‫ملحوظه ‪:‬‬
‫اللون االحمر يرمز لعنوان السؤال ‪.‬‬
‫اللون االخضر يرمز لجزء فرعى فى السؤال ‪.‬‬
‫اللون البنى يرمز لسؤال اجابته بالحب ‪.‬‬
‫اللون االزرق ألسئله المحاضرة االخيرة او المحاضرة الخامسه ولسا‬
‫مكتبتهمش ‪.‬‬
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Periodontology
* Functions of the periodontium:
1- To attach the tooth to the bone.
2- To compensate for the forces exerted by eating, mastication, speaking,
brushing..
3- To protect the body against the noxious substances which present in the oral
cavity.
4- To assist in maintaining the oral environment by continuous remodeling and
regeneration.
5- To assist in maintaining the integrity of the surface of the masticatory mucosa.
* Marginal gingiva : features in health
Width === 1 mm.
Apico-coronal and mesio-distal dimensions === 0.06 - 0.96 mm
Color ==== Coral pink.
Surface ==== Slightly dull.
Consistency ==== Firm.
Shape (Form) ==== Knife edged and closely adapted to the tooth surface
Contour ==== Scalloped.
Surface texture ==== Smooth.
* Interdental groove
Definition : A vertical groove parallel to the long axis of the teeth found in the
interdental area of attached gingiva.
Benefit of interdental sluice way groove : Help in sluice way extrusion of the food.
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* Attached gingiva : location ,features in health ,stippling and width
Location : the part of the masticatory mucosa which extends between the free
gingival groove and mucogingival junction.
- features in health ;
Color === Pale pink.
Consistency ==== Firm and Resilient
Surface texture === Stippled.
-stippling and width;
definition : It refers to the irregular surface of the gingiva that resembles the
surface of an orange peel.
found on the attached gingiva and The center of interdental papillae.
Benefit of stippling : It is an adaptation for function.
-The width of the attached gingiva
- It is the distance between the free gingival grove and the mucogingival junction.
-Width of attached gingiva = It varies in width from one person to another and
from one area to another in the same mouth → The range is 0 - 9 mm.
* Interdental gingiva and Interdental col
- Interdental gingiva It is that part of the gingiva that is located in the
interproximal space created by 2 adjacent teeth just beneath the contact area.
- Shape in the anterior region === Pyramidal.
- Shape in the premolar-molar region === More flatter in a buccoligual direction.
- interdental or gingival col : non keratinized stratified squamous epithelium
joining the the buccal and lingual peaks of The interdental papillae by a saddlelike depression.
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- Benefit of the interdental col : It joined the buccal and lingual interdental
papillae together, so it makes the interdental papillae to fill the interproximal
space .
* Effect of tooth contour on the shape of the interdental gingiva :
1-Flat proximal surface and broad )wide ) contact area cause short and narrow interdental gingiva.
2- convex proximal surface and small contact area cause high and broad
interdental gingiva.
3-overlapping crowded teeth make the interproximal space small , resulting in
gingiva that bulge out of the confines of the interproximal space.
* Clinical features of the gingiva
- The color of the attached and marginal gingiva is generally described as "coral
pink".
- shape == Knife-edge marginal gingiva and it is closely adapted to the tooth
surface, and the inter dental papilla (gingiva) fills the interproximal space.
-Contour === scalloped.
- Consistency === Firm and Resilient.
-Surface texture === Stippled (Absent over marginal gingiva).
- Width == 1 mm for marginal gingiva & 0-9 mm for attached gingiva.
Size == The size of the gingiva represents the bulk of cellular and intercellular
elements and the vascular supply.
- In healthy gingiva, there is no alteration in the size. Alteration in the size is a
common feature of gingival disease.
Position :
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position of the gingiva : Aberrant It depends on the level of marginal in relation
to the tooth surface.
Actual position of the gingiva : It refers to the level of the junctional epithelium in
relation to the tooth.
*Alveolar mucosa
- It is loosely attached to the underlying bone.
- Surface texture : Smooth.
- Color : Red and shiny.
- It is covered by a layer of non keratinized stratified squamous epithelium, so it
can't resist the frictional contact as the attached gingiva.
