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 o •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 o 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 o 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) oAdditional pulp changes •retrogressive changes –atrophy, fibrosis, vacuolization of odontoblasts, hyalinization • dystrophic calcification • pulp stones –internal resorption (sequel to persistent chronic inflammation) oNecrosis •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 oGangrene •Intermediate proteolytic products = Foul odour –indol, scatol –putrescin, cadaverin –indican •End products –hydrogen sulphide –ammonia •Endotoxins from bacteria •Foreign bacterial proteins •