PATHOGENESIS OF

PERIODONTAL
DISEASE
Pathogenesis
◦ Came from the Greek words pathos, which means "suffering or disease," and genesis, which
means "origin.“

◦ Defined as sequence of events that occur during the development of a disease or abnormal
condition.
 PERIODONTIUM IN
HEALTH AND DISEASE
THREE BASIC STATES OF
PERIODONTIUM
 CLINICAL PICTURE OF A HEALTHY
GINGIVA
A. COLOR:
PINK AND RESILIENT IN CONSISTENCY
B. GINGIVAL MARGIN:
SCALLOPED OUTLINE
LOCATED ABOVE THE CEJ
C. INTERDENTAL PAPILLAE:
FIRM AND OCCUPIES THE EMBRASURE SPACES APICAL TO THE
CONTACT AREAS
D. ABSENCE OF BLEEDING:
NO BLEEDING UPON PROBING
E. SULCUS
PROBING DEPTHS RANGE FROM 1 TO 3 mm
 MICROSCOPIC PICTURE OF A HEALTHY
GINGIVA
A. JUNCTIONAL EPITHELIUM:
THE JE IS FIRMLY ATTACHED BY HEMIDESMOSOMES TO THE
ENAMEL SLIGHTLY ABOVE THE CEJ
B. EPITHELIAL-CONNECTIVE TISSUE JUNCTION:
JE HAS NO EPITHELIAL RIDGES
C. GINGIVAL FIBERS:
INTACT SUPRAGINGIVAL FIBER BUNDLES SUPPORT THE JE
D. ALVEOLAR BONE:
CREST OF ALVEOLAR BONE IS INTACT AND LOCATED 2 TO 3 mm
BELOW THE BASE OF JE
E. PDL FIBERS:
INTACT PDL FIBER BUNDLES STRETCH BETWEEN THE BONY
WALLS OF THE TOOTH SOCKET TO THE CEMENTUM OF THE ROOT
F. CEMENTUM
CEMENTUM IS NORMAL
 CHARACTERISTICS OF GINGIVITIS
A. ONSET OF GINGIVITIS
- observed clinically from 4 to 14 days after plaque biofilm accumulates in the gingival sulcus.

1. Acute Gingivitis
- Gingivitis that lasts for a short period of time.
- Characterized by fluid in the gingival connective tissues that results in swollen gingiva
2. Chronic Gingivitis
- Lasts for months or years
- Body attempts to repair the tissue damage to form new collagen fibers
- Excess collagen fibers lead to gingival tissues that are enlarged and leathery consistency
- Excess collagen fibers conceal the redness caused by the increased blood flow, making
the tissue appear less red.
B. TISSUE ENLARGEMENT
- may be caused by swelling (acute gingivitis) or fibrosis (chronic gingivitis)

C. REVERSIBLE TISSUE DAMAGE

- damage is reversible
- with good patient self-care the body can repair the damage

D. DURATION OF GINGIVITIS
- may persist for years without ever progressing to the next stage, which is periodontitis.
 CLINICAL PICTURE OF GINGIVITIS
A. COLOR
- usually red or reddish blue in color
B. GINGIVAL MARGIN
- gingival margin is swollen and loses its knife-edge adaptation to the tooth
- gingival tissue may cover more crown of the tooth due to tissue swelling
or fibrosis.
C. INTERDENTAL PAPILLAE
- often bulbous and swollen
D. BLEEDING
- there is bleeding upon gentle probing
E. SULCUS
- probing depth is beyond 3mm due to swelling of tissues
- there is no apical migration of the junctional epithelium in gingivitis
 MICROSCOPIC PICTURE OF GINGIVITIS
A. JUNCTIONAL EPITHELIUM
- the hemidesmosomes still attach to the enamel coronal to the cementoenamel junction.
B. EPITHELIAL-CONNECTIVE TISSUE JUNCTION
- the junctional epithelium extends epithelial ridges down into the connective tissue
- such extension of the epithelial ridges only can occur because destruction of the gingival
fibers
creates space for the growing epithelium
C. GINGIVA FIBERS
- damage has occurred to the supragingival fiber bundles.
- damage is reversible if the bacterial infection is brought under control.
D. ALVEOLAR BONE
- the bacterial infection has not progressed into the alveolar bone.
- no destruction of alveolar bone
E. PERIODONTAL LIGAMENT FIBERS
- the bacterial infection has not progressed into the periodontal ligament fibers
F. CEMENTUM
- normal
 CHARACTERISTICS OF PERIODONTITIS
A. EXTENT OF TISSUE DESTRUCTION
- tissue damage of periodontitis is permanent
- characterized by the apical migration of the junctional epithelium, loss of connective tissue
attachment, and loss of alveolar bone.