* difference between Oral epithelium, Sulcular epithelium , Junctional
epithelium .
Oral epithelium
Sulcular epithelium
Junctional epithelium
Definition
It is that part of the
epithelium which faces
the oral cavity extending
from the mucogingival
junction into the crest of
the marginal gingiva.
Epithelium lining the
gingival sulcus .
It represents the
inner aspect of the
marginal gingiva.
The way of connection
between the tooth and
the gingival C.T.
Keratinization
keratinized stratified
squamous epithelium
with rete pegs.
Number of layers
composed of 4 layers
thin non keratinized
stratified squamous
epithelium without
rete pegs.
---------------------------
non keratinized
stratified squamous
epithelium without
rete pegs.
3 - 4 in early life and 10
- 20 later
Length
extending from the
mucogingival junction
into the crest of the
extends from the
0.25 - 1.35 mm.
coronal limit of the
junctional epithelium
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marginal gingiva.
to the crest of the
marginal gingiva.
*gingival sulcus ; definition and lining epithelium .
definition :The gingival margin forms with the tooth surface a shallow V-shaped
space called "Gingival sulcus or Gingival crevice ".
- Lining epithelium : It is a thin non keratinized stratified squamous epithelium
without rete pegs.
*gingival fibers groups and function :
-fibers of the gingiva
There are 3 types : Collagen - Reticular - Elastic.
- Gingival fibers :
1- Gingivodental group.
2- Circular group.
3- Transseptal group.
- Gingivodental group
Circular group
Transseptal group
Semicircular fibers
Transgingival fibers
Functions of the gingival fibers :
1- Brace the marginal gingiva firmly against the tooth, i.e. they provide the close
adaptation of the marginal gingiva to the tooth.
2- Unit the free marginal gingiva with the cementum of the root and the adjacent
attached gingiva.
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3- Provide the rigidity necessary to withstand the forces of mastication without
being deflected away from the tooth surface.
*periodontal ligament cell
1-. Connective tissue cells
a-Synthetic: Fibroblasts, Cementoblasts , Osteoblasts
b-Resorptive: Fibroblasts, Cementoclasts , Osteoclasts
2- Epithelial cell rests
3- Immune system cells
4- Neuro-vascular elements
* periodontal ligament fibers
1) The principal fibers
.a) Gingival fibers
.b) Transseptal or interdental ligament
c) Alveolodental ligament which is subdivided into the following five groups:
.Alveolar crest group, Horizontal group, Oblique group, Apical group
,Interradicular group
2) The accessory fibers
3) The oxytalan ( elastic ) fibers
*width of periodontal ligament and the effect of functional stress.
-Depending on age
11-16 yrs - 0.21mm
32-52 yrs - 0.18mm
51-67 yrs - 0.15mm
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-According to functional state of the tissues
Time of eruption - 0.1- 0.5mm
At function - 0.2-0.35mm
Hypo function - 0.1-0.15mm
*structure and function of the alveolar bone .
Structure:
-It is composed of two parts; the alveolar bone proper and the supporting bone.
-consists by weight of 25% mineralized tissue, 70% organic matrix (including cells
2–5%), and 15% water
Functions:
1-protection.
2-attachment.
3-support.
4-shock absorber.
* structure and function of cementum .
Structure:
1- 45-50 % Inorganic substances consists of calcium phosphate in the form of hydroxyapatite
crystals
2- 50-55% Organic substances :
A- Collagen fibers embedded in a ground substance .
B- protein
C- Polysaccharides
Functions of cementum :
1. Cementum furnishes a medium for the incorporation of the principal periodontal fibers,
thereby securing the binding of the tooth root to the alveolar bone proper .
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2. Cementum serves as a reparative tissue in case of root fracture or resorption .
3. Functional adaptation .
*defense mechanism of gingival epithelium .
1- Participating actively in responding to infection.
2- Signaling further host reactions.
3- Integrating the innate and acquired immune responses such as :
a- Respond to bacteria by increased proliferation.
b- Changing in the rate of cell differentiation and cell death.
c- Changing in the tissue homeostasis.
- The role of gingival epithelium in the defense mechanism of the gingiva is
achieved :by (mediated)
1- Its degree of keratinization.
