CHAPTER 27 

Chronic Periodontitis
Henrik Dommisch | Moritz Kebschull

CHAPTER OUTLINE
Clinical Features
Risk Factors for Disease

Chronic periodontitis is the most prevalent form of periodontitis, the area of the oral cavity but may be associated with severe sys-
and it generally shows the characteristics of a slowly progressing temic diseases such as cardiovascular disease, stroke, and diabetes
inflammatory disease. Periodontitis belongs to the group of complex mellitus.52,70,73,79
inflammatory diseases in humans. In this context, the word complex This chapter discusses clinical features that have been described
not only describes the fact that there are multiple clinical symptoms for chronic periodontitis, based on the consensus of the 1999 World
that account for the disease, but also explains the multiple factors that Workshop in Periodontics. In addition, the etiology is summarized
lead to and influence periodontal inflammation. Chronic periodontitis in categories explaining the known factors (microbiologic, immu-
occurs most frequently in adults. Nonetheless, it may also be diagnosed nologic, genetic, and environmental) involved in the pathology of
in children and adolescents when associated with chronic plaque chronic periodontitis.
and calculus accumulation. Therefore chronic periodontitis should At the time of writing of this chapter, a new World Workshop in
be understood as age-associated, but not age-dependent, complex Periodontics was jointly planned by the European Federation of
chronic inflammation of the periodontal tissues. As described in this Periodontology and the American Academy of Periodontology for
chapter, systemic or environmental factors (e.g., diabetes mellitus, November 2017, to further refine the classification of periodontal
smoking) modify the host immune response to the dental biofilm so diseases.
that the periodontal destruction becomes more progressive.
Periodontitis is a highly prevalent progressing disease, and it
affects approximately 10.5% to 12% of the world’s population.44
Clinical Features
Periodontitis has been found to exert adverse effects on systemic General Characteristics
health, and in this context, important pathologic interdependencies Characteristic clinical findings in patients with untreated chronic
with, for example, diabetes mellitus have been identified.9,32,55,73 Also, periodontitis include the following symptoms (see the case presentation
it is known that systemic inflammatory markers, such as the C-reactive in Figs. 27.1 to 27.6):
protein (CRP), are elevated in patients with periodontitis.69,96 In • Supragingival and subgingival plaque (and calculus)
general, chronic periodontitis is considered as a slowly progressing • Gingival swelling, redness, and loss of gingival stippling
disease, but in the presence of severe systemic conditions or envi- • Altered gingival margins (rolled, flattened, cratered papillae,
ronmental factors, such as smoking, this inflammatory disease recessions)
progresses more rapidly. • Pocket formation
The classic definition described chronic periodontitis as “an • Bleeding on probing
infectious disease resulting in inflammation within the supporting • Attachment loss
tissues of the teeth, progressive attachment loss, and bone loss.”24 • Bone loss (angular/vertical or horizontal)
The etiopathologic factors that lead to periodontal inflammation and, • Root furcation involvement
subsequently, destruction of periodontal tissues have been widely • Increased tooth mobility
studied, and the interplay between the microbial environment and • Change in tooth position
the individual host immune response has gained attention in the • Tooth loss
scientific community (discussed later). Chronic periodontitis can be clinically revealed by means of
Chronic periodontitis represents major clinical and etiologic periodontal screening and recording (PSR), diagnosed by an assess-
characteristics such as (1) microbial biofilm formation (dental plaque), ment of the clinical attachment level, and therewith the detection
(2) periodontal inflammation (gingival swelling, bleeding on probing), of inflammatory changes in the marginal gingiva (see Fig. 27.1).
and (3) attachment as well as alveolar bone loss. Measurements of periodontal probing pocket depth in combination
Besides the local immune response to the dental biofilm, periodontitis with the location of the marginal gingiva allow conclusions regarding
may also be associated with a number of systemic disorders and the loss of clinical attachment (see Figs. 27.3 and 27.6). Dental
defined syndromes. In most cases, patients with systemic diseases, radiographs reveal the extent of bone loss indicated by the distance
which lead to impaired host immunity, may also show periodontal between the cemento-enamel-junction and the alveolar bone crest
destruction. On the other hand, periodontitis is not only limited to (Fig. 27.2).

342
 CHAPTER 27  Chronic Periodontitis 342.e1

Abstract
This chapter focuses on the clinical characteristics, diagnostic findings,
and the etiopathology of chronic periodontitis. Subsequent to a brief
overview of the definition of chronic periodontitis and the epide-
miologic background, the clinical characteristics, disease distribution,
severity, symptoms, progression, and prevalence are discussed.
Furthermore, risk factors for chronic periodontitis, such as micro-
biologic, local, systemic, immunologic, genetic, and environmental
factors, are extensively presented in this chapter.

