Classification of Periodontal Diseases

CLASSIFICATION is a systematic
arrangement into groups or categories
2 Major categories of Periodontal Disease based on common attributes.
1. Gingivitis
2. Periodontitis Provide information necessary in :
- communicating clinical findings accurately
among clinicians, researchers, educators,
students, epidemiologists and public
health workers
- providing information to the patient
- Formulating individualized treatment plans
- And predicting treatment outcomes

There are 2 major categories of PD

A) Gingivitis B) Periodontitis
Gingivitis Periodontitis
GINGIVA:
GINGIVA: - is purplish or red with swollen gingiva
- (soft tissues) is red or bluish red - smokers gingiva may seem normal , pale pink
With swollen rounded margins without swelling , fibrosis of the gingival margins
- papillae is bulbous and swollen - The papillae do not fill the embrasure spaces
- Bleeding upon gentle probing ( probing - Bleeding upon gentle probing, there maybe pus
depths are greater than 3mm) (Probing depths greater than 4mm because of
- There is swelling but no apical migration of the apical migration of the junctional epithelium
the junctional epithelium and no bone loss - Bone loss
- Attachment loss is the hallmark of periodontitis; the
migration of the attachment apparatus is apical
to the level of the CEJ due the destruction of
fibers and bone that is supposed to support the
teeth.
1999 Classification of Periodontal Diseases and Conditions

Type 1 Gingival Diseases

Plaque Induced Gingivitis : Non-plaque -Induced gingival lesions of:

1. Caused solely plaque
2. Modified by systemic factors 1. Bacterial origin
3. Modified by medication 2. Viral origin
4. Modified by malnutrition 3. Fungal origin
4. Genetic origin
5. Systemic conditions
6. Traumatic lesions
7. Foreign body reactions
8. Not otherwise specified
Type II Chronic Periodontitis Type IV Periodontitis as a manifestation of
systemic diseases such as:
1. Localized Chronic periodontitis
2. Generalized Chronic Periodontitis 1. Blood disorders
2. Genetic factors
Type III Aggressive Periodontitis
Type V Necrotizing Periodontal Disease
1. Localized Aggressive Periodontis (LAP) Type such as :
2. Generalized Aggressive Periodontitis.
(GAP) 1. NUG
2. NUP
Type VI Associated with Endodontic Gingivitis is the most common form of
Lesions (perio-endo lesions) gingival disease
Inflammation is almost always present in all
Type VII Developmental or Acquired forms of gingival disease because
Deformities and Conditions bacterial plaque, which causes
1. Tooth related inflammation;
2. Muco-gingival conditions and irritating factor which favor plaque
3. Muco-gingival deformities accumulation are often present in the
4. Occlusal trauma gingival environment
5. Type VIII. Abscess of the Periodontium)
● Most common type of gingival disease is COURSE AND DISTRIBUTION
the simple inflammatory involvement
caused by bacterial plaque attached to the Acute gingivitis is a painful condition that
tooth surface comes on suddenly and is of short
● This type of gingivitis, called chronic duration
marginal gingivitis or simple gingivitis, Subacute gingivitis is a less severe phase of
may remain stationary for indefinite the aRecurrent gingivitis, reappears after
periods of time or may proceed to having been eliminated by treatment or
destruction of the supporting structures disappears spontaneously and then
reappears in an acute condition
Chronic gingivitis comes on slowly, is of long
duration, and is painless unless
complicated
DISTRIBUTION OF GINGIVITIS

Localized gingivitis is confined to the gingiva Papillary gingivitis involves the interdental
in relation to a single tooth or group of papillae and often extends into the
teeth adjacent portion of the gingival margin
Generalized gingivitis involves the entire Diffused gingivitis affects the gingival margin,
mouth the attached gingiva, and the interdental
Marginal gingivitis involves the gingival papillae
margin but may include a portion of the
contiguous attached gingiva
The distribution of gingival disease in individual cases is
described by combining the preceding terms, as follows:

Localized marginal gingivitis is confined to one Gingival Bleeding

or more areas of the marginal gingiva
Localized diffuse gingivitis extends from the Two earliest symptoms of gingival
margin to the mucobuccal fold inflammation, which precede
Localized papillary gingivitis is confined to one established gingivitis:
or more interdental spaces in a limited 1. Increase gingival fluid production
area rate
Generalized marginal gingivitis involves the 2. Bleeding from the gingival sulcus
gingival margins in relation to all of the on gentle probing
teeth
Generalized diffuse gingivitis involves the
entire gingiva
Gingival Bleeding caused by Local Factors

Chronic and Recurrent Bleeding Acute Bleeding

Most common cause of abnormal gingival bleeding
is chronic inflammation Gingival bleeding is caused by injury or occur
Is provoked by mechanical trauma such as spontaneously in acute gingival disease
improper brushing, toothpick, or food impaction, 1. Laceration of the gingiva by toothbrush
by biting into solid food, and by grinding teeth bristles during aggressive brushing
(bruxism) 2. Sharp piece of hard food cause gingival
bleeding even in the absence of gingival
disease
3. Gingival burns from hot foods or chemicals
increase the case of gingival bleeding
Hemorrhagic disorders in which abnormal gingival bleeding is encountered include the
following:
1. Vascular abnormalities (Vit. C deficiency or 4. Coagulation defects (hemophilia, leukemia,
allergy such as Schönlein-Henoch Christmas disease)
purpura) 5. Deficient platelet thromboplastic factor
2. Platelet disorders (idiopathic (PF3) resulting from uremia, multiple
thrombocytopenia purpura or myeloma and post-rubella purpura
thrombocytopenic purpura caused by Bleeding may follow the administration of
diffuse injury to bone marrow) excessive amounts of drugs such as
3. Hypoprothrombinemia (Vit. K deficiency salicylates and the administration of
resulting from liver disease or sprue) anticoagulants such as dicumarol and
heparin
Cyclic episodes of abnormal bleeding are
occasionally associated with the menstrual
period
 COLOR CHANGES IN THE GINGIVA