2- Turn over rate.
* method of collection of GCF.
1- Absorbing paper strips ( Periopapers): Placed either intrasulcular or
extrasulcular.
2-Preweighted twisted threads .
3- Micropipettes.
4- Intracrevicular washings .
* composition and and clinical significance of GCF.
- GCF contains : Enzymes - Cellular elements - Electrolytes (Inorganic
components) - Organic components - Metabolic and bacterial products Cytokines and Immunoglobulins - Antigens - Proteins.
- clinical significance of GCF.
a- Detect or diagnose active disease.
b- Predict patients at risk for disease.
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* composition and role of saliva in oral health and periodontal
pathology .
- Saliva contains : Enzymes - Enzymes inhibitors - Antibacterial factors Glycoproteins - Mucin - Buffers - Coagulation factors - Leukocytes.
- role of saliva in oral health.
1- Lubrication and physical protection via glycoproteins and mucoids.
2- Mechanical cleansing action of debris and bacteria via its flow.
3- Buffering action to neutralize acids produced by bacteria.
4- Maintenance of tooth integrity via glycoprotein pellicle and minerals by
remineralization.
5- Antibacterial action via IgA, lysosome and lactoperoxidase by control of
bacterial colonization and breakdown bacterial cell walls.
6- It initiates plaque accumulation, maturation and metabolism.
7- Its flow has an influence on calculus and caries formation.
8- Decrease salivary flow cause gingival inflammation and caries.
*classification of periodontal and peri-implant diseases and condition 2017.
*mucogingival deformities and condition around teeth.
*case definition of gingivitis in an intact peridontium.
* case definition of gingivitis in a reduced peridontium without history of
periodontits.
*structure and composition of dental plaque .
microorganisms (bacterial and non bacterial components) present within
intercellular (intermicrobia) matrix.
1- Densely packed microbial structure.
2- Insoluble salivary glycoprotein (The main component of the matrix).
3- Microbial intracellular product.
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4- To some extent, epithelial cells and debris arranged in an organized complex
intercellular matrix.
*difference between dental plaque , material alba , pellicle and calculus.
-dental plaque : A structured, soft yellowish-gray substance which is firmly
adhered to the teeth surfaces and other intraoral hard surfaces as removable and
fixed restorations.
- material alba: Soft accumulation of bacteria and tissue cells that lack the
organized structure of dental plaque, i.e. has no intermicrobial matrix, and easily
displaced by water spray.
Materia alba has an irritating effect on the gingiva and leads to gingivitis due to
the bacteria and their products that present in material alba.
-pellicle : Acellular layer of salivary proteins and other macromolecules,
approximately 2-10 μm thick, adsorbed on to the enamel surface by electrostatic
and hydrophobic forces.
- calculus : Hard deposit formed by mineralization of dental plaque and covered
by a layer of unmineralized plaque.
*formation of the dental pellicle.
1- Initial attachment of bacteria to the solid surface.
2- Formation of microcolonies on the surface.
3- Formation of the mature subgingival plaque biofilm.
* initial adhesion and colonization of bacteria .
- It occurs within few hours where bacteria connect to the pellicle.
- The initial colonizers are gram +ve facultative cocci and rods as S. sanguis and A.
viscosus.
10 ‫ صفحه رقم‬10 ‫لتفاصيل اكتر المحاضرة‬
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*secondary colonization and mature plaque formation .
Secondary colonization and coaggregation
1- Gram -ve cocci as veillonella parvula.
2- Gram -ve rods and filaments as :
a) Porphyromonas gingivalis.
b) Prevotella intermedia.
c) Prevotella loeschii.
d) Caponcytophaga species.
e) Fusobacterium nucleatum.
f) Spirochetes (Treponema).
COaggregation: Ability of different species and genera of bacteria to adhere
together by certain surface molecules and cell-to-cell interaction.
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*differences between tooth associated plaque and tissue associated plaque .
- tooth associated plaque:
- It is characterized by gram +ve cocci, rods and filaments as : S. sangius, S. mitis,
A. viscosus, A. naeslundii.
- The apical border of the plaque mass is separated from the J.E by a layer of host
leukocytes and the bacteria in this part mostly gram -ve rods.
