ISTOLOGY

Ma. Concepcion B. Medina, DDM.Oral Medicine Section

College of Dentistry, University of the Philippines ManilaTaft Avenue corner Pedro Gil St., Ermita, Manila

HI NFLAMMATION

Features of the Pulp• Low compliance environment

• Nature of its blood supply

• High pulpal tissue fluid pressure• Fluid in tubules

- Effect on DF flow?

• Protective mechanisms

Protective Response of Pulp to Caries1. Decrease in permeability

Kim, et.al., 2002

Sclerosis

Caries dentin is demineralized Precipitation of minerals

Stimulation of odontoblasts

Sclerosis

Protective Response of Pulp to Caries1. Decrease in permeability

2. Tertiary dentin formation

Kim, et.al., 2002

Tertiary dentin

Protective Response of Pulp to Caries1. Decrease in permeability

2. Tertiary dentin formationWhere formed?

Which histologic feature of the pulp is involved?

Mechanism?

Caries dentin is demineralized dentin proteins released Cytokine expression by pulp cells (odontoblasts, fibroblasts, dendritic cells) – IL-8 for PMNs; those that induce vascular permeability, promote dentinogenesis & repair, arrest caries progression (TNF, GFs)

Barkhorder, et.al, 1999; Tyler, et.al., 1999; Lim, et.al, 1994

Protective Response of Pulp to Caries1. Decrease in permeability2. Tertiary dentin formation

3. Inflammatory and adaptive immune reactions

Kim, et.al., 2002

• Innate immune response

• Adaptive immune response

Immune Response

Macrophages

PMNs

Lymphocytes

First line of defense

Initiates adaptive response

Injury: bacteria by productsOdontoblasts

Afferent nerves

Cells

INFLAMMATION

cytokines

neuropeptides

mediators of inflammation

• Vascular, cellular, neurogenic response to injury

• Acute phase – “exudative”

• Chronic phase – “proliferative”

• Protective reaction, BUT …

Inflammation

Vascular changesInjury VC VD

Plasma extravasation

Blood volumePCAPILLARIES

Permeability

redness heat

Vascular changesPlasma extravasation

Swelling

PT

ReversibleP nerves

localized inflammation (reversible)

remove cause

healing

Countermeasures vs increase in PT • Increased absorption by capillaries in adjacent uninflamed areas

• Increased lymphatic drainage

• No further filtration from capillaries

REMOVE CAUSE HEALING

Vascular changesPlasma extravasation

Swelling

PT PBV >Blood flow

Reversible

Vascular changesBlood flow P02

PCO2

pHNecrosis

Pus formation = microabscess

microabscessinflammation

Irreversible

Necrosed

inflammation

“Injury”

Vascular changesBlood flow P02

PCO2

pHNecrosis

Pus formation = microabscess

Cellular changesBlood flow

WBCs (PMNs)

Margination

Emigration

Phagocytosis

Pavementing

Aggregation

Proteolytic enzymes

Microabscess

Injury: bacteria by productsOdontoblasts

Afferent nerves

Cells

INFLAMMATION

chemokines

neuropeptides

mediators of inflammation

neuropeptides

Neurogenic changes• Neuropeptides (sensory nerves)

CGRP, SP, VIP,

Neuropeptide Y,

Neurokinin A

• Cause VD, inc. vascular permeability, pain modulation

• Regulate chemokine production by pulp cells

• Promote wound healing

Injury: bacteria by productsOdontoblasts

Afferent nerves

Cells

INFLAMMATION

chemokines

neuropeptides

mediators of inflammationmediators of inflammation

•Mediators of inflammationHistamine VD; inc. vascular permeabilityCytokines Kinins pain

Periradicular LesionsBacteria &/or by products

apical foramenInflammation :

Neuropeptides Chemokines

Inflammatory mediatorsChemokines Macrophages

PMNs Lymphocytes

Macrophages Osteoclasts Fibroblasts

Other likely inducers of chemokine production in PLs:

Periradicular Lesions

TraumaInjury from instrumentation

Irritation from endo materials

Silva, et.al., 2007

Injury VC VD

Plasma extravasation

Blood volumePCAPILLARIES

Permeability

redness heat

Periradicular Lesions

Plasma extravasation

Periradicular Lesions

Inflammatory exudate

Intraperiapical pressure

(+) percussion

Plasma extravasation

Swelling

PT PBV >Blood flow

Periradicular Lesions

Blood flow P02

PCO2

pHNecrosis

Pus formation

Periradicular Lesions

(+) palpation

Chronic state•Lymphocytes

•Plasma cells

•FibroblastsCollagen synthesis +

new blood vessels =

GRANULATION TISSUE

Adaptive IR

Chronic state• Granuloma

• Cyst

Localized abscess formation (grinding of rat molars)

12-24 hrs. phagocytosis

48 hrs. collagen synthesis by newly differentiated odontoblasts

Sveen, 1972

Localized abscess formation (grinding of rat molars)3-8 days mineralization 3oD or scar tissue formation

The inflammation that resulted from the inflicted trauma resolved.

Sveen, 1972

Localized abscess formation (humans)19 days post-injury differentiation of odontoblast-like cells

100 days reparative dentin barrier 0.12 mm. thick

Clinical implications• Healing may take place as a result of timely intervention.

(pre-injury status of pulp)

• Minimize trauma to provide the best possible opportunities for future pulpal healing.

Heyeraas, et.al, 2001

Clinical implications• Healing may take place as a result of timely intervention.

• Healing may be in the form of 3oD or scar tissue formation

Heyeraas, et.al, 2001

volume reparative ability

Clinical implications• Minimize trauma

Effective water cooling system

Light, intermittent pressure

Avoid prolonged air drying

Summary

• Inflammation is a protective response.

• Healing will take place if the cause is removed (ie., the cavity is cleaned and restored).

Summary

• It is the clinician’s duty to minimize trauma to the pulp during restorative procedures.

The principal threat to pulp health is caries. Ingle, et.al., 2008

The 2nd most significant threat is the treatment of caries.

Ingle, et.al., 2008

Cohen S and Burns R: Pathways of the Pulp 8th ed., 2002.

Walton R and Torabinejad M: Principles and Practice of Endodontics, 2002 and 2009.

References

Cohen and Hargreaves: Pathways of the Pulp 9th ed., 2006.

Janeway C and Travers P: Immunobiology 3rd ed., 1997.

References

Ingle, et.al.: Ingle’s Endodontics 6 2008.

Part 1. Normal structure and physiology. #6 pp. 427-446 Part 2. Initial reactions to preparation of teeth for restorative procedures. #7 pp. 537-551 Part 3. Pulpal inflammation and its sequelae. #8 pp. 611-625

Quintessence International 2001 Vol. 32: Pulp-dentin Biology in Restorative Dentistry

Chemokines in Oral Inflammatory Diseases: Apical Periodontitis and Periodontal Disease Silva, et.al.

Journal of Dental Research 2007 Vol. 86, No. 4