Color changes in Acute Gingivitis Color changes in Chronic Gingivitis

- Color changes vary with the intensity of the Chronic inflammation intensifies the red or
inflammation bluish red color, this is caused by vascular
- In all instances there is an initial bright red proliferation and reduction of keratinization
erythema due to epithelial compression by the
inflamed tissue
Venous stasis will add a bluish hue
 METALLIC PIGMENTATION

Bismuth, arsenic, and mercury produce a

> Heavy metals absorbed systemically from black line in the gingiva, which follows the
therapeutic use or occupational gingival contour of the margin
environments may discolor the gingiva and Lead results in a bluish red or deep blue
other areas of the mucosa linear pigmentation of the gingival margin
> This is different from tattooing produced by (burtonian line)
the accidental embedding of amalgam or Silver (argyria) causes a violet marginal line,
other metal fragments often accompanied by a diffuse bluish gray
discoloration throughout the mucosa
COLOR CHANGES ASSOCIATED WITH SYSTEMIC FACTORS

Endogenous oral pigmentation can be

due to melanin, bilirubin, or iron
3. Peutz-Jeghers syndrome which produces
Melanin oral pigmentation can be normal
intestinal polyposis and melanin
physiologic pigmentation and is
pigmentation in the oral mucosa and lips
commonly found in darker races
4. MAlbright’s syndrome (polyostotic fibrous
Diseases that increase melanin
dysplasia)
pigmentation include the following:
5. Von Recklinghausen’s disease
1. Addison’s disease which is caused by
(neurofibromatosis)
adrenal dysfunction and produces
6. Skin and mucous membrane can also be
isolated patches of discoloration
stained by bile pigments
varying from bluish black to brown
7. Jaundice is best detected by examination of
2. Iron in hemochromatosis may produce
the sclera, but the oral mucosa may also
a blue-gray pigmentation of the oral
acquire a yellowish color
mucosa
Exogenous factors are capable of producing Changes in the Consistency of the Gingiva
color changes in the gingiva include
atmospheric irritants, such as coal and Both chronic and acute inflammation produce
metal dust, and coloring agents in food changes in the normal firm, resilient
and lozenges consistency of the gingiva
Tobacco causes gray hyperkeratosis of the Chronic gingivitis is a conflict between
gingiva destruction and reparative changes, and
Localized bluish black areas of pigment are consistency of the gingiva is determined
commonly due to amalgam implanted in by the relative balance between the two
the mucosa
 Changes in the Surface Texture of the Gingiva

- Loss of surface stippling is an early sign of - Peeling of the surface occurs in

gingivitis desquamative gingivitis

- In chronic inflammation the surface is either - Hyperkeratosis results in a leathery texture

smooth and shiny or firm and nodular,
depending on whether the dominant
changes are exudative or fibrotic - Non-inflammatory gingival hyperplasia
produces a minute nodular surface
- Smooth surface texture is produced by
epithelial atrophy
Important Reminders when Diagnosing Periodontal Disease and Conditions

Careful Observation Use of Diagnostic Adjuncts

- Size, Shape, Contour, -Intraoral and Extraoral

Texture, Firmness and Photographs
Color - check for Radiographs
indication of -Probing Depths (CAL, PPD, GR
INFLAMMATION including Furcation
-Thorough History taking Involvement)
-History of Present Illness -Mobility and Percussion Test
based on the Chief -Plaque and Bleeding Indexes
Complaints -Oral Hygiene Index
-Dental History
-Medical History -Periodontal Diagnosis
-Social History Sequence: Severity, Extent ,
Disease
 Plaque- Induced Gingival Condition
● Localized, diffuse, intensely red area on • Generalized marginal gingivitis in the
the facial surface of tooth and dark-pink upper jaw with areas of diffuse gingivitis
marginal changes in the remaining anterior
teeth.
Non-Plaque Induced Gingival Conditions

● Bismuth gingivitis. Note the linear black ● Addison’s disease

discoloration of the gingiva in a patient
who is receiving bismuth therapy.
Non-Plaque Induced Gingival Conditions
● Neurofibromatosis Type I
● Polyostotic Fibrous Dysplasia
Periodontitis

1. Chronic Periodontitis
2. Aggressive Periodontitis
3. Periodontitis as a Manifestation of Systemic Disease
4. Necrotizing Periodontitis (Tissue necrosis with attachment
and bone loss)
Sample Case
Actual cases done at the
Centro Escolar University MScD Periodontics and Implantology Department

A 48 year old Filipina Female who lives in Taguig City.

