HOST MODULATION

By- Dr. Rupali Borade

 HOST- host can be defined as the organism from which a
parasite obtained its nourishment

MODULATION- is defined as the alteration of function or

status of something in response to stimulus or an altered
chemical or physical environment.
 The concept was 1st introduced in dentistry by willliams and
Goulb et al. and then expanded by many others.
PATHOGENESIS OF PERIODONTITIS

Periodontal disease does not appear to be a classic infection ,

but a more as an opportunistic infection.

Pathogenesis of periodontal disease is associated with

parasite- host interactions that are elicited predominantly by
plaque biofilm, endotoxins ,LPS which is a major component
of bacterial cell wall
Initiating a cascade of events.
 After accumulation of subgingival plaque bacteria , a variety
of microbial substances including chemo tactic factors such as
lipopolysacchrides, microbial peptides, and other bacterial
antigens .

Diffuses across the junctional epithelium into gingival

conn.tissue.
 Epithelial and conn. tissue cells thus stimulated to produces
inflammatory mediators which results in inflammatory
response in tissue.

Changes in gingival vasculature i.e vasodilatation leads to

increase permeability to fluids.

Migration of defence cell in GCF. neutrophils and PMNS in

early gingivitis.
 these cells phagocytose and kill plaque bacteria.
Bacterial killing by PMNs involves both

Intracellular mechanisms (after phagocytosis of bacteria

within membrane-bound structures inside the cell)

extracellular mechanisms by release of PMN enzymes and

oxygen radicals outside the cell).
 As bacterial products enter the circulation, committed
lymphocytes return to the site of infection, and It lymphocytes
are transformed to plasma cells, which produce antibodies
against specific bacterial antigens.

Antibodies are released in the gingival tissues and, in the

presence of complement, facilitate and enhance PMN
phagocytosis and bacterial killing.
 Thus, a host immune-inflammatory response is established in
the gingival tissues, and the clinical signs of gingivitis
develop.

Further defence cells secrete mediators like mmps cytokinins

and prostagalndins leading to conn. tissue breakdown and
bone loss

And clinical signs of periodontitis seen.

 Host modulatory therapy can be used to interrupt these
positive feedback loops and ultimately reduce the excessive
load of inflammatory mediators and enzymes resulting in
tissue destruction.
The periodontal balance
Risk factors in periodontal disease
Host modulation therapy
Host modulatory therapy (HMT) is a treatment concept that
aims to reduce tissue destruction and stabilize or even
regenerate the periodontium by modifying or down regulating
destructive aspects of the host response and up regulating
protective or regenerative responses.

A variety of different drug classes have been evaluated as host

modulation agents, including the nonsteroidal anti
inflammatory drugs (NSAIDs), bisphosphonates,
tetracyclines, enamel matrix proteins, growth factors, and
bone morphogenetic proteins.
 Systemically administrated agents
Non steroidal anti-inflammatory drugs
Bisphosphonates
Sub antimicrobial dose of doxycycline

Locally delivered drugs

NSAIDS
Enamel matrix proteins ,growth factors
Bone morphogennic proteins
 NSAIDs .
Inhibit formation of prostaglandins E2.
Produced by fibroblasts, neutrophils, macrophages and
gingival epithelial cells.

Reduce inflammatory response and inhibit osteoclastic

activity.
 Bisphosphonates
Bone seeking agents inhibit bone resorption by disrupting
osteoclastic activity
Mechanism action is unknown but they interfere with
osteoblast metabolism and secretion of lysosomal enzymes .
 SDD-
Previously called as low-dose doxycycline" (LDD)
Subantimicrobial dose doxycycline is 20mg dose of
doxycycline.
Periostat
Use as an adjunctive to SRP in treatment of chronic
periodontitis.
Dose- twice daily for 3 months ,up to maximum 9 months of
continues dosing.
 Effect by enzyme ,cytokine, and osteoclast inhibition rather
than antibiotic effect.
 Locally administrated drugs- NSAIDs

Enamel matrix proteins (emdogain)

Bone morphogenic proteins (BMP-2,BMP-7)
Growth factors like platelet derived growth factor
Insulin like growth factor and tetracycline.
THANK YOU