- tissue associated plaque :
- It contains gram -ve rods and cocci with large number of motile bacteria and
spirochetes.
- It extends to the J.E.
- The bacteria are more loosely organized and loosely adherent than the dense
tooth associated plaque.
-The most predominant bacteria are peptostreptococcus micros, F. nucleatum, P.
gingivalis.
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*physiologic properties of dental plaque.
1- The initial colonizers use oxygen and decrease the oxidation of the
environment which favors the growth of anaerobic species.
2- Gram +ve species use sugars as a source of energy and the saliva as a source of
carbon.
3- Bacteria in the mature plaque are anaerobic asaccharolytic bacteria used the
amino acids as a source of energy.
4- Streptococci and Actinomyces produce lactate which can be used for growth
and multiplication of the velionella species.
5- Actinomyces produce formate which can be used for growth and metabolism
of campylobacter species.
6- The growth of P. gingivalis is enhanced by succinate and succinic acid that are
the metabolic byproducts of C. ochracea & Campylobacter rectus.
7- The metabolism of P. gingivalis is enhanced by the iron (heme) produced from
the breakdown of host hemoglobin (RBCs), and also by menadione byproducts
produced from veilonella species.
8- P. intermedia also can utilize the iron.
9- The number of P. intermedia is increased by increase the level of steroid
hormone as in cases of hormonal disturbances as in pregnancy, puberty, and
using contraceptive pills.
*plaque hypothesis .
- There are 3 hypotheses :
1-The non specific plaque hypothesis .
2-The specific plaque hypothesis .
3- The plaque ecology hypothesis.
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*criteria for identification of periodontal pathogens.
1- Association between the disease and microorganisms : Microorganisms should
be present in large number in the disease site.
2- Elimination of these microorganisms should result in clinical improvement.
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3- Host response to pathogens by a humoral immune response by production of
antibodies or by a cellular immune response by mediators and cytokines directed
to the pathogen.
4- Virulence factors are produced by these pathogens.
5- Animal studies demonstrating tissue destruction.
*microorganism in periodontal health and different types of
periodontal diseases .
- periodontal health:
- Gram +ve and facultative anaerobic organisms such as : S. sanguis, S. mitis, A
viscosus, A. naeslundii.
- Few gram -ve bacteria such as : V. parvula, P. intermedia, F. nucleatum,
Capnocytophaga, few spirochetes and rods.
-in gingivitis :
- Gram +ve species such as : S. sanguis, S. mitis, A. viscosus, A. naeslundii, S.
intermedius, Peptostreptococcus micros.
- Gram -ve species such as : V. parvula, F. nucleatum, P. intermedia,
Capnocytophaga, Campylobacter species.
-in chronic periodontitis :
- ~ 75 % gram -ve (90 % strict anaerobes).
- P. gingivalis, A. actinomycetemcomitans, F. nucleatum, P. intermedia, Tannerella
forsythus , Treponema species, Campylobacter rectus, Capnocytophaga.
- High levels of P. gingivalis, T. forsythia, A. actinomycetemcomitans, C. rectus, P.
intermedia are associated with disease progression.
-in aggressive periodontitis:
- Localized aggressive periodontitis is strongly associated with A.
actinomycetemcomitans . with other bacteria as : P. gingivalis, Eikenella
corrodens, F. nucleatum, C. rectus, Capnocytophaga.
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- - Generalized aggressive periodontitis is associated with high levels of P.
gingivalis, A. actinomycetemcomitans, C. rectus, P. intermedia, E. corrodens.
-in Necrotizing ulcerative gingivitis :
- It is a specific, anaerobic, polymicrobial infection due to the combined activity of
fusobacteria (F. nucleatum), and oral spirochetes (Treponema spp.) forming
"Fusospirochaetal complex".
*direct mechanism of tissue destruction .
a) Attachment, colonization and invasion.
b) Production of virulence factors.
c) Evasion of host immunologic responses.
6 ‫ صفحه‬11 ‫لتفاصيل اكتر المحاضرة‬
*indirect mechanism of tissue destruction .