Chief Complaints:
“Umuuga mga ngipin ko.”
“Nag-iiba position ng ngipin ko.”
“Namaga yung gilagid ko.”
History of Present Illness:

In 1995, during her pregnancy she started to notice severe inflammation

described as having a warm feeling on her gums.
After giving birth to her first child in 1995, she noticed that her teeth where
“changing position” especially the Upper Central Incisors.
In 2015, the patient started to notice mobility of her Upper Central Incisors and
Lower Anterior Teeth.
Medical History: Dental History:

-In 2013, she was diagnosed of Stage I Hypertension -In 1995, after giving birth, she had extraction
and was prescribed with Amlodiphine 10mg and of her Molars(Upper and Lower).
Losartan 50mg
-In 2015, she had extraction of her Upper
-In 2016, she met an accident where her knee was
badly injured.
Lateral Incisors and had a Stayplate
-In September 2017, she had removal of cyst in her Removable Partial Denture fabricated for
breast. the Upper Arch.
-In March 2018, she had an Orthopedic Surgery of her -In 2017, she had a dental check up and had
injured knee; at the same time, she was extraction of tooth number 46 where it
diagnosed with osteoarthritis secondary to
fractured and the roots were not retrieved.
trauma.

Family History
Father: Died in 1986 due to Throat and Sinus Cancer
Mother: Died in 2013 due to Breast Cancer
Social History:

- 1990, the patient started to drink alcoholic beverages but only

occasionally.

- In September 2017, after removal of her cyst, she stopped drinking

alcoholic beverages.
Extraoral Examination:
Biologic Width
 Biologic Width
? Dimensional width of
the Dentogingival
junction is based on:
? First described by Sicher
(1969) and Gargiulo et al
(1961)
? The sulcus = 0.69 mm
? Junctional Epithelium
= 0.97mm
? Connective tissue
attachment =1.07mm

? SUM of BW = 2.04 mm
🙣 NOTE: Impingement on the zone of the biologic width may
result in bone resorption, gingival recession or gingival
inflammation or hypertrophy.
Tooth Movement
 Tooth Movement:
🙣 Pre-eruptive tooth movement: Made by the deciduous
and permanent tooth germs within tissues of the jaw
before they begin to erupt. (Ten Cate 8th ed.)

🙣 Eruptive tooth movement : Made by the tooth to move

from its position within the bone of the jaw to its
functional occlusion. (Ten Cate 8th ed.)

🙣 Active Eruption: Physical movement of the tooth from

its pre-functional subgingival position through the
gingival tissue into the oral cavity and finally into
functional occlusion. (Moss-Salentign and Klyvert,1990)
(Antonio Nanci, Ten Cate’s Oral Histology 8th ed.)
(Edward Cohen, Atlas of Cosmetic and Reconstructive Periodontal Surgery
3rd ed.)
 Tooth Movement:

🙣 Post-eruptive tooth movement: Maintaining the

position of the erupted tooth in occlusion while the jaws
continue to grow and compensate for occlusal tooth
wear. (Ten Cate 8th ed)

🙣 Passive Eruption: Continued apical movement of the

free gingival margin epithelial attachment or junctional
epithelium and connective tissue attachment that
occurs after the tooth reaches functional occlusion
(Gottlieb & Orban, 1922; Manson, 1963)

(Antonio Nanci, Ten Cate’s Oral Histology 8th ed.)

(Edward Cohen, Atlas of Cosmetic and Reconstructive Periodontal Surgery
3rd ed.)
 “Gummy Smile”
Excessive Gingival Display

🙣 “Altered passive eruption”: the failure of the tissue to

adequately recede to a level apical to the cervical
convexity of the crown. (Goldman and Cohen, 1968)

🙣 “Delayed passive eruption”: the tissue’s failure to

reach the CEJ . (Volcansky and Cleaton-Jones, 1974)

(Edward Cohen, Atlas of Cosmetic and Reconstructive Periodontal Surgery

3rd ed.)
The end
+

Periodontal Prognosis
+
PROGNOSIS
■ Prediction of the probable course, duration, and
outcome of a disease based on a general knowledge
of the pathogenesis of the disease and the presence
of risk factors for the disease

■ Established after diagnosis is made and before

treatment plan is established
+
Risk vs. Prognosis

■ Risk – likelihood that an individual will develop a

disease in a specified period

■ Risk factors – characteristics of an individual that

put the person at increased risk for developing the
disease

■ Prognosis – prediction of the course or outcome of

a disease

■ Prognostic factors – characteristics that predict the

outcome of disease once the disease is present
+
Types of Prognosis
based on Tooth Mortality

■ Good prognosis
■ Fair prognosis
■ Poor prognosis
■ Questionable prognosis

■ Hopeless prognosis
+
Good Prognosis
■ Control of etiologic factors and adequate periodontal
support ensure the tooth will be easy to maintain by the
patient and clinician
+
Fair Prognosis
■ Approximately 25% attachment loss and/or Class I furcation
involvement (location and depth allow proper maintenance
with good patient compliance)
+
Poor Prognosis
■ 50% attachment loss, Class II furcation involvement (location
and depth make maintenance possible but difficult
+
Questionable Prognosis
■ >50% attachment loss, poor crown to root ratio, poor root
form, Class II furcation (location and depth make access
difficult) or Class III furcation involvements; >2+ mobility;
root proximity
+
Hopeless Prognosis

