Etiology, pathogenesis of periodontitis · Lysozyme, 50 enzymes, complements of saliva Phagocytes...

Etiology, pathogenesis of periodontitis

doc. Popovich I.Yu.

Ukrainian Medical Stomatological Academy

Chair of Therapeutic Dentistry

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

Health

is the state of the full physical, psychical and social well-being,

not only the absence of diseases and physical defects

Risk factors

Risk factors

Local General

Reactivity Resistance

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

Classification of reactivity forms of the

organism

РЕАКТИВНОСТЬ

Race

Sex Constitution

PersonalityAge

Reactivity

2 31

Plaque

composition

Bite

pathologyTraumas

Local factors

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

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

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


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.


During from five to seven days if there is no hygienia of the oral cavity the

signs of the inflammation appear



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

The plaque can become mineralized to calculus


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

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

Gram-

positive

aerobes

decrease

Plaque

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

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

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

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

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

Crowding, teeth dislocation Vestibular localization 12

Palatal localization 13, 12, 11

Anomalies of teeth, bite pathology

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

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

Protictive mechanisms of an oral cavity

Proliferation AlterationExudation

Inflammation proses

Hypertrophic Catarrhal Ulcerous

Hypertrophic gingivitis

Inflammation proses

Pathological processes of periodont

Pathological processes of periodontal


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

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

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

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.


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.


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.

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.


nflammatory-dystrophic periodontal diseases



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

General factors influence of the

organism


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

Factors of human health

Style of life

50 %

Heredity

20 %

System of

health care

10 %

Environment

20 %

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

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

PeriodontInfection

diseases

Endocrine

disorders

Digestive diseases

Cardiovascular

dissesesBlood diseases

Allergic diseases

Hypo-vitaminosis

Pregnant’s

toxicity

Diseases of internal organs

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

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

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

Dietary factors

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

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

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)


organism

Pathological processes of periodontal

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

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

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

Be happy!

Be healthy

Thank you for attention!

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

Etiology, pathogenesis of periodontitis · Lysozyme, 50 enzymes, complements of saliva Phagocytes...

Documents

Transcript of Etiology, pathogenesis of periodontitis · Lysozyme, 50 enzymes, complements of saliva Phagocytes...