Keywords
chronic periodontitis
complex inflammatory disease
dental biofilm
generalized chronic periodontitis
localized chronic periodontitis
mild chronic periodontitis
moderate chronic periodontitis
periodontal microbiology
risk factors
severe chronic periodontitis
 CHAPTER 27  Chronic Periodontitis 343

A B C

D E
Fig. 27.1  Clinical features of generalized chronic periodontitis in a 49-year-old, medically healthy male patient
who presented to the clinic for the first time. The patient reported smoking 15 cigarettes per day. Note the
abundant dental plaque and calculus deposits, gingival redness and swelling, and alteration of the gingival
texture (loss of gingival stippling). The patient noticed multiple recessions. In this case, recessions were the
result from 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 M, Dommisch H: Resektive parodon-
talchirurgie. Zahnmedizin up-2-date. 2012; 525–545.)

Fig. 27.2  Collage of the radiographic periodontal status (a total of 11 x-rays) at the time of diagnosis (compare
Figs. 27.1 and 27.3). Generalized horizontal and localized angular, vertical bone loss on the mesial and distal
sites of molars was noted. Radiographs present deep subgingival restorations (teeth #2 and #19), overhanging
margins of restorations (teeth #14 and #15), carious lesion (tooth #14), and insufficient root canal treatment
(tooth #18). (Reprinted from Kebschull M, Dommisch H: Resektive parodontalchirurgie. Zahnmedizin up-2-date.
2012; 525–545.)
344 Part 2  Biologic Basis of Periodontology

Fig. 27.3  Documentation of the periodontal attachment level in the same patient (see Fig. 27.1) at the time
of the first visit. The red line displays the gingival margin reflecting recessions. Clinical attachment loss is
illustrated by the filled (blue) area on the root surfaces. The deepest periodontal pocket measured was 9 mm.
Class I (green) and class II (yellow) furcation involvement were documented. Bleeding upon periodontal probing
(gingival inflammation) is reflected by orange dots. Due to the 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 M, Dommisch H: Resektive parodontalchirurgie. Zahnmedizin
up-2-date. 2012; 525–545.)
 CHAPTER 27  Chronic Periodontitis 345

A B

C D

E F
Fig. 27.4  Subsequent to the anti-infective therapy and periodontal reevaluation, resective periodontal surgery
was performed in the patient introduced in Figs. 27.1, 27.2, and 27.3. Surgical method: apically repositioned
flap. (A) Intrasulcular incision at buccal sites; notice class I furcation involvement on tooth #14. (B) Paramarginal
incision at palatal sites, excision of a distal wedge. (C–D) Sutured using 5-0 Prolene, buccal and palatal view,
respectively. (E) Occlusal view after suturing. (F) Occlusal view 1 week post surgery. Tooth #14 received endodontic
therapy and crown restoration prior to periodontal surgery. (Reprinted from Kebschull M, Dommisch H: Resektive
parodontalchirurgie. Zahnmedizin up-2-date. 2012; 525–545.)
346 Part 2  Biologic Basis of Periodontology

B
Fig. 27.5  Subsequent to the anti-infective therapy and periodontal reevaluation, resective periodontal surgery
was performed in the patient introduced in Figs. 27.1 to 27.4. Surgical method: apically repositioned flap. (A)
Intrasulcular incision at buccal sites; notice class I furcation involvement on tooth #19 and horizontal bone loss
in teeth #18 to #20. (B) Sutured using 5-0 Prolene, buccal view. (Reprinted from Kebschull M, Dommisch H:
Resektive parodontalchirurgie. Zahnmedizin up-2-date. 2012; 525–545.)

The distinction between aggressive and chronic periodontitis is

Key Differences Between Gingivitis and Chronic Periodontitis
sometimes difficult, because the clinical features may be similar at
the time of the first examination. At later time points during treatment, Plaque-Induced Gingivitis Chronic Periodontitis
aggressive and chronic periodontitis may be differentiated by the
rate of disease progression over time, familial nature of aggressive Inflammation of the gingiva Inflammation of periodontal
disease, and presence of local as well as systemic factors. without attachment/bone apparatus with attachment/
loss. bone loss.
Disease Distribution With optimal oral hygiene, The attachment loss is
Chronic periodontitis exhibits a site-specific clinical picture, where this condition can be irreversible, in spite of
attachment and bone loss are not equally distributed throughout the resolved completely successfully controlling the
dentition as well as around teeth. Local inflammation, pocket forma- (reversible). inflammation.
tion, attachment loss, and bone loss are the sequelae of the direct Not all sites with gingivitis All patients with chronic
exposure to the subgingival plaque (dental biofilm) and local inflam- progress to periodontitis periodontitis must have
matory responses. Periodontal pocket formation, attachment, and experienced prior gingivitis
bone loss may develop on one or more sites of a tooth, while other
sites remain at a physiologic attachment level. Due to the site-specific The dental implant The dental implant counterpart of
nature and based on the number of teeth with clinical attachment counterpart of gingivitis is periodontitis is
loss, chronic periodontitis can be classified into the following peri-implant mucositis. peri-implantitis.
categories:
• Localized chronic periodontitis, meaning that less than 30% of
the teeth show attachment and bone loss Disease Severity
• Generalized chronic periodontitis, meaning that 30% or more of With chronic periodontitis, severity and extent of periodontal destruc-
the teeth show attachment and bone loss tion will occur over time in combination with systemic disorders
During chronic periodontitis, the local inflammatory response impairing or enhancing host immune responses. Patients with chronic
may lead to different patterns of bone loss, including vertical (angular) periodontitis experience a progression in attachment and bone loss
and horizontal bone destruction. Although vertical bone loss is as they become older. If untreated and oral hygiene behaviors remain
associated with intrabony pocket formation, horizontal bone loss is unchanged, chronic periodontitis eventually leads to tooth loss and
usually associated with suprabony (supraalveolar) pockets. may negatively impact distant organs by the uncontrolled progression
 CHAPTER 27  Chronic Periodontitis 347