■ Inadequate attachment to maintain health, comfort and

function
+
Types of Prognosis
based on obtaining stability of
Periodontium

■ Favorable Prognosis
■ Questionable Prognosis

■ Unfavorable Prognosis
■ Hopeless Prognosis
+
Favorable Prognosis
■ Comprehensive periodontal treatment and maintenance will
stabilize the status of the tooth. Future loss of periodontal
support is unlikely
+
Questionable Prognosis
■ Local and/or systemic factors influencing the periodontal
status of the tooth may or may not be controllable. If
controlled, the periodontal status can be stabilized with
comprehensive periodontal treatment. If not, future
periodontal breakdown may occur.
+
Unfavorable Prognosis
■ Local and/or systemic factors influencing the periodontal
status cannot be controlled. Comprehensive periodontal
treatment and maintenance are unlikely to prevent future
periodontal breakdown
+
Hopeless Prognosis
■ Tooth must be extracted
+
Provisional Prognosis

■ To be established until Phase I Therapy is

completed

■ Allows treatment to be initiated on teeth that are

doubtful, in a hope of a favorable response
+
Overall vs Individual Tooth
Prognosis
■ Overall Prognosis – dentition as a whole

■ Should treatment be undertaken?

■ Is treatment likely to succeed?
■ When prosthetic replacements are needed, are the remaining teeth
able to support the prosthesis?

■ Individual Tooth Prognosis – determined after

the overall prognosis
+

Factors Determining Prognosis

+

1. Overall Clinical Factors

2. Systemic and Environmental Factors
3. Local Factors
4. Prosthetic and Restorative Factors
+
Overall Clinical Factors

1. Patient age – older patients have better

prognosis but lesser reparative capacity

2. Disease Severity – previous periodontal disease

history, pocket depth, level of attachment,
degree of bone loss, bony defect

3. Plaque Control

4. Patient Compliance and Cooperation

+
+
Systemic and Environmental
Factors

1. Smoking

2. Systemic Disease or Condition – Type I and II

Diabetes, Parkinson’s Disease

3. Genetic factors – IL-1 genotype

4. Stress
+
Local Factors

■ Plaque and Calculus

■ Subgingival Restorations

■ Anatomic Factors – short, tapered roots with large

clinical crown, cervical enamel projections, root
morphology, developmentall grooves, root proximity,
access to furcation area

■ Tooth Mobility
+
Prosthetic and Restorative Factors

■ Endodontic Treatment

■ Abutment Teeth

■ Caries

■ Nonvital Teeth

■ Root Resorption
+

Diagnosis and Prognosis

+

For any given diagnosis, there should

be an expected prognosis under ideal
conditions.
+
Prognosis for Patients with
Gingival Disease

1. Plaque-Induced Gingival Disease

2. Non Plaque-Induced Gingival Lesions
+ I. Gingivitis associated with Dental Plaque Only
■ Prognosis is good, provided all other local irritants and factors
eliminated

II. Plaque-Induced GD modified by Systemic Factors

■ Long term Prognosis depends on control of plaque and
correction of systemic factor
+
III. Plaque-Induced GD modified by Medications
■ Drug-influenced gingival enlargements: Phenytoin,
Cyclosporine, Nifedipine, Oral Contraceptives
■ Long term Prognosis depends if patient systemic problem can be
treated with an alternate medication

IV. GD modified by malnutrition

■ Severe Vitamin C deficiency
+
Non Plaque Induced

■ Bacterial, fungal, and viral infections

■ Dermatologic disorders: lichen planus, pemphigoid, erythema
multiforme
■ Allergic, toxic and Foreign body reactions, mechanical and
thermal trauma
■ Prognosis depends on elimination of source of infectious and
causative agent, management of disorders,
+
Prognosis for Patients with
Periodontitis
1. Chronic Periodontitis
■ Can be localized or generalized
■ Prognosis is good for Slight to Moderate Periodontitis
■ Prognosis may be fair or poor for Severe Periodontitis

2. Aggressive Periodontitis
■ Can be localized or generalized
■ Rapid Attachment loss and bone destruction in a healthy patient &
Familial Aggregation
■ Prognosis is poor if microbial and immunological involvement
■ Prognosis is good, when treated early
+ 3. Periodontitis as Manifestation of Systemic Disease
a. PD assoc with hematologic disorders: leukemia and
acquired neutropenia

b. PD assoc with genetic disorders: familial and cyclic

neutropenia, Down Syndrome, hypophosphatasia

■ Systemic diseases alter the ability of the host to respond to the

microbial challenge

■ Prognosis is fair to poor

+ 4. Necrotizing Periodontal Disease
a. Necrotizing Ulcerative Gingivitis (NUG)

■ Prognosis may be fair

b. Necrotizing Ulcerative Periodontitis (NUP)

■ Associated with HIV patients

+

Reevaluation of Prognosis After

Phase I Therapy
Inflammation
Definition

● Inflammation is a non specific, localized immune reaction of the

organism, which tries to localized the pathogen agent. Many
consider the syndrome a self-defense mechanism.

● It consist of vascular, metabolic, cellular changes, triggered by the

entering of pathogen agent in healthy tissues of the body.
Etiology
● The causes of inflammation are many and varied:
● Exogenous causes:

● Physical agents

▪ Mechanic agents: fractures, foreign corps, sand, etc.

