression is measured by
determining the amount of attachment loss during a given period
as follows:
The continuous model suggests that disease progression is
slow and continuous, with affected sites showing a constantly
progressive rate of destruction throughout the duration of the
disease.
The random or episodic-burst model proposes that periodon-
tal disease progresses by short bursts of destruction followed
by periods of no destruction. This pattern of disease is random
with respect to the tooth sites affected and the chronology of
the disease process.
The asynchronous, multiple-burst model of disease progres-
sion suggests that periodontal destruction occurs around
affected teeth during defined periods of life and that these bursts

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316 PART 1 Biologic Basis of Periodontology
of activity are interspersed with periods of inactivity or remis-
sion. The chronology of these bursts of disease is asynchronous
for individual teeth or groups of teeth.
Prevalence
Chronic periodontitis increases in prevalence and severity with
age, and it generally affects both genders equally. Periodontitis is
an age-associated (not an age-related) disease. Nonetheless, the
prevalence of periodontitis increases with age so that 40% of
patients who are 50 years old or older and almost 50% of patients
who are 65 years old or older show moderate periodontal destruc-
tion. The prevalence of severe forms of periodontitis also increases
with age. Up to 30% of patients develop severe periodontitis by
the time they are 40 years old or older. Generally, 50% of the
human population experiences at least one form of periodontal
disease (Figures 23-7 and 23-8).9,16,20,25,58
Risk Factors for Disease
A number of different factors influence the etiopathology of chronic
periodontitis. The composition of the oral microflora is a major
etiologic factor that leads to periodontal destruction. In this context,
the extent of the periodontal destruction depends on the hosts
immune competence as well as genetic predispositions that influ-
ence individual susceptibility to disease. In addition, both systemic
diseases and environmental factors interfere with the development
and progression of chronic periodontitis.
Microbiological Aspects
Plaque accumulation on tooth and gingival surfaces at the dento-
gingival junction is considered the primary initiating agent in the
etiology of gingivitis and chronic periodontitis.34 Attachment and
bone loss are associated with an increase in the proportion of
100 %
none or mild periodontitis
moderate periodontitis
severe periodontitis
80 %
60 %
40 %
20 %
0%
1829 3039 4054
808 1200 1856
Figure 23-7 Prevalence of periodontitis in the United States and Germany, 2007-2009. ((Eke PI, Dye BA, Wei L, et al: Prevalence of periodontitis
in adults in the United States: 2009 and 2010. J Dent Res 91:914920, 2012.)
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gram-negative organisms in the subgingival biofilm, with specific
increases in organisms that are known to be exceptionally patho-
genic and virulent. Porphyromonas gingivalis, Tannerella for-
sythia, and Treponema denticolaotherwise known as the red
complexare frequently associated with ongoing attachment and
bone loss in patients with chronic periodontitis. The development
and progression of chronic periodontitis may not depend on the
presence of one specific bacterium or bacterial complex alone.
It is assumed that chronic periodontitis is the result of a multispe-
cies infection with a number of different bacteria that influence
the pro-inflammatory immune response of the host.50 Periodontal
pathogens may invade the periodontal tissue and thus induce
an immune response with increasing concentrations of pro-
inflammatory mediators that may enhance periodontal breakdown.
In addition, a number of periodontal pathogens are capable of
producing proteases that directly influence tissue stability and host
immune responses.40
As the dental biofilm develops, early signs of an inflammatory
reaction occur in the gingival margin (i.e., gingivitis), without
actual attachment loss. Generally, optimal plaque control leads to
the complete resolution of this early gingival inflammation. Alter-
natively, with neglected oral hygiene, inflammation will progress
and eventually result in the loss of attachment around teeth.32
Although not all patients with gingivitis develop periodontitis, it is
known that all patients with periodontitis experienced prior gingi-
vitis. The occurrence of periodontitis depends on the individual
immune response that modifies the onset and progression of the
disease.32,39,40
Local Factors
Plaque accumulation and biofilm development are the primary
causes of periodontal inflammation and destruction. Therefore,
5564 6581 Age
600 908 n (summarized)

100 %
mild periodontitis
moderate periodontitis
severe periodontitis
80 %
60 %
40 %
20 %
0%
3034 3549
435 1352
Figure 23-8 Prevalence of periodontitis in the United States, 2009-2010. (Eke PI, Dye BA, Wei L, et al: Prevalence of periodontitis in adults in the
United States: 2009 and 2010. J Dent Res 91:914920, 2012.)
