Histology and Physiology of the dental pulp Inflammation Prof. MUDr. M. Kukletová • Nature of inflammatory response • Inflammation is the reaction of living tissue to any type of injury • Mobilization and coordination of • vascular • neurologic processes • cellular • humoral Pathway of entry of microorganisms into the dental pulp • caries • trauma • from surrroundins • accessory root canals • retrograde (periodontal pockets) • anachoresis • Neurogenic pulpitis -irritation - traumatic occlusion • Objectives - to destroy the irritant • to neutralize it by dilution • heat • redness (rubor) • swelling (tumor) • pain (dolor) • loss of function (functio laesa) • to set the stage for repair Exudative - acute response • Initial response of the pulpal tissue to any irritant • mechanical, chemical, thermal, microbial • Emergency action - to neutralize the injurious action by: • an influx of fluid exudate (inflammatory edema) to dilute and detoxify • white cells (neutrofiles) to ingest and immobilize Proliferative (chronic) response • secondary (delayed) action • connective tissue forms • new cells (fibroblasts) • blood vessels and fibres • granulation tissue - formed to replace and repair the damaged tissue • granulomatous tissue = granulation tissue + lymphocytes, plasma cells, macrophages in great quantities • It is a defense tissue - microorganisms are destroyed • Primary factors that initiate the acute inflammation • Responsible for inflammation: • Neurogenic factor (neural response) • Tissue injury factor (cellular response) • The neurogenic factor - activation of neural response by environmental irritants (mechanical, chemical, microbial) • may cause • immediate and transient pain perception - result of nerve fibers irritation • vasodilatation - persists = increase in capillary permeability, fluid exudation, leucocytes infiltration= beginning of the exudative phase • increased intrapulpal pressure = result of the increased blood volume (hyperemia) and tissue exudate • secondary (spontaneous) pain response (C fibers) • The pain persists - the presence of necrotic tissue • The tissue injury factor - is due to release of mediators by the injured odontoblasts • chemical substances • the same effect as the nerve factor • prolonged vasodilatation, fluid exudation, leucocytes infiltration, increase of intrapulpal volume and pressure, pain Inflammation of the dental pulp • According to the nature • Reversible • Irreversible Reversible pulpitis - Hyperemia • Capillary bed - enlargement, vasodilatation, elevated capillary pressure, increased vascular permeability, potentially reversible response Irreversible pulpitis Acute - hyperactivity of exudative forces polymorphonuclear leucocytes, later macrophage Chronic - proliferative phase granulomatous tissue pain is usually absent lymphocytes, plasma cells, macrophages limited number of PMNS • Duration and severity • acute • chronic • subacute • Presence/absence of pain • painful • non painful acute chronic partial serous suppurative open ulcerative polypous total serous suppurative closed retrograde Acute - hyperactivity of exudative forces polymorphonuclear leucocytes, later macrophage Chronic - proliferative phase granulomatous tissue pain is usually absent lymphocytes, plasma cells, macrophages limited number of PMNS • Irreversible – painful pulpitis • acute pulpitis • subacute pulpitis – nonpainful pulpitis • chronic ulcerative pulpitis (due to caries) • chronic pulpitis (no caries) • chronic hyperplastic pulpitis (pulp polyp) Additional pulp changes • retrogressive changes – atrophy, fibrosis, vacuolization of odontoblasts, hyalinization • dystrophic calcification • pulp stones – internal resorption (sequel to persistent chronic inflammation) Necrosis • Is a sequel of acute and chronic inflammation • liquefaction necrosis • coagulation necrosis • products of necrosis - toxic to the periapical tissues = • inflammatory response, abscess formation, without the presence of microbes • anaerobic bacteria - decomposition of proteins Gangrene • Intermediate proteolytic products = Foul odour – indol, scatol – putrescin, cadaverin – indican • End products – hydrogen sulphide – ammonia • Endotoxins from bacteria • Foreign bacterial proteins