▪ Thermal agents: burns, freezing
● Chemical agents: toxic gases, acids, bases

● Biological agents: bacteria, viruses, parasites

● Endogenous causes:
● Circulation disorders: thrombosis, infarction, hemorrhage

● Enzymes activation – e.g. acute pancreatitis

● Metabolic products deposals – uric acid, urea

Cardinal Signs

● Celsus described the local reaction of injury in terms that have come
to be known as the cardinal signs of inflammation.
● These signs are:
● rubor (redness)
● tumor (swelling)
● calor (heat)
● dolor (pain)
● functio laesa, or loss of function (In the second century AD, the
Greek physician Galen added this fifth cardinal sign)
Inflammation

● The inflammatory reaction takes place at the microcirculation level

and it is composed by the following changes:
● Tissue damage

● Cellular – vascular - cellular response

● Metabolic changes

● Tissue repair
Tissue damage

● Changes begin almost immediately after injury:

● Because of the pathogen agent’s action in the affected tissue,
there’ll be release off inflammatory mediators responsible for the
following events of inflammation.
● Tissue macrophages, monocytes, mast cells, platelets, and
endothelial cells are able to produce a multitude of cytokines.
The cytokines tissue necrosis factor-a (TNF-a) and interleukin
(IL)–1 are released first and initiate several cascades.
Inflammatory Mediators
● TNF-a and IL-1 are responsible for fever and the release of stress
hormones (norepinephrine, vasopressin, activation of the renin-
angiotensin-aldosterone system).
● TNF-a and IL-1 are responsible for the synthesis of IL-6, IL-8, and
interferon gamma.
● Cytokines, especially IL-6, stimulate the release of acute-phase
reactants such as C-reactive protein (CRP).
● The proinflammatory interleukins either function directly on tissue or
work via secondary mediators to activate the coagulation cascade,
complement cascade, and the release of nitric oxide, platelet-
activating factor, prostaglandins, and leukotrienes.
Inflammatory Mediators
● Complement fragments and cytokines
● It stimulates chemotaxis of neutrophils, eosinophils and
monocytes;
● C3a, C5a increase vascular permeability;
● Cytokines
● Interleukins (IL1, IL 6, IL8)
● Stimulates the chemotaxis, degranulation of neutrophils and
their phagocytic activity
● Induce extravascularization of granulocytes
● Fever
● Tumor necrosis factor (TNF) and IL 8
● Leukocytosis
● Fever
● Stimulates prostaglandins production
Inflammatory Mediators
● Prostaglandins
● The prostaglandins are ubiquitous, lipid soluble molecules
derived from arachidonic acid, a fatty acid liberated from cell
membrane phospholipids, through the cyclooxygenase pathway.
● Prostaglandins contribute to vasodilation, capillary permeability,
and the pain and fever that accompany inflammation.
● The stable prostaglandins (PGE1 and PGE2) induce
inflammation and potentiate the effects of histamine and other
inflammatory mediators:
● They cause the dilation of precapillary arterioles (edema), lower
the blood pressure, modulates receptors activity and affect the
phagocytic activity of leukocytes.
● The prostaglandin thromboxane A2 promotes platelet
aggregation and vasoconstriction.
Inflammatory Mediators
● Leukotrienes
● The leukotrienes are formed from arachidonic acid, but through
the lipoxygenase pathway.
● Histamine and leukotrienes are complementary in action in that
they have similar functions.
● Histamine is produced rapidly and transiently while the more
potent leukotrienes are being synthesized.
● Leukotrienes C4 and D4 are recognized as the primary
components of the slow reacting substance of anaphylaxis (SRS-
A) that causes slow and sustained constriction of the bronchioles.
● The leukotrienes also have been reported to affect the
permeability of the postcapillary venules, the adhesion properties
of endothelial cells, and stimulates the chemotaxis and
extravascularization of neutrophils, eosinophils, and monocytes.
The cyclooxygenase and lipoxygenase
pathways
Inflammatory Mediators

● Histamine
● It is found in high concentration in platelets, basophils, and mast
cells.
● Causes dilation and increased permeability of capillaries (it
causes dilatation of precapillary arterioles, contraction of
endothelial cells and dilation of postcapillary venules).
● It acts through H1 receptors.
Inflammatory Mediators

● Platelet-activating factor (PAF)

● It is generated from a lipid complex stored in cell membranes;

● It affects a variety of cell types and induces platelet aggregation;

● It activates neutrophils and is a potent eosinophil

chemoattractant;
● It contributes to extravascularization of plasma proteins and so,
to edema.
Inflammatory Mediators
● Plasma Proteases
● The plasma proteases consist of:

● Kinins

▪ Bradykinin - causes increased capillary permeability

(implicated in hyperthermia and redness) and pain;
● Clotting factors

▪ The clotting system contributes to the vascular phase of

inflammation, mainly through fibrin peptides that are formed
during the final steps of the clotting process.
The Vascular Response
● Faze I = vasoconstriction (momentary constriction of small blood
vessels in the area).
● Vascular spasm begins very quickly (30 sec.) after the injury at it
last a few minutes.
● The mechanism of spasm is nervous – through catecholamine
liberated from sympatic nerves endings.
● Faze II = active vasodilation (through catabolism products that act
through receptors and directly stimulates vascular dilation – nervous
mechanism).
● Dilation of arterioles and capillaries (redness = rubor);

● Blood flow increases and gives pulsate sensation;