factors that facilitate plaque accumulation or that prevent plaque
removal by oral hygiene procedures can be detrimental to the
patient. Plaque-retentive factors are important for the development
and progression of chronic periodontitis, because they retain
microorganisms in proximity to the periodontal tissues, thereby
providing an ecologic niche for biofilm maturation. Calculus is
considered the most important plaque-retentive factor as a result
of its ability to retain and harbor plaque bacteria on its rough
surface as well as inside.56 As a consequence, calculus removal is
essential for the maintenance of a healthy periodontium. In addi-
tion, tooth morphology may influence plaque retention. Roots may
show grooves or concavities, and, in some instances, enamel pro-
jections on the surface or the furcation entrances. These morpho-
logic variations may facilitate plaque retention, subgingival
calculus formation, and disease progression.21,26,48 In addition, sub-
gingival and overhanging margins of restorations, carious lesions
that extend subgingivally, and furcations exposed by loss of
bone promote plaque retention.31,62 These potential risk factors
for periodontitis are discussed further in Chapter 32, and their
impact on the prognosis of periodontal treatment is discussed in
Chapter 33.
Systemic Factors
Chronic periodontitis is a complex disease that may not only be
limited to the infection of local sites. In several instances, periodon-
titis is also associated with other systemic disorders, such as Haim
Munk syndrome, PapillonLefvre syndrome, EhlersDanlos
syndrome, Kindlers syndrome, and Cohen syndrome. Patients with
diseases that impair the host immune response (e.g., human immu-
nodeficiency virus, acquired immunodeficiency syndrome) may
also show periodontal destruction. It is also known that osteoporo-
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CHAPTER 23 Chronic Periodontitis 317
5064 65+ Age
1128 828 n
sis, a severely unbalanced diet, and stress as well as dermatologic,
hematologic, and neoplastic factors interfere with periodontal
inflammatory responses.
In addition to being associated with defined syndromes,
periodontitis also occurs with severe systemic diseases, such
as diabetes mellitus, cardiovascular disorders, stroke, and lung
disorders.1,28,38,40,60
For diabetes mellitus and periodontitis, it is known that there is
an interaction during which both diseases mutually correlate with
each other. Patients with diabetes mellitus exhibit a higher risk for
the development of periodontitis, and periodontal infection and
inflammation may negatively interfere with the glycemic control
of the diabetic patient.43 A number of studies showed that the
prevalence, severity, and prognosis of periodontitis are associated
with the incidence of diabetes mellitus. It was found that the
average pocket depth as well as the clinical attachment loss was
increased in patients with diabetes mellitus (independent of the
type of diabetes mellitus).10,43 Patients with poor glycemic control
(i.e., a glycated hemoglobin level of >9%) tend to experience a
more severe progression of periodontitis as compared with patients
with good glycemic control (i.e., a glycated hemoglobin level of
<9%). With regard to the progression of severe periodontitis, no
difference was found between patients with good glycemic control
and non-diabetic patients.61 With diabetes mellitus, advanced gly-
cation end products may arise and lead to the release of free oxygen
and pro-inflammatory mediators (i.e., cytokines). Advanced glyca-
tion end products may also promote chemotaxis and the adhesion
of inflammatory cells to periodontal tissues, and the increased
apoptosis of fibroblasts and osteoblasts may occur.23 Further-
more, patients with diabetes mellitus tend to show a higher body