Fig. 27.6  Documentation of the periodontal attachment level in the same patient (see Figs. 27.1 to 27.5)
after active periodontal therapy was completed and the supportive periodontal therapy was initiated. The red
line displays the gingival margin reflecting recessions after therapy. Clinical attachment loss is illustrated by
the filled (blue) area on the root surfaces. The deepest periodontal pocket measured was 4 mm. (Reprinted
from Kebschull M, Dommisch H: Resektive parodontalchirurgie. Zahnmedizin up-2-date. 2012; 525–545.)

of periodontal inflammation and by the systemic spread of infection. • Severe chronic periodontitis: clinical attachment loss of 5 mm
Relative to the degree of attachment and bone loss, disease severity or more
can be described as mild, moderate, or severe. These degrees are
defined as follows: Symptoms
• Mild chronic periodontitis: clinical attachment loss of 1 to 2 mm Chronic periodontitis is commonly a slowly progressing complex
• Moderate chronic periodontitis: clinical attachment loss of 3 to disease without a pain experience. Therefore most patients are unaware
4 mm that they have developed a chronic disease. For the majority of
348 Part 2  Biologic Basis of Periodontology

patients, gingival bleeding during oral hygiene procedures or eating Although some sites exhibit more rapid periodontal breakdown over
may be the first sign of disease occurrence. Areas with advanced time, the attachment level remains static at other sites in the dentition
periodontal inflammation may present with purulence emanating for longer time periods.58 Interestingly, disease progression is more
from the periodontal pocket. As a result of gingival recession, patients rapid at interproximal sites compared to oral or buccal areas of
may notice black triangles between teeth or tooth sensitivity in neighboring teeth.56,59 This phenomenon may be explained by the
response to temperature changes (cold and heat). In addition, food fact that these interproximal areas become wider along with disease
impaction may occur in the space of interdental triangles, leading progression, recession development, and the related increased prob-
to increased discomfort and bad breath. In cases with advanced ability of plaque accumulation and food impaction in those areas.
attachment and bone loss, tooth mobility, tooth movement, fanned Plaque control becomes more difficult, and interproximal furcation
out or elongated front teeth, and, in rare occasions, tooth loss may areas, interproximal caries, root caries, overhanging restoration
be reported. In cases with advanced disease progression, areas of margins, and tooth crowding may further promote interproximal
localized dull pain or pain sensations radiating to other areas of the attachment loss.
mouth or head may occur. As chronic periodontitis exhibits individual and heterogeneous
progression patterns throughout the dentition, three different models
have been proposed to describe the rate of disease progression and
KEY FACT determine the degree of attachment loss over time17 as follows92:
Site Specificity of Chronic Periodontitis • The continuous model:
Not all sites in the mouth are equally prone to chronic periodontitis, and • Describes slow and continuous disease progression
it exhibits site specificity. The progression of the disease occurs in certain • Suggests that sites exhibit a constant progression rate of
sites but not uniformly. Interproximal sites, in general, are more prone to attachment loss throughout the duration of the disease
periodontal destruction, compared to buccal/facial sites. • The random or episodic-burst model:
• Describes the episodic occurrence of short progressive bursts
of periodontal destruction followed by periods of stagnation
Disease Progression • Sites, teeth, and the chronology of bursts and stagnation are
Chronic periodontitis may develop at any time in life. First clinical subject to random effects
signs of inflammation may occur even during adolescence when the • The asynchronous, multiple-burst model:
oral hygiene is neglected and dental plaque and calculus were allowed • Describes the occurrence of periodontal destruction (bursts)
to accumulate. In general, the progression rate of chronic periodontitis during defined periods, which are asynchronously interrupted
is slow, so that symptoms of the disease appear around the age of by periods of stagnation or remission for individual sites and
40 or later in life. Onset and the rate of disease progression, however, teeth
may be influenced by a number of modifiable (e.g., smoking, diet)
and nonmodifiable (e.g., genetic disorders and risk issues) factors. Prevalence
In this context, patients who develop a metabolic disorder, such as Chronic periodontitis is considered to be one of the most common
diabetes mellitus, may exhibit a much higher progression rate of chronic diseases in humans, and the prevalence of the disease increases
chronic periodontitis along with increased alveolar bone loss, with age equally in both genders. In general, 40% of patients ≥50
periodontal bleeding, and pocketing.73,95,100 Thus diabetes mellitus years old and almost 50% of patients ≥65 years old show signs of
and the degree of blood sugar control belong to the most important mild to moderate periodontal destruction. The prevalence of severe
systemic factors that are directly correlated with periodontal disease. forms of periodontitis also increases with age. From 11% to 30%
The progression pattern of chronic periodontitis does not show of patients develop severe periodontitis at the age of 40 years or
equal degrees of attachment loss on each affected site over time. older (Figs. 27.7 and 27.8).14,22,28,39,94 The worldwide prevalence for