B. PROCESS OF TISSUE DESTRUCTION

- tissue destruction in periodontitis is not continuous process, rather it occurs in an intermittent manner with
extended periods of disease inactivity followed by short periods of destruction.
- progresses at different rates throughout the mouth.
- destruction does not occur in all parts of the mouth at the same time but instead destruction usually
occurs in only a few specific sites at a time.
 CLINICAL PICTURE OF PERIODONTITIS
A. COLOR
- the gingival tissue shows visible alterations in color, contour,
and consistency.
1. Edematous tissue (spongy tissue) – bluish or purplish-red
with a smooth, shiny appearance
2. Fibrotic tissue (firm, nodular tissue) – light pink with a
leathery consistency
B. GINGIVAL MARGIN
1. The gingival margin may be swollen and doesn’t have a close
knife-edged adaptation to the tooth
2. The position of the gingival margin varies greatly in
periodontitis.
3. The margin may be apical to the cementoenamel junction
resulting in a portion of the root being visible in the mouth.
C. INTERDENTAL PAPILLAE
- the interdental papillae may not fill the interdental embrasure
spaces.
D. BLEEDING
- there often is bleeding upon probing, and suppuration may be
visible
E. POCKET
- probing depth is 4mm or greater because the junctional
epithelium is attached to the root surface
- pus may be evident upon probing
- pain is usually absent, however probing may cause some pain
due to ulcerations of the pocket epithelium
 MICROSCOPIC PICTURE OF PERIODONTITIS
A. JUNCTIONAL EPITHELIUM
- located on the cementum, below its normal location (also known
as APICAL MIGRATION OF THE JUNCTION EPITHELIUM)
- the coronal-most portion of JE detaches from the tooth surface
- the extracellular matrix of the gingiva and the attached collagen
fibers at the apical edge of the junctional epithelium are destroyed
B. EPITHELIAL-CONNECTIVE TISSUE JUNCTION
- the junctional epithelium proliferates and extends epithelial ridges
into the connective tissue
- the sulcular epithelium of the pocket wall thickens and extends
epithelial ridges deep into the connective tissue. Small ulcerations of the
pocket epithelium expose the underlying inflamed connective tissue.
C. GINGIVAL CONNECTIVE TISSUE
- changes in the gingival connective tissue are severe and the collagen
destruction in the area of inflammation is almost complete.
- there is widespread destruction of the supragingival fiber bundles, reducing
them to fiber fragments.
- the transseptal fiber bundles, however, are regenerated continuously across the
crest of bone.
- epithelium grows over the root surface in areas where the fiber bundles have
been destroyed.
D. ALVEOLAR BONE
- there is permanent destruction of the alveolar bone that supports the teeth.
- tooth mobility may be present
E. PERIODONTAL LIGAMENT FIBERS
- there is permanent destruction of some or all of the periodontal ligament fiber
bundles
F. CEMENTUM
- exposed to dental plaque biofilm
INFLAMMATORY RESPONSE
IN PERIODONTAL DISEASE
The molecules that play a role in the pathogenesis of periodontitis can be broadly divided into two main groups:
- derived from the subgingival microbiota (i.e., microbial virulence factors)
- derived from the host immune–inflammatory response.

