Carranza 2015

1. Chronic Periodontitis

2. Introduction
 the major clinical and etiologic characteristics
 (1) microbial biofilm formation (dental plaque);
 (2) periodontal inflammation (e.g., gingival swelling, bleeding on probing);
 (3) attachment as well as alveolar bone loss.
 Chronic periodontitis is the most prevalent form of periodontitis

3. Clinical Features
 Supragingival and subgingival plaque and calculus
 Gingival swelling, redness, and loss of gingival stippling
 Altered gingival margins (e.g., rolled, flattened, cratered papillae, recessions)
 Pocket formation
 Bleeding on probing
 Attachment loss (angular or horizontally)
 Bone loss
 Root furcation involvement (exposure)
 Increased tooth mobility
 Change in tooth position
 Tooth loss

4.  The condition is diagnosed via the assessment of the clinical attachment level
and the detection of inflammatory changes in the marginal gingiva.
 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.
 Dental radiographs display the extent of bone loss, which is indicated by the
distance between the cementoenamel junction and the alveolar bone crest.

5.  The distinction between aggressive and chronic periodontitis is sometimes
difficult, because the clinical features may be similar at the time of the first
examination.
 At later time points during treatment, aggressive and chronic periodontitis
may be differentiated by
 the rate of disease progression over time,
 the familial nature of aggressive disease,
 the disease’s resistance to periodontal anti-infective therapy,
 the presence of local factors.

6.  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).
 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

7.  the local inflammatory response may lead to different patterns of bone loss,
including vertical (angular) and horizontal bone destruction.
 vertical bone loss is associated with intrabony pocket formation.
 horizontal bone loss is usually associated with suprabony (supra-alveolar)
pockets.

8.  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.

9.  • Mild chronic periodontitis: when no more than 1 mm to 2 mm of clinical
attachment loss has occurred
 • Moderate chronic periodontitis: when 3 mm to 4 mm of clinical
attachment loss has occurred
 • Severe periodontitis: when 5 mm or more of clinical attachment loss has
occurred

10. 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.
 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).

11.  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 progression, 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 patient’s discomfort.
 Gingival tenderness or “itchiness” may also be found.

12. 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 first signs may be detected during adolescence
 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.

13.  Chronic periodontitis does not progress at an equal rate in all affected sites
throughout the mouth.
 More rapidly progressive lesions occur most frequently in interproximal areas
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

14.  progression is measured by determining the amount of attachment loss during a given period.
 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 periodontal 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 progression suggests that periodontal
destruction occurs around affected teeth during defined periods of life and that these bursts
of activity are interspersed with periods of inactivity or remission. The chronology of these
bursts of disease is asynchronous for individual teeth or groups of teeth.

15.  Chronic periodontitis generally affects both genders equally.
 Periodontitis is an age-associated (not an age-related) disease.
 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 destruction.
 Up to 30% of patients develop severe periodontitis by the time they are 40 years
old or older.
 50% of the human population experiences at least one form of periodontal disease

17. Risk Factors for Disease

18. Microbiological Aspects
 Plaque accumulation on tooth and gingival surfaces at the dentogingival junction is
considered the primary initiating agent in the etiology of gingivitis and chronic
periodontitis.
 Attachment and bone loss are associated with an increase in the proportion of
gram-negative organisms in the subgingival biofilm, with specific increases in
organisms that are known to be exceptionally pathogenic and virulent.
 Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola—
otherwise known as the “red complex”—are 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

19.  Periodontal pathogens may invade the periodontal tissue and thus induce an
immune response with increasing concentrations of proinflammatory
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

20. Local Factors
 Plaque-retentive factors are important for the development and progression of
chronic periodontitis, because of 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.
 tooth morphology: Roots grooves or concavities, enamel projections
 subgingival and overhanging margins of restorations,
 carious lesions that extend subgingivally,
 Exposed furcations

21. Systemic Factors
 Periodontitis is also associated with other systemic disorders, such as Haim– Munk
syndrome, Papillon–Lefèvre syndrome, Ehlers–Danlos syndrome, Kindlers syndrome,
and Cohen syndrome
 Patients with diseases that impair the host immune response may also show
periodontal destruction
 It is also known that osteoporosis, 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.

22.  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.
 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)

23.  Patients with poor glycemic control tend to experience a more severe
progression of periodontitis as compared with patients with good glycemic
control.
 With regard to the progression of severe periodontitis, no difference was
found between patients with good glycemic control and non-diabetic patients

24.  With diabetes mellitus, advanced glycation end products may arise and lead
to
 the release of free oxygen and pro-inflammatory mediators (i.e., cytokines).
 chemotaxis and the adhesion of inflammatory cells to periodontal tissues,
 and the increased apoptosis of fibroblasts and osteoblasts may occur

25.  Patients with diabetes mellitus tend to show a higher body mass index;
therefore, increased concentrations of adipokines that directly influence
inflammatory responses will likely be found.
 Hyperglycemia itself leads to the release of pro-inflammatory mediators in
the bloodstream, which in turn promote increased glycose concentration.
 It has been shown that systematic periodontal therapy leads a 0.4% reduction
of glycated hemoglobin.

26. Immunologic Factors
 Patients may show alterations in their peripheral monocytes, which are
related to the reduced reactivity of lymphocytes or an enhanced B-cell
response.
 B-cells, macrophages, periodontal ligament cells, gingival fibroblasts, and
epithelial cells synthesize pro-inflammatory mediators (e.g., interleukin-1β,
interleukin-6, interleukin-8, prostaglandin E2, tumor necrosis factor-α) that
modify innate and adaptive immune responses at periodontal sites

27.  Pro-inflammatory mediators regulate the synthesis and secretion of, for example,
matrix metalloproteinases and receptor activator of nuclear factor-κβ ligand
(RANKL).
 In periodontal lesions, matrix metalloproteinases contribute to soft and hard-
tissue degradation during active inflammatory reactions.
 RANKL binds to its receptor activator of nuclear factor-κβ on the cell surface of
premature osteoclasts, thereby initiating osteoclast differentiation that leads to
the degradation of alveolar bone.
 Physiologically, osteoprotegerin is the opponent of RANKL; during periodontitis, an
imbalance between osteoprotegerin and RANKL promotes further bone
degradation.

28.  Congenital neutropenia (Kostman syndrome) 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 (α-
defensins), which impair the innate immune response.

29.  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–Lefèvre syndrome; Haim–
Munk syndrome).

30. Genetics
 The data from those studies have demonstrated variable results, with a
likelihood of heritability of up to 50% for AP and CP.
 SNPs
 Interleukin-1: controversial
 CDKN2BAS: Association between periodontitis and coronary heart disease.
 DEFB1:(untranslated region) aggressive and chronic periodontitis.
 GLT6D1: aggressive periodontitis.
 COX-2: aggressive periodontitis
 In vitro studies have shown that the periodontal pathogen Porphyromonas
gingivalis induced the gene expression of ANRIL in human gingival fibroblasts.

31.  Smoking is a major risk factor for the development and progression of
generalized chronic periodontitis.
 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
 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

32.  Smoking causes:
 Increased periodontal pocket depth of more than 3 mm
 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

33.  Positive correlations between cortisol levels and periodontal indices (e.g.,
plaque index, gingival index), bone loss, and missing teeth have been
recorded.
 In addition, stress as an etiologic factor was even more strongly associated
with periodontitis when patients were smokers as compared with non-smokers

34. Thanks for attention