100 %
None or mild periodontitis
Moderate periodontitis
Severe periodontitis
80 %

60 %
Fig. 27.7  Prevalence for periodontitis
in the United States and Germany
(2007–2009). (Data from Genco et al.,
40 % 2007,28 and Holtfreter et al., 2009,39 and
reviewed in Demmer & Papapanou,
2010.14)

20 %

0%
18–29 30–39 40–54 55–64 65–81 Age

808 1200 1856 600 908 n (summarized)

 CHAPTER 27  Chronic Periodontitis 349

100 %
Mild periodontitis
Moderate periodontitis
Severe periodontitis
80 %

60 %
Fig. 27.8  Prevalence for periodontitis in the
United States (2009–2010). (Data from Eke PI,
Dye BA, Wei L, et al: Prevalence of periodontitis
40 %
in adults in the United States: 2009 and 2010.
J Dent Res 91:914–920, 2012.)

20 %

0%
30–34 35–49 50–64 65+ Age
435 1352 1128 828 n

severe chronic periodontitis is estimated at 10.5% to 12% of the As the dental biofilm develops, early signs of an inflammatory reaction
world’s population.44 occur in the gingival margin (gingivitis) without attachment loss.
Generally, optimal plaque control leads to the complete resolution
of this early gingival inflammation.62 With neglected oral hygiene
Risk Factors for Disease on the other hand, inflammation will progress and eventually result
A number of factors influence the etiopathogenesis of chronic in the loss of attachment around teeth.56 Although not all patients
periodontitis. The composition of the oral microflora and the amount with gingivitis develop periodontitis, it is known that all patients
of dental biofilm (plaque) are major etiologic factors. In this context, with periodontitis experienced prior gingivitis. The occurrence of
the extent of the periodontal destruction depends on the host immune periodontitis depends on the individual immune response that modifies
competence as well as genetic predispositions influencing the the onset and progression of the disease.56,68,70
individual susceptibility to disease. In addition, both systemic diseases Attachment and bone loss are associated with an increase in the
and environmental factors interfere with the development and progres- proportion of gram-negative organisms in the subgingival biofilm,
sion of chronic periodontitis. The risk factors described in the fol- with specific increases in organisms known to be pathogenic and
lowing sections (microbiological, local, systemic, immunologic, virulent. Porphyromonas gingivalis, Tannerella forsythia, and
genetic, environmental, and behavioral) may occur simultaneously, Treponema denticola, otherwise known as the red complex bacteria,
or a selection of factors is present in patients with chronic periodontitis. are frequently associated with ongoing attachment and bone loss in
The degree of the individual risk factor contribution differs among chronic periodontitis.91 Development and progression of chronic
patients, so it is worthwhile to not only identify the risk factors but periodontitis may not depend on the presence of one specific bacterium
also to specify each risk factor’s degree of contribution. or bacterial complex alone. It is assumed that chronic periodontitis
The prior history of gingivitis and periodontitis should be con- is the sequelae of a multispecies infection with a number of different
sidered as general predictors for the development or progression of bacteria that influence the proinflammatory immune response of the
chronic periodontitis.56 It is possible that the disease could not be host.46,82 Furthermore, the concept of host-microbial interactions has
successfully treated in the first place. The reason for an unsuccessful gained scientific attention. It has been found that increased numbers
treatment outcome can be as simple as the patient’s unwillingness of periodontal pathogens contribute to the development of a dysbiotic
(noncompliant patients) to understand the disease or perform proper microbial environment, which is triggered by the inflammatory milieu
oral hygiene. On the other hand, reasons for disease progression can in the periodontal pocket.2,36 This concept describes a shift from a
also be more complex when nonmodifiable factors—such as genetic symbiotic microbial environment to the development of dysbiosis
predispositions/syndromes, severe immunologic disorders, other within the biofilm involving so-called keystone pathogens, such as
therapies (e.g., organ transplantations) that affect the patient’s immune P. gingivalis, as a polymicrobial synergistic effect.33–35 Periodontal
status, lack of dexterity, or other systemic diseases—are present. pathogens like P. gingivalis may then invade the periodontal tissue
This highlights the complexity of not only the development but also and therewith induce further immune responses with increasing
the progression/reoccurrence of chronic periodontitis. Several risk concentrations of proinflammatory mediators that may enhance
factors that contribute to the patient’s susceptibility to chronic periodontal breakdown. In addition, a number of periodontal pathogens
periodontitis are discussed next. are capable of producing proteases that directly affect the tissues
and host immune responses.70
Microbiologic Aspects
Plaque accumulation on tooth and gingival surfaces (dental biofilm Local Factors
formation) at the dentogingival junction is considered the primary Plaque accumulation and biofilm development are the primary causes
initiating agent in the etiology of gingivitis and chronic periodontitis.56 of periodontal inflammation and destruction. Therefore factors that
350 Part 2  Biologic Basis of Periodontology

