Transcript ISTOLOGY
H ISTOLOGY I NFLAMMATION Ma. Concepcion B. Medina, DDM. Oral Medicine Section College of Dentistry, University of the Philippines Manila Taft Avenue corner Pedro Gil St., Ermita, Manila Features of the Pulp • Low compliance environment • Nature of its blood supply • High pulpal tissue fluid pressure - Effect on DF flow? • Fluid in tubules • Protective mechanisms Protective Response of Pulp to Caries 1. Decrease in permeability Kim, et.al., 2002 Caries dentin is demineralized Precipitation of minerals Stimulation of odontoblasts Sclerosis Protective Response of Pulp to Caries 1. Decrease in permeability 2. Tertiary dentin formation Kim, et.al., 2002 Tertiary dentin Protective Response of Pulp to Caries 1. Decrease in permeability 2. Tertiary dentin formation Where 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 Caries 1. Decrease in permeability 2. Tertiary dentin formation 3. Inflammatory and adaptive immune reactions Kim, et.al., 2002 Immune Response • Innate immune response Macrophages First line of defense PMNs adaptive response Initiates • Adaptive immune response Lymphocytes Injury: bacteria by products Odontoblasts cytokines Afferent nerves neuropeptides Cells mediators of inflammation INFLAMMATION Inflammation • Vascular, cellular, neurogenic response to injury • Acute phase – “exudative” • Chronic phase – “proliferative” • Protective reaction, BUT … Vascular changes Injury VC VD Blood volume PCAPILLARIES Permeability redness heat Plasma extravasation Vascular changes Plasma extravasation Swelling PT Reversible P 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 changes Plasma extravasation Swelling PT > PBV Blood flow Reversible Vascular changes Blood flow P02 PCO2 pH Necrosis Pus formation = microabscess microabscess inflammation inflammation Irreversible “Injury” Necrosed Vascular changes Blood flow P02 PCO2 pH Necrosis Pus formation = microabscess Cellular changes Blood flow Pavementing Emigration Proteolytic enzymes Microabscess WBCs (PMNs) Margination Aggregation Phagocytosis Injury: bacteria by products Odontoblasts chemokines Afferent nerves neuropeptides Cells mediators of inflammation INFLAMMATION Neurogenic changes Neuropeptides • Cause VD, inc. (sensory vascular nerves) permeability, pain modulation CGRP, SP, VIP, • Regulate chemokine production Neuropeptide Y, by pulp cells Neurokinin A • Promote wound healing Injury: bacteria by products Odontoblasts chemokines Afferent nerves neuropeptides Cells mediators of inflammation INFLAMMATION •Mediators of inflammation Histamine VD; inc. vascular permeability Cytokines Kinins pain Periradicular Lesions Bacteria &/or by products apical foramen Inflammation : Neuropeptides Macrophages Chemokines PMNs Osteoclasts Inflammatory mediators Lymphocytes Fibroblasts Periradicular Lesions Other likely inducers of chemokine production in PLs: Trauma Injury from instrumentation Irritation from endo materials Silva, et.al., 2007 Periradicular Lesions Injury VC VD Blood volume PCAPILLARIES Permeability redness heat Plasma extravasation Periradicular Lesions Plasma extravasation Inflammatory exudate Intraperiapical pressure (+) percussion Periradicular Lesions Plasma extravasation Swelling PT > PBV Blood flow Periradicular Lesions Blood flow Necrosis Pus formation (+) palpation P02 PCO2 pH Chronic state •Lymphocytes •Plasma cells Adaptive IR •Fibroblasts Collagen synthesis + new blood vessels = GRANULATION TISSUE 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 o 3 D 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 odontoblastlike 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 volume reparative ability Heyeraas, et.al, 2001 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. nd principal 2 most The threat significant to pulp threat health is the treatment is caries. of caries. Ingle, et.al., 2008 Ingle, et.al., 2008 References Cohen S and Burns R: Pathways of the Pulp 8th ed., 2002. Cohen and Hargreaves: Pathways of the Pulp 9th ed., 2006. Walton R and Torabinejad M: Principles and Practice of Endodontics, 2002 and 2009. References Janeway C and Travers P: Immunobiology 3rd ed., 1997. Ingle, et.al.: Ingle’s Endodontics 6 2008. Quintessence International 2001 Vol. 32: Pulp-dentin Biology in Restorative Dentistry 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 Journal of Dental Research 2007 Vol. 86, No. 4 Chemokines in Oral Inflammatory Diseases: Apical Periodontitis and Periodontal Disease Silva, et.al.