● Active hyperemia in skin territory and increased metabolism

leads to higher local temperature (heat = calor).
The Vascular Response
● Faze III = passive vasodilation
● Blood vessels in the affected area loose their reactivity to
nervous and humoral stimuli and passive vasodilation occurs.
● Progressively fluid move into the tissues (increased vascular
permeability and structural alteration of blood vessels) and cause
swelling (tumor), pain, and impaired function.
● The exudation or movement of the fluid out of the capillaries and
into the tissue spaces dilutes the offending agent. As fluid moves
out of the capillaries, stagnation of flow and clotting of blood in
the small capillaries occurs at the site of injury.
● This aids in localizing the spread of infectious microorganisms, if
case.
Cellular Response
● The cellular response of acute inflammation is marked by movement
of phagocytic white blood cells (leukocytes) into the area of injury.
● Two types of leukocytes participate in the acute inflammatory
response - the granulocytes and monocytes.
● The sequence of events in the cellular response to inflammation
includes:
● pavementing

● emigration

● chemotaxis

● phagocytosis
Pavementing

● The release of chemical mediators (i.e., histamine, leukotrienes and

kinins) and cytokines affects the endothelial cells of the capillaries
and causes the leukocytes to increase their expression of adhesion
molecules.
● As this occurs, the leukocytes slow their migration and begin to
marginate, or move to and along the periphery of the blood vessels.
Emigration and chemotaxis

● Emigration is a mechanism by which the leukocytes extend

pseudopodia, pass through the capillary walls by ameboid
movement, and migrate into the tissue spaces.
● The emigration of leukocytes also may be accompanied by an
escape of red blood cells.
● Once they have exited the capillary, the leukocytes move through
the tissue guided by secreted cytokines, bacterial and cellular
debris, and complement fragments (C3a, C5a).
● The process by which leukocytes migrate in response to a chemical
signal is called chemotaxis.
Phagocytosis
● During the next and final stage of the cellular response, the
neutrophils and macrophages engulf and degrade the bacteria and
cellular debris in a process called phagocytosis.
● Phagocytosis involves three distinct steps:
● Adherence plus opsonization
● Engulfment
● Intracellular killing
● through enzymes, toxic oxygen and nitrogen products
produced by oxygen-dependent metabolic pathways (nitric
oxide, peroxyonitrites, hydrogen peroxide, and hypochlorous
acid)
● If the antigen is coated with antibody or complement, its adherence
is increased because of binding to complement. This process of
enhanced binding of an antigen caused by antibody or complement
is called opsonization.
Phagocytosis
Metabolic changes
● Protein metabolism
● Is increased – cell destruction, metabolic products lead o
increased osmotic pressure in interstitial space which attracts
water and contributes to edema (swelling = tumor);
● The metabolic changes, including skeletal muscle catabolism,
provide amino acids that can be used in the immune response
and for tissue repair;
● Glucose metabolism
● Anaerobe utilization of glucose is increased because of hypoxia
with increased formation of lactic and pyruvic acid;
● Lipid metabolism
● Increased formation of ketons and fatty acids

● Mineral metabolism
● Increased extracellular K+ concentration

● Acid – base balance

● Metabolic acidosis (ketons, lactic acid)
Inflammation
● Stage I:
● Following an insult, local cytokine is produced with the goal of
inciting an inflammatory response, promoting wound repair and
recruitment of the reticular endothelial system.
● Stage II:
● Small quantities of local cytokines are released into circulation to
improve the local response. This leads to growth factor
stimulation and the recruitment of macrophages and platelets.
This acute phase response is typically well controlled by a
decrease in the proinflammatory mediators and by the release of
endogenous antagonists. The goal is homeostasis.
● Stage III:
● If homeostasis is not restored, a significant systemic reaction
occurs. The cytokine release leads to destruction rather than
protection. A consequence of this is the activation of numerous
humoral cascades and the activation of the reticular endothelial
system and subsequent loss of circulatory integrity. This leads to
organ dysfunction.
Systemic manifestations of
inflammation
● Under optimal conditions, the inflammatory response remains
confined to a localized area. In some cases local injury can result in
prominent systemic manifestations as inflammatory mediators are
released into the circulation.
● The most prominent systemic manifestations of inflammation are:
● The acute phase response
● Alterations in white blood cell count (leukocytosis or leukopenia)
● Fever
● Sepsis and septic shock, also called the systemic inflammatory
response, represent the severe systemic manifestations of
inflammation
The acute phase response

