etiology, pathogenesis of periodontitis · lysozyme, 50 enzymes, complements of saliva phagocytes...
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Etiology, pathogenesis of periodontitis
doc. Popovich I.Yu.
Ukrainian Medical Stomatological Academy
Chair of Therapeutic Dentistry
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Plan:
1. Health and its components.
2. Starting mechanism of development of
periodontal disease
3. Local factors
4. Mechanism of periodontal pocket formation.
5. Mechanism of host response
6. General factors
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Health
is the state of the full physical, psychical and social well-being,
not only the absence of diseases and physical defects
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Risk factors
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Risk factors
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Risk factors
Local General
Reactivity Resistance
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Reactivity is the ability of an organism to react
adequately on the changed conditions of intra and
extra mediums.
Resistance is the quantitative concept describing the
degree of stability of the organism to the certain
pathogenic factor.
Reactivity Resistance
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Classification of reactivity forms of the
organism
РЕАКТИВНОСТЬ
Race
Sex Constitution
PersonalityAge
Reactivity
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2 31
Plaque
composition
Bite
pathologyTraumas
Local factors
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ORAL BIOFILMS it is special complex ecosystems commensal microbes. They
reside on the surfaces of the mucosal epithelia that line the oral cavity,
respiratory tract, esophagus, gastrointestinal tract, and urinary tract.
The adult human body consists
of 1013 somatic cells, and 1014
normal or commensal microbes.
The oral cavity contains almost
half the commensal bacteria in
the human body; approximately
6 billion microbes representing
from 300 to 500 species reside in
the oral cavity.
Plaque
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I phase : Transport to the surface => is the formation of
the biofilm on the surface of enamel of the tooth
I phase
Phases of the formation of the dental biofilm
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I phase. During from a few minutes to an hour, an absolutely clean
tooth is covered by a 0.1—0.8 um thick pellicle composed of salivary
glycoproteins
Phases of the formation of the dental biofilm
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II phase
II phase: Initial adhesion =>This stage results in an initial,
reversible adhesion of the bacterium, initiated by theinteraction between the bacterium and the surface.
Phases of the formation of the dental biofilm
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During from five to seven days if there is no hygienia of the oral cavity the
signs of the inflammation appear
Phases of the formation of the dental biofilm
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Phases of the formation of the dental biofilm
III phase: Attachment => – appearance and formation of thick biofilm (to 30 days) - structure-complicatedpolymicrobic, the most aggressive formation with the thickness to 200 mkm
III phase
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The plaque can become mineralized to calculus
Phases of the formation of the dental biofilm
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plaque Calcculus
Producing of toxins by bacterias
Disorder of vessels
Producing of proteolytic enzymes
Development of the microbial sensibility
Mechanical injuries
Chemical irritations
Pathological processes in periodontalInflammation
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The intensity of gingivitis and periodontitis is determined by the quantity and quality of
the microorganisms. When plaque accumulation is great and gram-negative anaerobes
increase, gingivitis develops
Plaque
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Gram-
positive
aerobes
decrease
Plaque
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Periodontal pathogenic bacteria
With expressed association
with periodontal diseases With moderate association
with
periodontal diseases
Actinobacillus
actinomycetemcomitans
Porfhyromonas gingivalis
Bacteroides forsythus
Treponema denticola
Prevotella intermedia
Campylobacter rectus
Peptostreptococcus micros
Eikenella corrodens
Fusobacterium spp.
Eubacterim spp.
Staphylococcus spp.
Pseudomonas spp.
Candida spp.
Can influence
in the rare cases
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Factors of pathegenity of microorgasms
The ability to adhesive to epithelium
Ability to invade into tissue (hyaluronidase, chondroitin sulfatase,
proteolitic enzymes)
Resistance to antibiotics due to production of β-lactamaze.
1
2
3
4
5
6
Resistance to the host response can evade the neutrophil-protective
response by killing neutrophils
Starting of factors of resorbtion of the bone
Production of endotoxins
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Factors of pathegenity of microorgasms
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mechanical injuries by tooth-brush,
instruments while treatment , acute edges
of carious cavities; wrong filling at the
proximal surfaces;
mistakes in prosthetic and orthodontic
treatment;
chemical injections (iatrogenic factor),
etc.;
habits;
disorders in nasal breathing
Local mechanical factors
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Overhanging margins of restorations accumulate additional plaque. The
composition of the plaque changes.
Gross iatrogenic irritants such as poorly designed clasps and prosthesis saddles
may exert a direct traumatic influence on periodontal tissues.
.