facilitate plaque accumulation or prevent plaque removal by oral chemotaxis and adhesion of inflammatory cells to periodontal tissues,
hygiene procedures can be detrimental to the patient. Plaque-retentive and increased apoptosis of fibroblasts and osteoblasts may occur.31
factors are important in the development and progression of chronic Furthermore, patients with diabetes mellitus tend to show a higher
periodontitis because they retain microorganisms in proximity to body mass index, and therefore increased concentrations of adipokines
the periodontal tissues, providing an ecologic niche for biofilm that directly influence inflammatory responses were found.74 Hyper-
maturation. Calculus is considered the most important plaque-retentive glycemia per se leads to the release of proinflammatory mediators
factor because of its ability to retain and harbor plaque bacteria on in the bloodstream, which in turn promote increased glucose concentra-
its rough surface as well as inside.42,89 As a consequence, calculus tion.73 Periodontal therapy may contribute to glycemic control of
removal is essential for the maintenance of a healthy periodontium. the diabetic patient. It was shown that the systematic therapy of
In addition, the tooth morphology may influence plaque retention. chronic periodontitis leads to an at least short-term reduction
Roots may show grooves or concavities, and in some instances, of glycated hemoglobin (HbA1c) of approximately 0.3% up to
enamel projections on the surface or furcation entrances. Those 0.6%.7,9,41,57,90 Each therapy regimen that contributes to achieve
morphologic variations may facilitate plaque retention, subgingival reduction of glycated hemoglobin may decrease the risk of diabetes-
calculus formation, and disease progression.29,40,78 In addition, sub- related long-term consequences, such as myocardial infarction,
gingival and overhanging margins of restorations, carious lesions microvascular complications, and many others.73
that extend subgingivally, and furcations exposed by loss of bone In the context of diabetes mellitus, a number of patients exhibit
promote plaque retention.50,101 an increased body weight (obesity), which also correlates with the
prevalence and severity of periodontal attachment and bone loss.66
The negative effect of a high body mass index with regard to the
Common Retentive Local Factors That Contribute to Chronic outcome of periodontal therapy was comparable to the negative
Periodontitis effect that has been described for smoking.93
• Dental calculus
• Crown margins Immunologic Factors
• Restoration overhangs Chronic periodontitis is a disease induced by bacteria organized in
• Furcation involvement the dental biofilm. Onset, progression, and severity of the disease
• Deep probing depths depend, however, on the individual host immune response.26,68 Patients
• Anatomic grooves on the roots may show alterations of peripheral monocytes, which relate to reduced
• Subgingival caries or resorptive lesions reactivity of lymphocytes or enhanced B-cell response.68,70 Not only
B cells and macrophages, but also periodontal ligament cells, gingival
fibroblasts, and epithelial cells synthesize proinflammatory
mediators—such as interleukin-1 beta (IL-1 beta), IL-6, IL-8,
Systemic Factors prostaglandin-E2 (PGE2), tumor-necrosis factor alpha (TNF-alpha),
Chronic periodontitis is a complex disease that may not be limited and many others—that modify innate and adaptive immune responses
to infection at local sites, but in several instances periodontitis is at periodontal sites.11,18–21,48,75 Proinflammatory mediators regulate
