Dental Pulp Disorders V. Žampachová Dental pulp npulp tissue confined to a space limited by hard tissues nno collateral circulation nbiopsies or direct application of medication impossible, would lead to entire pulp necrosis nlimited clinical signs – npain, but problematic localization nlevel of sensitivity Pulpitis ncommon inflammatory reaction npathologic external stimuli → cytokine release → vasodilatation + edema → increased pulpal pressure in the limited space → compression of venous return → possible arterial strangulation → possible necrosis + spread nnormal intrapulpal pressure 5-20 mm Hg, npulpitis → 60 mm Hg Pulpitis - causes ndental caries nirritation thermal/chemical incl. iatrogenic ntrauma ncracked tooth ncrown fracture ntraumatic pulp exposure (cavity preparation) nsecondary progression of periapical/periodontal inflammation from adjacent teeth Pulpitis - etiology nmechanical damage (trauma, dental procedure, attrition, abrasion, barotrauma) nthermal injury (in dental procedures, uninsolated metallic materials) nchemical irritation (in erosion, acidic dental materials), possible reactionary dentin formation. nbacteria (directly in caries, haematogenous; indirectly – toxins) Barotrauma (aerodontalgia) nFlying at high altitude in unpressurized aircraft, or rapid decompression in divers. nAttributed to formation of nitrogen bubbles or fat emboli in pulp tissue or vessels (decompression sy). nNot a direct cause, but rather an exacerbating cause in presence of caries. n n Pulpitis nDynamic process with continuous spectrum of changes, depending on cause and host defenses n- Acute or chronic. n- Partial or total. n- Open or closed. n- Exudative or suppurative. n- Reversible or irreversible. n nPoor correlation between microscopic changes and clinical symptoms. n Pulpitis nModifying factors: nNature, severity and duration of insult. nQuality of dental tissues (abrasion, attrition, ...) nEfficiency of host defenses. nEfficiency of pulpo-dentinal complex defenses. nreactionary dentine (pulp capping, regular tubules) nreparative dentine (irregular structure) ncalcific barriers n Pulpitis nPatient history nClinical examination nTests npercussion nheat ncold nelectric Pulpitis (clinical) nAcute pulpitis: nSevere throbbing, lancinating pain on thermal stimulation or lying down, keeps patient awake. nGenerally for 10-15 minutes (reversible pulpitis). nWith progression, may become spontaneous + continuous (irreversible pulpitis). nChronic pulpitis nBouts of dull aching, an hour or more. nPain on thermal stimulation or spontaneously. nMay be asymptomatic. n n n Acute pulpitis nprogression of focal reversible pulpitis npossible exacerbation of preexisting chronic pulpitis nusually pain constant, severe, localized nheat/cold sensitive nstage nearly – electric hyperreactivity nlate – reduced/missing response ncommonly +/- normal percussion test n Chronic pulpitis nlow grade, long term injury nintermittent, mild symptoms nno symptoms possible nreduced response to stimulation Pulpitis nMost important decision clinically is whether pulpitis is reversible or irreversible → different management. nDecision based on many factors including: nSeverity of symptoms. nDuration of symptoms. nSize of carious lesion. nPulp tests. nDirect observation during operative procedure. nAge of the patient. n Pulpitis - signs nreversible – possible regeneration; sudden short pain in local thermal and/or chemical stimuli (cold, sweet, sour); no percussion sensitivity, no change in radiograph n nirreversible – no regeneration, common bacterial invasion nearly – longer, more intensive pain, may be continuous; still may be localised nlate – severe continuous pain, radiation to jaw, face, neck, … (trigeminal irritation) Reversible pulpitis nClinical examination: nintermittent pain nvitality test: positive, „short” response nFocal change, acute nTreatment: nremoving of the offending agent nmaking a filling (or pulp capping) copy Irreversible pulpitis nAnamnesis: nmild or severe spontaneous pain ndifficult to localise nClinical examination: nvitality test: „long”, sharp response nTreatment: nroot canal treatment copy Pulpal necrosis nAnamnesis: nasymptomatic nClinical examination nvitality test: negative nTreatment: nroot canal treatment copy Hyperplastic pulpitis chronically inflammed open pulp nAnamnesis: nasymptomatic nClinical examination: nvitality test: positive nopen pulp chamber with polypous tissue nTreatment: nroot canal treatment copy Bacteria in the dentin nBacteria extending down the dentinal tubules into the pulp tissue itself 47big 48big copy Odontoblast changes 33big n Early change of the pulp as a result of some irritants. nNormal odontoblastic nuclei in the dental tubules. nCapillaries grow in the subodontoblastic zone in the presence of deep caries or a deep filling (in an intact uninflamed pulp not present). copy Pulp hyperemia n nPulpal congestion (hyperemia) multiple dilated capillaries, obliteration of the cell free zone . nOdontoblastic layer intact. nPredentine and irregular reparative dentin, probably a response to severe irritation (deep caries, filling material, tooth preparation). 