Local mechanical factors
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Mechanical injuries of periodontGetting stuck of food
Changing of hydrostatic pressure in vessels of periodont
Appearance of swelling near the vessels
Agrigation of trombocells
Formation of dental plaque
Increasing activity of pathogenic flora
Pathological processes in periodontal Inflammation
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Crowding, teeth dislocation Vestibular localization 12
Palatal localization 13, 12, 11
Anomalies of teeth, bite pathology
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Low fixation of upper labial frenulumNormal fixation of lower
and upper labial frenulums
Small depth of vestibulum Short lingual frenulum
Level of labial and lingual frenulums fixing
Anomalies fixation soft tissue, bite pathology
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Anomalies of teeth localization, crowding, bite pathology Anomalies fixation soft tissue
Small depth of vestibule
Disorder of trofic of periodontal tissues
Increasing activity of pathogenic microflora
Pathological processes in periodontal
Inflammation
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Protictive mechanisms of an oral cavity
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Proliferation AlterationExudation
Inflammation proses
Hypertrophic Catarrhal Ulcerous
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Hypertrophic gingivitis
Inflammation proses
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Pathological processes of periodont
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Pathological processes of periodontal
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Protictive mechanisms of an oral cavity
Nonspecific protective factors Specific protective factors
Mechanical ChemicalPhysiological
1. Barrier function of the epithelium of an
oral cavity
2. Self-cleaning
3. Adgesiving on the cells of scrubbing
epithelium
Lysozyme, 50 enzymes,
complements of saliva
Phagocytes in an oral cavity
Immunoglobulins
Intrinsic
Extrinsic
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Cell type
Protective mechanisms of an oral cavity
chemotaxis- adherence
phagocytosis — phagolysosome formation degradation
microbicidal processes (cytotoxicity)
phagocytosis, pinocytosis
microbicidal processes (cytotoxicity)
antigen processing and presentation
regulation of lymphocyte function
cell mediated immunity
helper T-cells: interaction with B-cells, leading to antibody
production
suppressor T-cells: inhibit B-cell response
killer T-cells
humoral immunity, immunoglobulin synthesis
B-lymphocyte: immunoglobulin, antigen-specific, variable Ig
classes
plasma cell: immunoglobulin, antigen- and class-specific
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Cellular immunity: T-lymphocytes elicit a delayed hypersensitivity reaction by production of various
lymphotoxins and lymphokines that influence the activation and migration of macrophages and the
proliferation of lymphocytes
3. Humoral immunity: Under the influence of antigens, B-lymphocytes proliferate and differentiate into
plasma cells. Activated B-cells produce immunoglobulins (antibodies). These three basic protective immune
mechanisms may be modulated by additional leukocytes (eosinophils, basophils, mast cells), by the
complement system, and by the kinins to provide an enhanced defensive response to particular antigenic or
other challenge to the host. The natural, nonspecific immunity activates specific immunity.
Specific immunity
specific
(acquired)
immunity
Nonspecific immunity
Protctive mechanisms of an oral cavity
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Neutrophils migrate to the area of periodontal infection and induction of
antibodies, both of which appear to be protective. Proteases are activated by
cytokins.
Extracellular matrix components of the ginagiva and periodontal ligament are
destroyed and alveolar bone is resorbed .This leads to connective tissue
destruction.
Protctive mechanisms of an oral cavity
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Production of proinflammatory cytokines, such as IL-1, resulting in alveolar bone
resorption. These cytokines can cause activation of fibroblasts, which then
produce major metalloproteinases that destroy the extracellular matrix. In
addition, proinflammatory cytokines such as IL-1, IL-6, and TNF-a lead to
activation of osteoclasts, which leads to bone resorption.
Protctive mechanisms of an oral cavity
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Protctive mechanisms of an oral cavity
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Protictive mechanisms of an oral cavity
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Mechanism of periodontal pocket formation
Gram-negative anaerobic motile bacteria quickly become predominant. A direct invasion
(infection) of the tissues by microorganisms occurs. The tissue responds with a massive acute
defense reaction,. Periodontal tissue is lost. The acute infection sets in motion the
mechanisms that lead to bone destruction. Products of both hummoral and cellular immunity
and bacterial products can cause bone loss.
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The immune response causes resorbton of bone, deeping of the periodontal
pocket and accumulation of dental plaque, resulting in a repeat of the cycle
and recurrence of periodontitis.