also associated with other systemic disorders, such as Haim–Munk synthesis and secretion of matrix-metalloproteinases (MMPs) and
syndrome, Papillon–Lefèvre syndrome, Ehlers–Danlos syndrome, receptor-activator-of-NF-kappaB-ligand (RANKL). In periodontal
Kindler syndrome, and Cohen syndrome. Patients who suffer from lesions, MMPs contribute to soft and hard tissue degradation during
diseases that impair host immune responses (e.g., HIV/AIDS) active inflammatory processes.26 RANKL binds to its receptor RANK
may also show periodontal destruction. Further, it is also known on the cell surface of premature osteoclasts, and therewith it initiates
that osteoporosis, severe unbalanced diet, and stress, as well as osteoclast differentiation leading to degradation of alveolar bone.26,48,75
dermatologic, hematologic, and neoplastic factors, interfere with Physiologically, osteoprotegerin (OPG) is an inhibitor of RANKL,
periodontal inflammatory responses. In addition to defined syndromes, and during periodontitis, an imbalance between OPG and RANKL
periodontitis is also associated with severe systemic diseases, such promotes further bone degradation.26
as diabetes mellitus, cardiovascular disorders, stroke, and lung In addition, reduced counts in neutrophils (polymorphonuclear
disorders.1,9,45,67,70,98,99,102 neutrophils [PMNs]) influence the degree of periodontal inflamma-
Periodontitis is now considered as the sixth complication of tion. Congenital neutropenia (Kostmann syndrome) leads not only
diabetes mellitus.27,61 For diabetes mellitus and periodontitis, there to an increased susceptibility to infection in general, but also to
is a known interaction during which both diseases mutually correlate severe chronic periodontitis. Patients with Kostmann syndrome show
to each other.54 Patients with diabetes mellitus exhibit a higher risk reduced levels of antimicrobial peptides, such as the cathelicidin
to develop periodontitis, and the periodontal infection/inflammation (LL-37) and neutrophil peptides (alpha defensins), which impair
may negatively interfere with the glycemic control of the diabetic their innate immune response.8,76 LL-37 is an effective antimicrobial
patient.73 A number of studies showed that prevalence, severity, and peptide that is synthesized from inactive precursors, and mutations
prognosis of periodontitis are associated with the incidence of diabetes in the cathepsin C gene hinder cleavage, and therewith activation,
mellitus. It was found that the average pocket depth as well as the of LL-37. Those genetic alterations contribute to the severity and
clinical attachment loss was increased in patients with diabetes mellitus progression of chronic periodontitis (Papillon–Lefèvre syndrome,
(independently from the type of diabetes mellitus).15,47,73,81 Patients Haim–Munk syndrome).13,38
with poor glycemic control tend to experience more severe progression
of periodontitis compared to patients with good glycemic control. Genetic Factors
Regarding the progression of severe periodontitis, no difference was Periodontitis is considered to be a complex inflammatory disease
found between patients with good glycemic control and nondiabetic influenced by local, systemic, and immunologic factors (discussed
patients.100 With diabetes mellitus, advanced glycation end products earlier). Each factor is in turn directly related to individual genetic
(AGEs) may arise, which lead to the release of free oxygen and conditions. Several genetic disorders are known to show periodontal
proinflammatory mediators (cytokines). AGEs may also promote destruction as one of their major symptoms. For example,
 CHAPTER 27  Chronic Periodontitis 351