mass index; therefore, increased concentrations of adipokines that
318 PART 1 Biologic Basis of Periodontology
directly influence inflammatory responses will likely be found.44
Hyperglycemia itself leads to the release of pro-inflammatory
mediators in the bloodstream, which in turn promote increased
glycose concentration.43 Periodontal therapy may contribute to the
glycemic control of the diabetic patient. It has been shown that
systematic periodontal therapy leads a 0.4% reduction of glycated
hemoglobin. Each therapy regimen that contributes to achieve
a reduction in the glycated hemoglobin level decreases the risk
of diabetes-related long-term consequences, such as myocardial
infarction, microvascular complications, and many others. 43
Immunologic Factors
Chronic periodontitis is a disease that is induced by bacteria orga-
nized in the dental biofilm. However, the onset, progression, and
severity of the disease depend on the individual hosts immune
response.19,39 Patients may show alterations in their peripherial
monocytes, which are related to the reduced reactivity of lympho-
cytes or an enhanced B-cell response.39,40 B-cells, macrophages,
periodontal ligament cells, gingival fibroblasts, and epithelial
cells synthesize pro-inflammatory mediators (e.g., interleukin-1,
interleukin-6, interleukin-8, prostaglandin E2, tumor necrosis
factor-) that modify innate and adaptive immune responses at
periodontal sites.7,12-14,29,45 Pro-inflammatory mediators regulate the
synthesis and secretion of, for example, matrix metalloproteinases
and receptor activator of nuclear factor- ligand (RANKL). In
periodontal lesions, matrix metalloproteinases contribute to soft-
and hard-tissue degradation during active inflammatory reactions.19
RANKL binds to its receptor activator of nuclear factor- on the
cell surface of premature osteoclasts, thereby initiating osteoclast
differentiation that leads to the degradation of alveolar bone.19,29,45
Physiologically, osteoprotegerin is the opponent of RANKL;
during periodontitis, an imbalance between osteoprotegerin and
RANKL promotes further bone degradation.19
In addition, reduced neutrophil counts influence the degree of
periodontal inflammation. Congenital neutropenia (Kostman syn-
drome) leads not only to an increased susceptibility to infection
in general but also to severe chronic periodontitis. Patients with
Kostman syndrome show reduced levels of antimicrobial peptides,
such as the cathelicidin LL-37 and neutrophil peptides (-defensins),
which impair the innate immune response.5,46 LL-37 is an effective
antimicrobial peptide that is synthesized from inactive precursors.
Mutations in the cathepsin C gene hinder cleavage and thus the
activation of LL-37. Such genetic alterations contribute to the
severity and progression of chronic periodontitis (i.e., Papillon
Lefvre syndrome; HaimMunk syndrome).8,24
Genetic Factors
Periodontitis is considered to be a multifactorial disease that
is influenced by local, systemic, and immunologic factors, as
described previously. Each factor is in turn directly related to indi-
vidual genetic conditions. Genetic variations such as single nucleo-
tide polymorphisms (SNPs) and genetic copy number variations
may directly influence innate and adaptive immune responses as
well as the structure of periodontal tissues. Periodontal destruction
has been found among family members and across different gen-
erations within a family, thereby suggesting a genetic basis for the
susceptibility to periodontal disease. In a number of studies, the
prevalence of aggressive and chronic periodontitis has been inves-
tigated in families with a history of one or more family members
with periodontitis. The data from those studies have demonstrated
variable results, with a likelihood of heritability of up to 50%.