In terms of the relative importance of each, it is now clear that most of the tissue breakdown results from the host’s
inflammatory processes.
 MICROBIAL VIRULENCE FACTORS
LIPOPOLYSACCHARIDE

- Large molecule composed of a lipid component (lipid A) and a polysaccharide component.

- They are found in the outer membrane of gram-negative bacteria, they act as endotoxins, and they elicit strong
immune responses in animals.
BACTERIAL ENZYMES AND NOXIOUS PRODUCTS

- Plaque bacteria produce proteases, which are capable of breaking down structural proteins of the periodontium such
as collagen, elastin, and fibronectin.

- Bacterial proteases disrupt host responses, compromise tissue integrity, and facilitate the microbial invasion of the
tissues.

- P. gingivalis produces two classes of cysteine proteases that have been implicated in periodontal pathogenesis known
as gingipains, and they include the lysine-specific gingipain Kgp and the arginine-specific gingipains RgpA and
RgpB.
MICROBIAL INVASION

– In histologic specimens, bacteria (including cocci, filaments, and rods) have been identified in the intercellular spaces
of the epithelium.

– Periodontal pathogens such as P. gingivalis and Aggregatibacter actinomycetemcomitans have been reported to
invade the gingival tissues, including the connective tissues.

– Fusobacterium nucleatum can invade oral epithelial cells, and bacteria that routinely invade host cells may facilitate
the entry of noninvasive bacteria by coaggregating with them. It has also been shown that A. actinomycetemcomitans
can invade epithelial cells and persist intracellularly.
FIMBRIAE

– The fimbriae of certain bacterial species, particularly P. gingivalis, may also play a role in periodontal
pathogenesis.

– Monocytes are also stimulated by P. gingivalis FimA.

– Bacterial fimbriae are therefore, important for modifying and stimulating immune responses in the periodontium.
BACTERIAL DEOXYRIBONUCLEIC ACID AND EXTRACELLULAR DEOXYRIBONUCLEIC ACID

– Bacterial deoxyribonucleic acid (DNA) stimulates immune cells through TLR-9, which recognizes hypomethylated
CpG regions of the DNA.

– Extracellular DNA (eDNA) is a ubiquitous constituent of all biofilms and of particular interest in biofilms
associated with chronic diseases such as periodontitis.
HOST-DERIVED INFLAMMATORY MEDIATORS
CYTOKINES

– Cytokines play a fundamental role in inflammation, and they are key inflammatory mediators in
periodontal disease

– Cytokines are produced by a large number of cell types, including infiltrating inflammatory cells (e.g.,
neutrophils, macrophages, lymphocytes), as well as resident cells in the periodontium (e.g., fibroblasts,
epithelial cells)
PROSTAGLANDINS

– The prostaglandins (PGs) are a group of lipid compounds derived from arachidonic acid; a
polyunsaturated fatty acid found in the plasma membrane of most cells.

– Arachidonic acid is metabolized by cyclooxygenase-1 and 2 (COX-1 and COX-2) to generate a series of
related compounds called the prostanoids, which include the PGs, the thromboxanes, and the
prostacyclins.

– PGs are important mediators of inflammation, particularly prostaglandin E2 (PGE2), which results in
vasodilation and induces cytokine production by a variety of cell types.
MATRIX METALLOPROTEINS

– MMPs are a family of proteolytic enzymes that degrade extracellular matrix molecules such as
collagen, gelatin, and elastin. They are produced by a variety of cell types, including neutrophils,
macrophages, fibroblasts, epithelial cells, osteoblasts, and osteoclast.

– Key MMPs in periodontitis include MMP-8 and MMP-9, which are produced by neutrophils as they migrate
through the periodontal tissues, thus contributing to periodontal tissue breakdown.