Papillon–Lefèvre syndrome is a well-known genetic disorder (a defect also with cardiovascular disease, which underlines potential systemic
on chromosome 11) that exhibits not only palmoplantar hyperkeratosis interactions.12,85–87 The role of ANRIL during the development of
but also severe periodontitis.23,37,51 Besides Papillon–Lefèvre syndrome, periodontitis is subject to ongoing investigations. It is known that
Haim–Munk syndrome, Ehlers–Danlos syndrome, Down syndrome, it represents a noncoding regulatory RNA, which is involved during
Kindler syndrome, Cohen syndrome, and congenital neutropenia the regulation of cell division and in affecting other genes that play
(Kostmann syndrome) are other genetic disorders that have been a role in the glucose and lipid metabolism (ADIPOR1, VAMP3,
related to periodontal disease. These genetic conditions are discussed C11ORF10).6,16,103 In addition to ANRIL, genetic variances (SNPs)
extensively in Chapter 11. in the sequences of the glucosyltransferase-6 domain containing 1
Periodontal disease has been found in different family members gene (GLT6D1), the plasminogen gene (PLA), and the neuropeptide
(twins, siblings) and generations of one family. Early twin studies Y gene (NPY) have been associated with periodontal disease.25,84,88
suggested the involvement of genetic susceptibility factors in the Due to the current technical and scientific progress, it may be expected
etiopathogenesis of periodontitis.63 In a number of studies, the that more genes will be identified to be associated with periodontitis
prevalence of aggressive and chronic periodontitis has been inves- in the future.
tigated in families with a history of one or more family members
with periodontitis. The data from those studies showed variable results Environmental and Behavioral Factors
with a likelihood for heritability of up to 50%. Variations are mainly In addition to microbial, immunologic, and genetic factors, the
due to different study designs as well as the number of evaluated development and progression of chronic periodontitis is further
individuals.3,60,64,83 influenced by environmental and behavioral factors such as smoking
and psychological stress68,70 Smoking is a major risk factor for the
development and progression of generalized chronic periodontitis.4
Treatment of Chronic Periodontitis Periodontitis is influenced by smoking in a dose-dependent manner.
Chronic periodontitis can be treated effectively by a systematic peri- The intake of more than 10 cigarettes per day tremendously increases
odontal therapy that includes optimal long-term plaque control, the risk of disease progression when compared to nonsmokers and
debridement of soft and hard deposits, or surgical pocket reduction former smokers, respectively.97
(case-dependently either resective osseous surgery or regenerative Compared to nonsmokers, the following features are found in
surgery; Figs. 27.4 and 27.5). Depending on the individual periodontal smokers5,43,72,80:
risk, each patient should be remotivated, reinstructed, and retreated • Increased periodontal pocket depth with more than 3 mm
(if necessary) during a systematic supportive periodontal therapy regimen • Increased attachment loss
(revisits every 3, 6, or 12 months; Fig. 27.6). • More recessions
• Increased loss of alveolar bone
• Increased tooth loss
In addition, other genetic variations (single nucleotide polymor- • Fewer signs of gingivitis (less bleeding upon probing)
phisms [SNPs], genetic copy number variations) that have so far • A greater incidence of furcation involvement
not been identified as responsible for certain syndromes may also Due to the consumption of tobacco, reactive oxygen (radicals) is
directly influence innate and adaptive immune responses as well as released that chemically irritates periodontal tissues by DNA damage,
the structure of periodontal tissues. The identification of genes that lipid peroxidation of cell membranes, damage of endothelial cells,
are relevant to the development of periodontitis has led to new and the induction of smooth muscle cell growth.65
scientific concepts and findings. There are at least two different Psychological factors, such as stress and depression, also negatively
strategies (candidate genes and genome-wide associations) to identify influence the progression of chronic periodontitis.30 Patients with
genetic variances in relation to disease. In candidate gene studies, periodontitis often report the experience of family- or work-related
certain already known variances (SNPs) are correlated to a specific stress.71 Positive correlations between cortisol levels and periodontal
phenotype such as periodontitis. Therefore a hypothesis is required indices (plaque index, gingival index), bone loss, and missing teeth
in order to choose specific SNPs in relevant genes. The data from were recorded.17,30,77 In addition, stress as an etiologic factor was
those studies showed variable results, making it challenging to draw even strongly associated with periodontitis when patients were smokers
clear conclusions. In this context, studies on SNPs in the IL-1 gene compared to nonsmokers.10
led to the early conclusion that alterations in sequences of immunologi-
cally relevant genes may explain the heritability of periodontitis.49
Stress and Periodontal Disease: Potential Mechanisms
Conflicting data in the literature, however, indicate inconclusive
1. Immunosuppression via cortisol secretion
knowledge regarding SNPs in the IL-1 gene and their potential role
2. Poor oral hygiene compliance in patients with chronic stress
in the heritability and etiopathogenesis of periodontitis.53 Also, it
3. Patients with stress are less likely to seek professional care
seems implausible that a single polymorphism in a specific gene
4. Patients with stress may smoke more frequently
sequence can cause a complex inflammatory disease, such as peri-
odontitis, without causing any other symptoms relevant to one’s
systemic health. Thus genome-wide association studies (GWASs) Case Scenarios are found on the companion website
have become more relevant. Here, a high number of DNA-sequence www.expertconsult.com.
variances are evaluated at the same time. In contrast to candidate
gene studies, no hypotheses are required for GWASs, so that there
is no potential bias during analysis. In several GWASs, a number References
of new genes have been identified to be associated with periodontitis.
One of the best replicated genes is called ANRIL (antisense RNA in References for this chapter are found on the companion
website www.expertconsult.com.
the Inc locus). ANRIL is associated not only with periodontitis but
 CHAPTER 27  Chronic Periodontitis 351.e1