● Usually begins within hours or days of the onset of inflammation or

infection.
● Includes:
● changes in the concentrations of plasma proteins - liver
dramatically increases the synthesis of acute-phase proteins
such as fibrinogen and C-reactive protein
● increased erythrocyte sedimentation rate
● fever
● increased numbers of leukocytes
● skeletal muscle catabolism
● negative nitrogen balance
The acute phase response
● These responses are generated after the release of the cytokines,
IL-1, IL-6, and TNF:
● These cytokines affect the thermoregulatory center in the
hypothalamus to produce fever;
● IL-1 and other cytokines induce an increase in the number and
immaturity of circulating neutrophils by stimulating their
production in the bone marrow;
● Lethargy, a common feature of the acute-phase response, results
from the effects of IL-1 and TNF on the central nervous system.
Tissue repair
● The primary objective of the healing process is to fill the gap created
by tissue destruction and to restore the structural continuity of the
injured part.
● The effect of all this is restitutio ad integrum.
● Concomitantly with tissue damage, at the peripheral of inflammatory
process, begins the repair process, in order to limit the extension of
it.
● Reparatory processes:
● Cell proliferation
● Conjunctive tissue proliferation
● Blood vessels neoformation = angiogenesis
● Lymphatic drainage of exudates
● Phagocytosis
● Injured tissues are repaired by regeneration of parenchymal cells or
by connective tissue repair in which scar tissue is substituted for the
parenchymal cells of the injured tissue (could lead to malfunction of
organs - fibrosis).
Tissue repair
● Chemical mediators and growth factors orchestrate the healing
process.
● Some growth factors act as chemoattractants, enhancing the
migration of white blood cells and fibroblasts to the wound site,
and others act as mitogens, causing increased proliferation of
cells that participate in the healing process (e.g. platelet-derived
growth factor, which is released from activated platelets, attracts
white blood cells and acts as a growth factor for blood vessels
and fibroblasts).
● Many of the cytokines discussed function as growth factors that
are involved in wound healing.
Tissue repair
● Fibroblasts and vascular endothelial cells begin proliferating to form
a specialized type of soft, pink granular tissue, called granulation
tissue.
● This tissue serves as the foundation for scar tissue development. It
is fragile and bleeds easily because of the numerous, newly
developed capillary.
● The newly formed blood vessels are leaky and allow plasma
proteins and white blood cells to leak into the tissues.
● At approximately the same time, epithelial cells at the margin of the
wound begin to regenerate and move toward the center of the
wound, forming a new surface layer.
● As the proliferative phase progresses, there is continued
accumulation of collagen and proliferation of fibroblasts.
● Collagen synthesis reaches a peak within 5 to 7 days and continues
for several weeks, depending on wound size.
● By the second week, the white blood cells have largely left the area,
the edema has diminished, and the wound begins to blanch as the
small blood vessels become thrombosed and degenerate.
Factors That Affect Wound Healing
● Malnutrition
● Protein deficiencies prolong the inflammatory phase of healing
and impair fibroblast proliferation, collagen and protein matrix
synthesis, angiogenesis, and wound remodeling.
● Carbohydrates are needed as an energy source for white blood
cells.
● Fats are essential constituents of cell membranes and are
needed for the synthesis of new cells.
● Vitamins A and C have been shown to play an essential role in
the healing process.
● Vitamin C is needed for collagen synthesis.
● Vitamin A functions in stimulating and supporting
epithelialization, capillary formation, and collagen synthesis.
The B vitamins are important cofactors in enzymatic reactions
that contribute to the wound-healing process.
● Vitamin K plays an indirect role in wound healing by preventing
bleeding disorders.
Factors That Affect Wound Healing

● Blood Flow and Oxygen Delivery

● Pre-existing health problems

● Arterial disease and venous pathology

● Molecular oxygen is required for collagen synthesis.

● It has been shown that even a temporary lack of oxygen can
result in the formation of less stable collagen.
● Wounds in ischemic tissue become infected more frequently.
● PMNs and macrophages require oxygen for destruction of
microorganisms.
Resolution of inflammation
● The inflammatory response must be actively terminated when no
longer needed to prevent unnecessary "bystander" damage to
tissues.
● Failure to do so results in chronic inflammation, and cellular
destruction.
● Resolution of inflammation occurs by different mechanisms in
different tissues. Mechanisms which serve to terminate inflammation
include:
● Short half-life of inflammatory mediators in vivo;
● Production and release of transforming growth factor (TGF) beta from
macrophages;
● Downregulation of pro-inflammatory molecules, such as leukotrienes;
● Upregulation of anti-inflammatory molecules such as the Interleukin 1
receptor antagonist or the soluble tumor necrosis factor receptor;
● Apoptosis of pro-inflammatory cells;
● Downregulation of receptor activity by high concentrations of ligands;
● IL-4 and IL-10 are cytokines responsible for decreasing the production of
TNF-a, IL-1, IL-6, and IL-8.
Resolution of inflammation
● Production of anti-inflammatory lipoxins
● Evidence now suggests that an active, coordinated program of
resolution initiates in the first few hours after an inflammatory
response begins.
● After entering tissues, granulocytes promote the switch of
arachidonic acid–derived prostaglandins and leukotrienes to
lipoxins, which initiate the termination sequence. Neutrophil
recruitment thus ceases and programmed death by apoptosis
is engaged.
● These events coincide with the biosynthesis, from omega-3
polyunsaturated fatty acids, of resolvins and protectins, which
critically shorten the period of neutrophil infiltration by initiating
apoptosis.
● Consequently, apoptotic neutrophils undergo phagocytosis by
macrophages, leading to neutrophil clearance and release of
anti-inflammatory and reparative cytokines such as
transforming growth factor-β1.
● The anti-inflammatory program ends with the departure of
macrophages through the lymphatics.
Outcomes
● Resolution
● The complete restoration of the inflamed tissue back to a normal
status. Inflammatory measures such as vasodilation, chemical
production, and leukocyte infiltration cease, and damaged
parenchymal cells regenerate. In situations where limited or short
lived inflammation has occurred this is usually the outcome.
● Fibrosis
● Large amounts of tissue destruction, or damage in tissues unable
to regenerate, can not be regenerated completely by the body.
Fibrous scarring occurs in these areas of damage, forming a scar
composed primarily of collagen. The scar will not contain any
specialized structures, such as parenchymal cells, hence
functional impairment may occur.
Outcomes
● Abscess formation
● A cavity is formed containing pus, an opaque liquid containing
dead white blood cells and bacteria with general debris from
destroyed cells.
● Chronic inflammation
● In acute inflammation, if the injurious agent persists then chronic
inflammation will ensue. This process, marked by inflammation
lasting many days, months or even years, may lead to the
formation of a chronic wound. Chronic inflammation is
characterised by the dominating presence of macrophages in the
injured tissue. These cells are powerful defensive agents of the
body, but the toxins they release (including reactive oxygen
species) are injurious to the organism's own tissues as well as
invading agents. Consequently, chronic inflammation is almost
always accompanied by tissue destruction.
PERIODONTICS 2