34big copy Reparative dentine nSeverely inflamed pulp despite the blockage of caries progress through the primary dentin with reparative dentin 35big copy Dentine caries and pulpitis n nRelationship of pulp to caries. nDeep dentinal caries extending into pulp horn with inflammatory reaction, spread of the inflammation down the length of the canals. nThe reaction decreases with the distance from the noxious stimuli. 36big Acute pulpitis – later phase nReappearance of the odontoblastic layer, acute inflammatory reaction in the pulp still present. 40big copy Pulpitis progression nPulp abscess with penetrating caries, dark necrotic material in the pulp horn n no odontoblastic layer naccumulation of chronic inflammatory cells. 44big copy Pulp abscess nthe junction of the abscess with the remaining portion of the pulp nfibrin attempting to wall-off the abscess area, reactive macrophages, starting formation of pyogenic membrane 45big copy Chronic and acute pulpitis nJunction of the acute and chronic processes, acute inflammatory reaction; nchronic: normal-appearing pulp with slight chronic inflammation 42big copy Chronic pulpitis nCarious invasion of the pulp horn. The odontoblastic layer is intact around almost the entire periphery, n presence of congested capillaries and increased inflammatory infiltrate. 37big copy Chronic pulpitis nThin odontoblastic layer nCapillaries in the subodontoblastic cell-free zone nPredominantly chronic inflammatory infiltrate (lymphocytes, plasma cells), few neutrophils in pulpal stroma 46big copy Chronic hyperplastic pulpitis nin children, young adults nlarge open pulp chambers (molars), dentinal defect, wide apices and good blood supply nlarge carious cavities nproliferation + protrusion of granulation tissue npossible epithelialization by spontaneous grafting of desquamated oral epithelial cells from saliva. ncommonly asymptomatic, if ulcerated may bleed n Chronic hyperplastic pulpitis nRed, dome-shaped pulp polyp, predominantly in young patients, in permanent or deciduous molars n 49big Chronic hyperplastic pulpitis n 50big Chronic hyperplastic pulpitis n severe tooth destruction. 51big copy Chronic hyperplastic pulpitis nThe polypous lesion projecting out of the pulp chamber. 53big Chronic hyperplastic pulpitis ngranulation tissue with numerous capillary buds, fibroblasts and chronic inflammatory cells, ncovered by stratified squamous epithelium with reactive pseudoepiteliomatous hyperplasia 54big Chronic hyperplastic pulpitis nChronic inflammation in stroma nPeripheral resorption and repair – deposition of new cementum/bone 56big copy Effects of cavity preparation and restorative materials nCavity preparation: speed, heat, pressure and coolant may all cause pulp irritation. nAspiration or displacement of odontoblasts into dentinal tubules, with reduction of numbers (dead tracts). nPossible further complications of pulpitis caused by caries or other causes. nThickness and nature (quality, opened tubules) of remaining dentin may affect pulp response to dental material. n Pulp healing nInjured odontoblasts replaced by new cells from pulp. nPulpitis may resolve after removal of irritant. nIt may resolve due to reactionary dentine formation even without removal of caries. nPulp capping after traumatic pulp exposure or pulpotomy: calcium hydroxide agents – high pH, kill bacteria, stimulate formation of a calcified barrier (dentin). nVariable barrier quality, possible leakage of toxins n Pulp calcification n~20% on X-ray (size>200 μm) nPulp stones (denticles): calcified bodies, organic matrix n true – developmental, with tubules + odontoblasts, possible covering of predentin nfalse - concentric calcifications ngrowth with age (number, size), in trauma or caries nusually asymptomatic True denticle nnodule of dentin, secondary adherence to the pulpal surface of the tooth dentin. n 62big copy True denticle nOdontoblastic differentiation of mesenchymal cells nPrimary dentin, nwith tubules, outer layer of predentin + odontoblasts 61big copy False denticles npulp stones with concentric lamellations of growth and central nidus of debris. 57big copy Pulp calcification nDystrophic calcifications: amorphous calcified material, mostly in roots, may obstruct endodontic treatment. nIn form of diffuse linear calcifications – irregular fibrillar, parallel with nerves + vessels nNot visible on X-ray Dystrophic calcification namorphous nsurrounded by areas of congestion. 58big Dystrophic calcification nDiffuse calcifications nDystrophic calcification in or around nerves and blood vessels 59big Pulp obliteration nby irregular dentin after traumatic vessel injury not sufficient to cause necrosis. npossible in dentinogenesis imperfecta and dentinal dysplasia. n Pulp necrosis nMay follow pulpitis or trauma to apical blood vessels. nCoagulative necrosis after ischemia. nLiquefactive necrosis after pulpitis nGangrenous (with foul odor) due to infection by putrefactive caries bacteria. nPulp necrosis in sickle cell anemia (blockage of microcirculation). n Age changes in the pulp nGradual decrease in volume due to secondary dentin formation. nDecreased vascularity and cellularity. nIncreased collagen fiber content. nImpaired response to injury and healing potential. nIncrease of pulp stones and diffuse calcification. n Periapical granuloma or cyst n 034a.jpg copy Selected sources nOdell EW: Cawson‘s Essentials of Oral Pathology and Oral Medicine, 9th ed., Elsevier 2017 nRegezi JA,Sciubba JJ, Jordan RKC: Oral pathology: Clinical Pathologic Correlations, 7th ed., Elsevier 2017