Mechanism of periodontal pocket formation
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nflammatory-dystrophic periodontal diseases
Mechanism of periodontal pocket formation
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Mechanism of periodontal pocket formation
Microorganisms
and their toxins
Decreasing of local
protection factors
in oral cavity
Decreasing of general
protection factors
of organism
Increasing of pathogenic properties of microorganisms
Infiltrtate formation (lymphocytes, macrophages,
plasmocytes, polymorphnucleatic leucocytes)
in connective stroma under epithelium connection
Cytokines: IL – 1, IL – 2, IL – 8, prostoglandines
Decreasing of function
fibroblasts, periodontal l
ligament destruction
Periodontal
pocket formation
Fromation of ulcerous
defect in connected
epithelium, changing it
to granulation tissues
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General factors influence of the
organism
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General factors influence of the
organism
1. Stress factors
2. Genetic factors
3. Diseases of internal organs
4. Intoxication
5. Dietary factors
6. Atherosclerosis of periodontal microvessels
7. Disorder of nerve-endocrine regulation homeostasis
8. Changing of the immunity system
9. Style of life
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Factors of human health
Style of life
50 %
Heredity
20 %
System of
health care
10 %
Environment
20 %
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Genetic links are noticed between the intenivity and spreading of
the periodontitis in females
Periodontos is the most influenced by genetic factors when the
periodontitis is less
At the age of 12-17 genetic factors influence on the periodontal
inflammatory diseases
Genetic factors
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Stress factors
Stress goes through the hypothalamic-pituitary-adrenal axis to promote
the release of corticotropic releasing hormone from hypothalamus and
glucocorticoids from adrenal cortex. Influence of acute and chronic stress
leads to the activation of peroxide-oxidation of lipids, disorders in
hemocirculation , increasing of anti-aggregation activity of soft tissues,
delaying of collagen synthesis, increasing alveolar bone resorption
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PeriodontInfection
diseases
Endocrine
disorders
Digestive diseases
Cardiovascular
dissesesBlood diseases
Allergic diseases
Hypo-vitaminosis
Pregnant’s
toxicity
Diseases of internal organs
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50 somatic diseases damage of periodontal are known. Among them there are
a lot of with 100% guaranty
Changing of functions of internal
organs causes disorders of functions
of the oral cavity
Inflammatory-dystrophical process
in periodontal tissue is the source
of chronic intoxication of the
organism
Diseases of internal organs
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Role of organic and functional disorders of
endocrine system
94% of patients with diabeteshave the periodontitis
with acute inflammation
Patients with thyreoid and parathyreoid gland disorders
complain on generalized periodontitis
Females with disorders of ovary have the patholgy of
periodont
At period of menstrual pause osteoporosis can be
observed, especially at alveolar bone
Endocrine glands function plays the main role on periodontal diseases
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Dietary factors
Vitamin C
The earliest signs of avitaminosis:
gingival bleedings,
teeth mobility
Vitamin B2 provides trophic of oral mucosa
Vitamin A enforces oral mucosa barrier function.
Vitamin D stimulate Ca –P exchange
Ca is a building material of the bone
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Dietary factors
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Smoking
• Decreasing of plague and calculus
• Increasing of pathogenic properties of
bacteria
• Decreasing of local protective factors of
the periodontal tissue
• Disorders of microcirculation in
periodontal tissues
• Change of the viscosity and composite of
saliva
• Hipocsia of the periodontal tissue
Smoking has a general and local influent
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Vascular theory A.I.Evdokimov was
described already 50 years ago. Main role at
this theory is to the organic (morphological)
changes of periodontal vessels walls.
Hyalinosis and atherosclerosis of periodontal
micro vessels walls leads to narrowing of
the small vessels as a result dystrophic
changes appear in periodontal tissues
Complex organic changes follow after
functional nonorganic changes . All of them lead to the dystrophic changes in periodont
Role of organic and functional disorders of
cardiovascular system
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Role immunological mechanisms
IgG and IgM bind antigen, forming antigen-
antibody (immune) complexes.
These activate complement, which results in
PMN chemotaxis and activation.
PMNs then release tissue damaging enzymes.
Tissue damage present in autoimmune diseases
and chronic infectious diseases can be
attributeds, in part, to immune complex
reactions.
Vascular pathology in the periodont (АR ІІІ type)
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Role immunological mechanisms
Vascular pathology in the periodont (АR ІІІ type)
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Role immunological mechanisms
Vascular pathology in the periodont (АR ІІІ type)
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General factors influence of the
organism
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Pathological processes of periodontal
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Role immunological mechanisms
Vascular pathology in the periodont (АR ІІІ type)
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Pathogens of generalized inflammatory-dystrophic injueries
of periodontal tissues
Includesimmunity system
activation of peroxide-oxidation of lipids,
changing of metabolism of tissue
changing of microcirculation
lack of homeostatic system
disorder of nerve-endocrine regulation
changing of psycho-somatic balance
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Primary inflammatory variant
Primary dystrophic variant with the secondary
development of the inflammation
Simultaneous development of the inflammatory and
dystrophic changes
Variants of the development of the generalized periodontitis
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If GP combined with arterial hypertonic we have
primary dystrophic process in the periodont
(Н.А.Колесова, А.М.Политун, Н.В.Колесова, 2008)
Development of generalized periodontitis
if a person has somatic pathology
If GP combined with chronic diseases digestive system we
have primary inflammatory process in the periodont
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Be happy!
Be healthy
Thank you for attention!
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Decreasing of the resistance
of the organismChanging of reactivity
Decreasing of the resistance
of the periodontal tissues
т
Loosing by periodontal
tissues of their protectionIncreasing activity of
microorganisms
Pathalogical
process
in periodont
Iliness factors
Starting mechanism of development of periodontal disease
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Factors of pathegenity of microorgasms