Rationale for Periodontal

Treatment
Prepared by: Dr. Almira Dulce Garcia- Icaro
Short Term Goals: elimination of all infectious and
inflammatory processes that cause periodontal and other problems
that hinder patient’s general health.
• To bring the oral cavity back to health
• Periodontal procedures: pocket eradication or reduction, the
establishment of good gingival contours and mucogingival
relationship
• Endodontics, Surgery, Restoration

Long Term Goals: reconstruction of a healthy dentition that

fulfill all functional and esthetic requirements
• Prosthetic reconstruction
• Implant Surgery, Orthodontics
Treatment Plan
Blueprint for case management and includes all procedures required for the
establishment and maintenance of oral health:

● Emergency Treatment
● Extractions
● Periodontal Pocket Therapy both surgical and non-surgical
● Endodontic Treatment
● Occlusal correction, Orthodontic treatment
● Implant Surgery
● Restorations
● Prosthetic replacements
● Esthetic Periodontal treatment
Extracting or Preserving Tooth

• Treatment: establish and maintain the health of the periodontium

throughout the mouth rather than attempting spectacular efforts to
“tighten loose teeth”
• Teeth at the borderline of hopeless prognosis: do not contribute to the
overall usefulness of the dentition.
• When do you extract a teeth?
■ So mobile that function becomes painful
■ Cause acute abscess during therapy
■ No use for it in the overall treatment plan
Extracting or Preserving Tooth
• When do you postpone the decision to extract?
■ It maintains posterior stops. Extraction after treatment when it can be replaced by
an implant or prosthesis.
■ It may be functional after implant placement in adjacent areas. After implant
placement, proceed with extraction
■ Anterior teeth, retain the tooth during periodontal treatment, extract after
completion of treatment. When a restorative procedure can be performed.
■ Extraction during periodontal surgery of the adjacent teeth.

• Importance of the Esthetic zone

• Interdisciplinary consultation with other specialties
• Systemic conditions are carefully evaluated
• Supportive periodontal care for case maintenance
PERIODONTICS 2

Periodontal
Treatment Plan

DR. ALMIRA DULCE GARCIA-ICARO

 ● Eliminate pain
● Eliminate exudation
● Eliminate gingival inflammation and
bleeding
● Reduce periodontal pockets
Benefits of ● Eliminate infection
● Arrest the destruction of soft tissue
and bone
Periodontal ● Reduce abnormal tooth mobility
● Establish optimal occlusal function
Treatment ● Restore tissue destroyed by disease
● Reestablish physiologic gingival
contour
● Prevent recurrence of the disease
 LOCAL
• Removal of plaque and other
local factors
• Elimination of trauma

SYSTEMIC
Local and • Only an adjunct to local measures
• Controlling systemic complications
• Systemic antibiotics
Systemic
Therapy
FACTORS THAT AFFECT HEALING

LOCAL SYSTEMIC
• Excessive tissue • Age
manipulation during • Generalized infections
treatment • Diabetes and debilitating
• Trauma to the tissues diseases
• Presence of foreign bodies • Insufficient food intake
• Repetitive treatment • Nutrient deficiency
procedures that disrupt the • Hormones
healing process • Stress
• Removal of degenerated
necrotic tissue
• Immobilization of healing
area
• Pressure on the wound
 HEALING AFTER TREATMENT

• Removal of degenerated tissue debris and

• Replacement of tissues destroyed by the disease

REGENERATION
• Natural renewal of the structure produced by growth and
differentiation of new cells
• A normal physiologic process = wear and tear repair

1. Mitotic activity in the epithelium of the gingiva and CT of

the PDL
2. Formation of new bone
3. Continuous deposition of cementum
 HEALING AFTER TREATMENT

REPAIR
● Restores the continuity of the diseased marginal gingiva and
reestablishes a normal gingival sulcus at the same level on the root as
the base of the preexisting pocket = healing by scar

● Arrests bone destruction but does not result in gain of gingival

attachment or bone height
Healing After
Treatment
NEW ATTACHMENT
● Embedding of new periodontal ligament fibers
into new cementum and the attachment of the
gingival epithelium to a tooth surface previously
denuded by disease
REATTACHMENT
● Repair of areas of the root not previously
exposed to the pocket (after surgical
detachment of tissues)
EPITHELIAL ADAPTATION
● Close apposition of the gingival epithelium to the
tooth surface with no gain in height of gingival
fiber attachment.
Healing After
Treatment
• PERIODONTAL RECONSTRUCTION
• Regeneration of cells and fibers and
remodeling of the lost periodontal
structures that results in:

1. Gain of attachment level

2. Formation of new periodontal ligament
fibers
3. Level of alveolar bone coronally to that
present before treatment
Healing After Treatment