Variations are mainly the result of different study designs as well
as the number of evaluated individuals.2,35,51
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Studies of SNPs in the interleukin-1 gene led to early conclu-
sions that alterations in sequences of immunologically relevant
genes may explain the heritability of periodontitis.30 Conflicting
data in the literature indicate inconclusive knowledge of SNPs in
the interleukin-1 gene as well as of SNPs potential role in the
heritability and etiopathology of periodontitis. 15,17
Genome-wide association studies have revealed a significant
association between periodontitis and coronary heart disease as a
result of a variation in the CDKN2BAS gene (cyclin-dependent
kinase inhibitor 2B antisense [formerly antisense non-coding RNA
in the INK4 locus, ANRIL]). In vitro studies have shown that the
periodontal pathogen Porphyromonas gingivalis induced the gene
expression of ANRIL in human gingival fibroblasts, thereby sug-
gesting the potential regulation of ANRIL during periodontal infec-
tion and inflammation.52 Another study identified a SNP in an
untranslated region of the human -defensin-1 gene DEFB1, and
this genetic alteration was significantly associated with aggressive
and chronic periodontitis. Human -defensin-1 is an antimicrobial
peptide that plays an important role in innate immune responses.7,54
In a different genome-wide association study, a SNP in the glyco-
syltransferase gene GLT6D1 was found to be associated with
aggressive periodontitis. The exact physiological role of GLT6D1
is currently unknown.55 In addition, genetic alterations in the
cyclooxygenase-2 gene (COX-2) were also significantly associated
with aggressive periodontitis. COX-2 is involved in eicosanoid
metabolism and therefore important during inflammatory reac-
tions.53 Although four different genetic variations have been identi-
fied and validated, it is most likely that a higher number of genes
require variations to result in the development of periodontitis.36
Environmental and Behavioral Factors
In addition to microbial, immunologic, and genetic factors, the
development and progression of chronic periodontitis is further
influenced by environmental and behavioral factors, such as
smoking and psychological stress.39,40 Smoking is a major risk
factor for the development and progression of generalized chronic
periodontitis.4 Periodontitis is influenced by smoking in a dose-
dependent manner. The intake of more than 10 cigarettes per day
tremendously increases the risk of disease progression as compared
with non-smokers and former smokers.59
As compared with non-smokers, the following features are
found in smokers3,27,42,49:
Increased periodontal pocket depth of more than 3mm
Increased attachment loss
More recessions
Increased loss of alveolar bone
Increased tooth loss
Fewer signs of gingivitis (e.g., less bleeding with probing)
Greater incidence of furcation involvement
As a result of the consumption of tobacco, reactive oxygen
(i.e., radicals) is released that chemically irritates periodontal
tissues via DNA damage, the lipid peroxidation of cell membranes,
the damage of endothelial cells, and the induction of smooth
muscle cell growth.37
Psychological factors (e.g., stress, depression) also negatively
influence the progression of chronic periodontitis.22 Patients
with periodontitis often report the experience of family- or work-
related stress.41 Positive correlations between cortisol levels and
periodontal indices (e.g., plaque index, gingival index), bone loss,
and missing teeth have been recorded.11,22,47 In addition, stress
as an etiologic factor was even more strongly associated with
periodontitis when patients were smokers as compared with
non-smokers.6

Suggested Readings
Chung WO, Dommisch H, Yin L, etal: Expression of defensins in gingiva
and their role in periodontal health and disease. Curr Pharm Des
13:30733083, 2007.
Eke PI, Dye BA, Wei L, etal: Prevalence of periodontitis in adults in the
United States: 2009 and 2010. J Dent Res 91:914920, 2012.
Flemmig TF: Periodontitis. Ann Periodontol 4:3238, 1999.
Kebschull M, Demmer RT, Papapanou PN: Gum bug, leave my heart
alone!epidemiologic and mechanistic evidence linking periodontal
infections and atherosclerosis. J Dent Res 89:879902, 2010.
Lang NP, Schatzle MA, Loe H: Gingivitis as a risk factor in periodontal
disease. J Clin Periodontol 36(Suppl 10):38, 2009.
Lindhe J, Okamoto H, Yoneyama T, etal: Longitudinal changes in peri-
odontal disease in untreated subjects. J Clin Periodontol 16:662670,
1989.
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CHAPTER 23 Chronic Periodontitis 319
Pihlstrom BL, Michalowicz BS, Johnson NW: Periodontal diseases. Lancet
366:18091820, 2005.
Preshaw PM, Alba AL, Herrera D, etal: Periodontitis and diabetes: a
two-way relationship. Diabetologia 55:2131, 2012.
Schaefer AS, Richter GM, Nothnagel M, etal: A 3 UTR transition within
DEFB1 is associated with chronic and aggressive periodontitis. Genes
Immun 11:4554, 2010.
Tonetti MS: Cigarette smoking and periodontal diseases: etiology and man-
agement of disease. Ann Periodontol 3:88101, 1998.
References
References for this chapter are found on the companion
website www.expertconsult.com.

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