Pathogenesis of periodontal

disease
By
Dr Kamlesh Singh
 Why?
Neutrophil s/n
Stages of pathogenesis s/n

Date 06/02/2018, 20 February 2018, 27/2/2018, 21 Feb.

2020, 23/2/2021, 3/3/2021, 20/10/2021
 Definition

Biological mechanism that leads to the diseased state

Etiology factor:

Dental plaque
Microbial challenge
 V. parvula Socransky et al. 1998
A. odontolyticus
S. mitis C. rectus
S. oralis C. gracilis
S. sanguis
P. intermedia
S. gordonii P. nigrescens P. gingivalis
S. intermedius P. micros E. nodatum B. forsythus
S. constellatus
F. nucleatum T. denticola
F. periodonticum

E. corrodens
C. showae
C. gingivalis
C. sputigena
S. noxia
C. ochracea
A. actino. a A. actino. b ***
p. gingivalis, t. forsythia, t. denticolla
 Presence of bacteria

•Inflammation
•
Clinical healthy gingival tissues

• Excellent oral hygiene, no visible

plaque.
• Junctional epithelium(non
keratinized)
1. Lies at -----------
2. It is a unique epithelium structure-
attached to the tooth.
• Extracellular space between the
junctional epithelium are also greater
than other epithelium. Low density
of desmosomes.
• Widen intercellular space- pmn and
macropha, gcf outflow(dilution effect
and flushing action).
• Presence of PMN in junctional epith
 Stages in pathogenesis(short note)

• Initial lesion

• Early lesion

• Established lesion

• Advanced lesion
 Initial lesion : clinical healthy gingiva

• 2-4 days.

• Slight elevated vascular permeability, vaso.

• Dilated vessels and blood flow increased- increa GCF

• Exudation of fluid in to the sulcus

• Increased migration of leucocytes into the J.E and sulcus

• Loss of peri-vascular collagen.

Initial lesion
 Early lesion: early gingivitis that is evident
clinically

1 week

Increased Vascular permeability, vasodilation, proliferation.

Infiltration by PMN and LYMPHOCYTES CELLS

Increase collagen loss

Rete pege in junctional epi

BOP (MCQ), ERYTHEMA

Early lesion
 Established lesion: chronic gingivitis

14 – 21 days

• Predominance of plasma cells (MCQ) with out bone loss..

• Presence of immunoglobulin extra vascularly…

• Continuing loss of C.T

• Proliferation, apical migration and lateral extension of J.E

established
 Advanced lesion;transition from gingivitis to
periodontitis
• Persistence of features…
• Extension of lesion into alveolar bone and PDL
• Continued loss of collagen… and fibrosis at different sites..
• Plasma cell in C.T
• Epithelium and gingival sulcus: PMN
Advanced
 Histology of J.E

• Dense infiltration pmn

• Rete peg formation
• Ulceration
• Cell lose cohesiveness
• Great majority of tissue break down results
from

• bacteria?

• Host response?
 Disease
• Host
bacteria
response
 Immunity
•
 Host response
Predominant
leucocyte

Present in
gingiva

Use
chemokines
 Neutrophils migration

• Two mechanisms

Expression of leukocyte adhesion

molecules…ICAM,ECAM
Low molecular weight cytokines
Neutrophils
 Chemo taxis
• leukotriene B 4
 Microbicidal activity

Oxygen independent Oxygen dependent

 Lysozyme  myeloperoxidase

 Lactoferrin  Chloramines

 Hydrogen peroxide
 Defensins
 Superoxide anion
 Cathepsins
 Singlet oxygen
 Azurocidin
 Hydroxyl radicals
 Complement system
• Enhancing the quality of other person or
thing
Cytokines and Chemokines
• IL 4, 10 , 11 13.
•
Risk factors
Genetic influences
Which genetic
factor ?????
•
Environmental and acquired risk factors
stress
Thank you