Bacteria and their products (virulence factors) activate host immune responses
leading to release of biologic mediators and cytokines from the host cells leading
to tissue destruction.
*bacterial virulence factors .
1- Exotoxins.
2- Enzymes.
3- Endotoxins.
4- Metabolic toxic / noxious products.
5- Bacterial capsule.
6- Surface associated materials (SAM).
7- Bacteriocins.
8- Modulation of cytokine function.
9- Reduction PMN function.
10- Altered lymphocyte function.
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*evasion of host immunologic response.
Overcoming of the host defense mechanisms.
- Antibodies in the subgingival area prevent the attachment of bacteria rendering
them susceptible to phagocytosis.
-Factors :
1- Capsule as it helps the bacteria escape phagocytosis by resisting the
opsonization.
2- Exotoxins as they damage PMNs, monocytes, T& B lymphocytes.
3- Proteases as they degrade immunoglobulins and complement.
4- Some bacteria can change their surface antigenicity as modulation of host
responses by binding serum components on the bacterial cell surface, and
invasion of gingival epithelial cells.
*role of protease in periodontal pathology.
1- Degrade the basement membrane and extracellular proteins leading to
destruction of C.T facilitating bacterial invasion.
2- Degrade the immunoglobulins and complement proteins as IgA and IgG
proteases produced from P. gingivalis and P. intermedia.
3- Interfere with tissue repair by inhibiting clot formation or lysing of fibrin matrix
to promote bleeding and provide heam (iron) which is utilized by P. gingivalis as
nutrient, i.e. proteases has fibrinolytic activity and act as a fibrinolysin.
4- Activate latent host collagenases (matrix metalloproteinases).
*proteolytic and hydrolytic enzymes in periodontal pathology.
- proteolytic enzyme:
1- Collagenase : A. actinomycetemcomitans, P. gingivalis, T. denticola and disrupt
C.T.
2- Trypsin like enzymes : P. gingivalis, T. denticola, T. forsythus.
3- Chymotrypsin like enzymes : T. denticola, Capnocytophaga.
4- Aminopeptidase : T. denticola, Capnocytophaga.
5- Elastase like enzymes : Capnocytophaga
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- hydrolytic enzyme:
1- Hyaluronidase and chondroitin sulphatase.
2- Acid and alkaline phosphatase .
*role of endotoxins in periodontal pathology .
1- They have a direct toxic effect on fibroblasts, osteoblasts and epithelial cells.
2- They are potent antigens inducing immune response. Immune system can
recognize LPS by a family of cell surface receptors called "toll-like" receptors
(TLRs).
3- They induce PMNs chemotaxis.
4- They induce bone resorption and activated complement leading to
macrophage activation and secretion of prostaglandins (PG). PG itself leads to
bone resorption, and PG E causes stimulated lymphocytes to produce osteoclast
activating factor leading to bone resorption.
*virulence factor produced by A. actinomycetemcomitans .
1- Endotoxins resorb the bone.
2- Leukotoxin kills human neutrophils (-> release of lysosomal enzymes) &
macrophages.
3- Epithellotoxins affects fibroblasts.
4- Bacteriocin.
5- LPS activates the alternate complement pathway.
6- Hydrolytic enzymes as collagenase.
7- SAM.
8- Immunosuppressive factor inhibits B-cell growth.
9- Capsule resists phagocytosis.
10- Fimbriae help adhesion.
11- Ability to invasion.
*virulence factor produced by P. gingivalis.
Capsular polysaccharides, collagenase , keratinase, phospholipase , trypsin-like
proteases (gingipain), hyaluronidase, hemolysins, endotoxins, flbrinolysins,
hydrogen sulphide, methylmercaptan.
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*virulence factor produced by T. forsythus.
Trypsin like enzyme and the ability to invasion .
*virulence factor produced by T. denticola.
Proteolytic enzymes , Hydrolytic enzymes , Altered lymphocyte function
*changes occurring in initial gingivitis stage l.
Plaque at junctional epithelium, increased flow of GCV, migration of neutrophils
due to acute inflammation. Mostly Gram + cocci
*changes occurring in early gingivitis stage ll.