CASE SCENARIO 27.1 

Patient:  46-year-old female
Chief Complaint:  “My lower incisors are becoming loose.”
Background Information
This patient is a smoker (20 cigarettes per day, 30 pack-years) with
controlled hypertension. She did not report any other systemic
conditions. The patient is currently taking lisinopril for hypertension
management and receives annual medical examinations. She reports
brushing once a day but not using interdental cleaning aids. For 2 years,
she recognized tooth loosening in the lower incisor region.
Current Findings:  Probing depths were in the range of 5 to 8 mm,
bleeding on probing was 65%, poor oral hygiene.

CASE-BASED QUESTIONS SOLUTION AND EXPLANATION

1. Which type of nonsurgical periodontal therapy is most effective in Answer: D
reducing periodontal probing depths and gaining clinical attachment Explanation: According to a current systematic review of the Cochrane
level in patients with chronic periodontitis? Collaboration, no one periodontal nonsurgical treatment modality is
A. Quadrant-wise scaling and root planing superior to others with regard to its efficacy in reducing probing pocket
B. Full-mouth scaling depth, clinical attachment gain, and reduction of bleeding on probing.44
C. Full-mouth disinfection
D. All of the above
2. Does the adjunctive administration of systemic antibiotics provide Answer: B
added benefit for reducing periodontal probing depth in smokers with Explanation: A current systematic review and meta-analysis showed no
generalized chronic periodontitis, in addition to nonsurgical benefit for smokers after systemic adjunctive antibiotic therapy. Instead,
periodontal therapy? a majority of studies noted that smokers benefited from locally
A. Yes administered antibiotics.73
B. No
3. Smoking is a well-known risk factor for chronic periodontitis. Does Answer: B
the risk for chronic periodontitis change in patients who quit smoking Explanation: The risk for periodontal disease after smoking cessation
compared to patients who continue to smoke? lowers continuously. In the first few years after smoking cessation, the
A. The risk for future periodontal disease immediately following risk ranges between the risk for smokers and that for never-smokers.9
smoking cessation is comparable to never-smokers. Three years following smoking cessation, the risk for periodontal
B. The risk lowers continuously, and 11 years after smoking disease is three times higher in former smokers when compared to the
cessation the risk is comparable to a never-smoker. risk of never-smokers. After eleven years, the risk for periodontal
C. The risk for periodontal disease does not change after smoking disease is similar between former smokers and never-smokers.32
cessation.

REFERENCES 3. Haffajee AD, Socransky SS: Relationship of cigarette smoking to attachment

1. Eberhard J, et al: Full-mouth treatment modalities (within 24 hours) for chronic level profiles, J Clin Periodontol 28:283–295, 2001.
periodontitis in adults, Cochrane Database Syst Rev CD004622, 2015. 4. Tomar SL, Asma S: Smoking-attributable periodontitis in the United States:
2. Chambrone L, et al: Efficacy of local and systemic antimicrobials in the findings from NHANES III. National Health and Nutrition Examination Survey,
non-surgical treatment of smokers with chronic periodontitis: a systematic J Periodontol 743–751, 2000.
review, J Periodontol 87:1320–1332, 2016.

Clinical image courtesy Prof. Dommisch, Charité–Universitätsmedizin, Berlin, Germany.

351.e2 Part 2  Biologic Basis of Periodontology

CASE SCENARIO 27.2 

Patient:  48-year-old male
Chief Complaint:  “My gum is bleeding so much.”
Background Information
This patient is a nonsmoker suffering from type 2 diabetes mellitus. His
hemoglobin A1c parameter has ranged from 8.5% to 9.3% within the
past 10 years. He takes 500 mg metformin three times a day.
Furthermore, he reports a high normal blood pressure and is not taking
antihypertensive medications. The patient reports brushing his teeth
twice a day and not using interdental cleaning aids.
Current Findings:  Probing depths were in the range of 4 to 7 mm,
bleeding on probing was 72%, poor oral hygiene.

CASE-BASED QUESTIONS SOLUTION AND EXPLANATION

1. What percentage change of glycated hemoglobin (HbA1c as a Answer: A
percentage) can be expected 3 months after nonsurgical periodontal Explanation: A current systematic review and meta-analysis detected an
therapy in patients with diabetes mellitus and chronic periodontitis? improvement of 0.48% (95% confidence interval: 0.18%–0.78%)
A. Approximately 0.5% regarding the glycated hemoglobin (HbA1c) 3 months after nonsurgical
B. Approximately 1% periodontal therapy in patients with diabetes mellitus. Systemic
C. More than 1% adjunctive antibiotics did not result in additional improvements in
hemoglobin A1c reduction.44
2. Does locally administered antibiotics in combination with nonsurgical Answer: B
periodontal therapy lead to improvements of periodontal pocket Explanation: Current data indicate an improvement of clinical
depths in patients with chronic periodontitis and diabetes? periodontal parameters (pocket probing depths and clinical attachment
A. Yes, independent of the glycemic control, there will be an level), especially in patients with well-controlled diabetes.73
improvement in periodontal probing depths.
B. Yes, especially well-controlled diabetic patients benefit from
locally administered antibiotics.
C. No, periodontal parameters will not improve after usage of locally
administered antibiotics in diabetic patients.
3. Do diabetic patients with chronic periodontitis benefit from Answer: A
adjunctive systemic antibiotics? Explanation: Adjunctive use of systemic antibiotics in diabetic patients
A. Yes provides a small but measurable additional benefit in terms of
B. No reductions in mean periodontal pocket depths and mean percentage of
bleeding on probing.9

REFERENCES 3. Santos CM, et al: Systemic antibiotics in periodontal treatment of diabetic

1. Teshone A, Yitayaeh A: The effect of periodontal therapy on glycemic control patients: a systematic review, PLoS ONE 10:e0145262, 2015.
and fasting plasma glucose level in type 2 diabetic patients: systematic review
and meta-analysis, BMC Oral Health 17:31, 2016.
2. Rovai ES, et al: Efficacy of local antimicrobials in the non-surgical treatment
of patients with periodontitis and diabetes: a systematic review, J Periodontol
87:1406–1417, 2016.

Clinical image courtesy Dr. Hoedke, Charité–Universitätsmedizin, Berlin, Germany.

 CHAPTER 27  Chronic Periodontitis 351.e3

23. Fischer J, Blanchet-Bardon C, Prud’homme JF, et al: Mapping of

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