– MMPs are also inhibited by the tetracycline class of antibiotics, which has led to the development of a
sub antimicrobial formulation of doxycycline as an adjunctive systemic drug treatment for
periodontitis. Doxycycline, like all the tetracyclines, possesses the ability to down regulate MMPs, and
this was recognized as representing a potential novel treatment strategy for periodontitis.
 STAGES OF
HISTOPATHOLOGY
The development of gingivitis and periodontitis can be divided into a series of stages: initial, early, established, and
advanced lesions
 INITIAL LESION

◦ During the initial lesion, an acute exudative

vasculitis in the plexus of the venules lateral to the
junctional epithelium, migration of
polymorphonuclear (PMN) cells through the
junctional epithelium into the gingival sulcus, co-
exudation of fluid from the sulcus, and the loss of
perivascular collagen were observed.
 EARLY LESION

◦ This lesion is characterized by a dense

infiltrate of T lymphocytes and other
mononuclear cells, as well as by the
pathological alteration of the fibroblasts
 ESTABLISHED LESION

◦ This lesion is dominated by activated B cells (plasma cells) and

accompanied by further loss of the marginal gingival
connective tissue matrix, but no bone loss is yet detectable.

◦ Several PMN continue to migrate through the junctional

epithelium, and the gingival pocket is gradually established.
 ADVANCED LESION
◦ In the advanced lesion, plasma cells continue to predominate
as the architecture of the gingival tissue is disturbed, together
with the destruction of the alveolar bone and periodontal
ligament.

◦ It is characterized by a conversion of junctional epithelium

to the pocket epithelium, formation of denser inflammatory
infiltrate composed of plasma cells and macrophages, loss of
collagen attachment to the root surface, and resorption of the
alveolar bone 
 PATHOGENESIS OF
BONE DESTRUCTION
The pattern of bone destruction that occurs depends on the pathway of
inflammation as it spreads from gingiva into the alveolar bone.

It is important to understand the changes that occur in the alveolar bone

because it is the reduction in bone height that eventually results in tooth
loss.
 CHANGE IN ALVEOLAR BONE HEIGHT IN DISEASE
1. REDUCTION IN BONE HEIGHT
A. Bone height in Health and Gingivitis
- in health and gingivitis, the crest of the alveolar bone is located
approximately 2 mm apical to the CEJ’s of the teeth.
 B.Bone height in Periodontitis
- bone destruction in Periodontitis may be severe.

- as periodontal diseases progresses, tooth loss may occur from lack of alveolar bone
support.
PATTERNS OF BONE LOSS IN PERIODONTITIS
1. HORIZONTAL BONE LOSS
- most common pattern of bone loss

- results in fairly even overall reduction

in the height of the alveolar bone

- alveolar bone is reduced in height,

but the margin of the alveolar crest
remains more or less perpendicular to
the long axis of the tooth
2. VERTICAL BONE LOSS
(ANGULAR BONE LOSS)

- less common pattern of bone loss

- in an uneven reduction in the height
of the alveolar bone
- the resorption progresses more
rapidly in the bone next to the root
surface
- the uneven pattern of bone loss
leaves a trenchlike area of missing
bone alongside the root
PATHWAYS OF INFLAMMATION INTO THE ALVEOLAR BONE

A. Pathway of Inflammation in Horizontal Bone Loss

- inflammation spreads in this order:
A. Pathway of Inflammation in Vertical Bone Loss
- inflammation spreads in this order:
 BONE DEFECTS IN PERIODONTAL DISEASE
A. INFRABONY DEFECTS
- results when bone resorption occurs in an uneven, oblique direction
- the bone resorption primarily affects one tooth.
- infrabony defects are classified on the basis of the number of osseous walls, it may have one, two, or
three walls
B. OSSEOUS CRATERS
- bowl-shaped defect in the interdental alveolar bone, with bone loss nearly equal on the roots of two adjacent
teeth
- presence of an osseous crater causes dental plaque biofilm to collect and makes it difficult to clean the
interdental area
 BONE LOSS IN FURCATION AREAS

- Furcation involvement occurs on a

multirooted tooth when periodontal
infection invades the area between and
around the roots, resulting in a loss of
alveolar bone between the roots of the
teeth.

- Bone loss in the furcation area may be

hidden by the gingival tissue or may be
clinically visible in the mouth.