Gingival infiltrate dominated by lymphocytes (75%) and macrophages, with some
plasma cells at the periphery. Actinomyces, spirochetes and capnophilic
organisms
*changes occurring in established gingivitis stage lll.
Predominance of plasma cells and B lymphocytes. P. gingivalis and Prevotella
intermedia
*role of neutrophil in tissue destruction.
Lysosomal leakage while digesting bacteria
Release of endotoxin from digested bacteria
Release of collagenase
*role of macrophage in periodontal destruction.
*pro-inflammatory cLysosomal leakage while digesting bacteria
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*role of lL-1 periodontal tissue destruction.
*role of TNF in a periodontal tissue destruction.
*inflammatory mediators .
*Role of prostaglandin E2 in periodontal destruction.
*reparative and anabolic cytokines.
*composition of supragingival calculus and subgingival calculus.
3 ‫ صفحه‬9 ‫للتفاصيل المحاضرة‬
*method of attachment of calculus to the tooth surface .
1- Attachment by means of an organic pellicle on the enamel.
2- Mechanical locking into surface irregularities, such as resorption lacunae and
caries.
3- Close adaptation of the calculus under surface depressions to the gently
sloping mounds of the unaltered cementum surface.
4- Penetration of the calculus bacteria into the cementum.
*the thories of calculus formation .
1- the 1st theory
2-The 2nd - theory : Epitactic concept or more appropriately Heterogeneous
nucleation.
6 ‫ صفحه‬9 ‫لتفاصيل اكتر المحاضرة‬
*role of microorganism in mineralization of calculus.
Bacterial plaque may actively participate in the mineralization of calculus by
forming phosphatases, which change the pH of the plaque and induces
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mineralization, but the prevalent opinion is that these bacteria are only passively
involved. The occurrence of calculus-like deposits in germ free animals supports
this opinion.
*role of malocclusion as a local predisposing factor in periodontal
diseases.
- Irregular alignment and crowding of the teeth leads to more plaque
accumulation and difficult plaque control (removal).
*periodontal complication associated with orthodontics therapy.
1- Favor plaque retention.
2- Modify plaque composition with increasing gram -ve microorganisms.
3- Gingival inflammation and enlargement.
4- Gingival trauma due to forceful placement of orthodontic bands beyond the
level of epithelial attachment (JE) leading to apical proliferation of the JE leading
to detachment of the gingiva from the tooth leading to gingival recession and may
pocket formation.
5- Higher degree of alveolar bone loss (resorption) during adult orthodontic care
than that occurs in adolescents.
* periodontal complication associated with impacted 3 molar .
- Vertical defects distal to the 2nd molar (Bone resorption at the distal aspect of
the 2nd molar) occur if the extraction of 3rd molar occurs after 25 years old
regardless of the flap design, so extraction of the concerned 3rd molar should be
done before 25 years old.
* periodontal complication associated with habits and self inflicted
injuries.
- Toothbrush trauma : Aggressive brushing is a horizontal or rotary manner leads
to gingival abrasions and tooth alterations especially with highly abrasive
toothpaste.
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*effect of tobacco use on the periodontium .
1- Higher prevalence of necrotizing ulcerative gingivitis (NUG).
2- Higher prevalence of refractory periodontitis.
3- Deeper pockets, greater attachment loss, more bone loss and furcation
involvement.
4- Less probing depth reduction, less gain in clinical attachment and bone height
with nonsurgical treatment (as scaling) and surgical treatment (as periodontal flap
surgery) even with guided tissue regeneration (GTR).
5- Lower rate of implant success.
*local risk factor in periodontal disease .
1- Calculus.
2- Iatrogenic factors.
3- Malocclusion.
4- Periodontal complications associated with orthodontic therapy.
5- Extraction of impacted 3rd molars.
6- Habits and self-inflicted injuries.
7- Tobacco use (Smoking).
8- Radiation therapy.
*systemic risk factor in periodontal disease.
1- Hematologic disorders.
2- Genetic disorders.
3- Endocrinal disorders.
4- Nutritional influence.
5- Medications.
*endocrine disorder as a risk factor in periodontal disease.
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*hormonal changes as a risk factor in periodontal disease.
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