Summary

This document provides a detailed overview of dental pulp diseases, covering topics such as classifications, causes, symptoms, and treatment options. It delves into the anatomical and histological aspects relevant to various types of pulpitis, highlighting the clinical features and the diagnostic considerations in the management of these conditions.

Full Transcript

Dental pulp The dental pulp is a delicate connective tissue (CT) interspersed with tiny blood vessels, lymphatices, myelinated and unmyelinated nerves and undifferentia...

Dental pulp The dental pulp is a delicate connective tissue (CT) interspersed with tiny blood vessels, lymphatices, myelinated and unmyelinated nerves and undifferentiated CT. Like other CT, throughout the body, it reacts to bacterialinfectionor to other stimuli by an inflammatory response. Certain anatomic faturs of this specialized CT, howevr, tend to aletcr the nature and course of this response. The enclosure of the pulp tissue within the calcified walls of the dentin precludes the excessive swelling of tissue that occurs in the hyperemic and edematous phases of inflammation in other tissues. The fact that the blood vessels supplying the pulp tissue must enter the tooth through the tiny apical foramen prevents the development of an extensive collateral blood supply to the inflamed part. Etiology of pulp diseases: I- Most cases of pulpitis are a result of dental caries in which the bacterial invasion of the dentine and pulp tissue occur. However, many authors reported that changes in the pulp may occur in very early dental caries, repoted that changes in the pulp may occur even with very early dental cares, represented by demineralizationlimited to the enamel alone, appearing as (white spots) without actual activation. 2-Bacterial invasion in absenc of caries, as in case of tooth fracture that exposed the pulp tissue to oral fluid and microorganisms. 3- Bacterial invasion as a result bacteremia (bacterial circulating in the blood stream) tend to settle out at sites of pulpal inflammation, such as that which might follow some chemical or mechanical injury to the pulp , it was termed (anachoretic pulpitis) Although anachoresis represents a distinct mechanism for bacterial infection of an intact pulp. 4-chemical irritation of the pulp, e.g. irritating filling material. So it occurs in both exposed and unexposed pulp. 5- sever thermal changes in togth, As in.teeth with large metallic restorations, particularly when there is inadequate isolation. 6- Electrosurgical current on metallic restorations produces major damage to both pulp and peridontal tissue. 7- Aerodontologia: a condition clinically simulating pulpitis was reported in world war Il in flying personnel at high attitudes, it is associated with recently filled tooth. Classification of pulp diseases; * -Acute pulpitis - Chronic pulpitis -18- Depends on the extent of inflammation: -partial pulpitis total pulpitis Depends on the communication to oral cavity: -open pulpitis -closed pulpitis l- Focal reversible pulpitis(pulp hyperemia) It is one of the earliest form of pulpitis CLnical Picture: The-tooth is sensitive to thermal changes, particularly cold. this pain disappears The application of ice or cold fluids to the tooth results in pain but temperature. upon removal ofthennal irritant or restoration of the normal current It respondsto stimulationby the electric pulp tester at a lower level of (indicating a lower pain threshold or greater sensitivity than that of the adjacent normal tooth). The tooth shows: -a) deep carious lesions -b) large metallic restorations, particularly without adequate isolation or restorations with defect margins. Histopathological features: Dilatation of the pulp vessels. Edema fluid may collect because of damage to the capillary walls, allowing actual extravasation of RBCs or some diapedesis of WBCs. Slowing of the blood flow & haemoconcentation due to transduction of fluid from the vessels could cause thrombosisive margins. Treatment& prognosis: It is reversible condition, provided focal pulpitis. so the carious lesion should be excised and restored & defective filling should be replaced as soon as it is discovred. If the primary cause is not corrected,extensive pulpitis will result, with subsequent death of the pulp. 2-Aute pulpitis Extensive acute inflammation of the pulp, it is frequent immediate sequelae Of focal reversible pulpitis, although it may also occur as an acute exacerbation of chronic inflammation. -19- Clinical features: acute pulpitis usually occurs in a tooth with a large carious lesion or a restoration. Sever pain is elicatd by thermal changes, particularlynthos caused by ice or cold fluids (this pain persists even after removing the stimulus). As agreat portion of the pulp becomes involvedwith intrapulpal abscess formation, the painmay become even more sever and is often described may be as a (lancinating type), it contiuous and its intensity may increased when the patient lies down. - The application of heat may cause an acute exacerbation of pain. The tooth reacts to the electric pulp tester at a lower level of current, indicating increased sensitivity of the pulp. When necrosis of pulp tissue occurs, this sensitivity is lost. If the entrance to diseased pulp not wide open pressure increase because of lack of escape of inflammatory exudates causing rapid spread of inflammation throughout the pulp with pain & necrosis. In case of large open cavity, there no opportunity for a build —upof preasure.thus the inflammatory process does not tend to spread rapidly throughout the pulp. In such cas, the pain is described as (dull pain) or (throbbing ache). Until this inflammation or necrosis extends beyond thepulp tissue within the root apex, the tooth is not particularly sensitive to percussion. Histopathologic features: Early acute pulpitis is characterized by the continuedvascular dilation seen in focal reversible pulpitis, accompanied by accumulationof edema fluid in the connective tissue surrounding the tiny bood vessels. The pavementing polymorphonuclear leukocytes (PMLs) become apparent along the walls of these vascular channels, they rapidly migrate through the endothelium - lined structure, and this migration is increasing. Soon, great collection of PMLs may be found, especially beneath the area of caries penetration. By this stage,the odontoblasts in this area have usually been desroyed Early in the course of the disease, PMLs are confined to a localized area, & the remainder of the pulp tissue appears relatively normal. Even at this period ,there may be localized destruction of pulp tissue & the formation of small abscess, known as (pulp abcess), continuing pus arising from breakdown of PMLs and bacteria as well as from digestion of tissue (abscess=PMLs+ bacteria-F digestive tissue). In tissue sections, because of loss of liquid pus, this abscess frequently appears as a smallvoid surrounded by a dense band of leukocytes. Eventually in some cases, in a only a few days, the acute inflammatory process spread to involve most of the pulp so that PMLs file the pulp & the entire odontoblastic layer degenerates. If the pulp is closed to the outside, there is considerable pressure formed, and the entire pulp tissue undergoes rapid disintegration. Numerous small abscesses may form & eventually the entire pulp undergoes liquefaction & necrosis. This is sometimes referred to as "acute suppurative pupitis". The pulp, especially in the later stages of pulpitis following carious invasion, contains large numbers of bacteria. Treatment and prognosis: In very early cases of acute pulpitis involving only a limited area of tissue, there is some evidence to indicate that pulpotomy (removal of coronal pulp) and placing a bland material that favors calcification such as "calcium hydroxide" may be used in case of mechanical pulp exposure without obvious infection. Teeth involved with acute pulpitis may be treated by filling the root canals treatment (complete removal of damaged pulp tissue, ( pulpectomy) followed by root canal filling. Occasionally, acute pulpitis, especially with an open cavity may enter a chronic state,but this is unusual and appears to occur most frequently in persons who have a high tissue resistance or in case of infection with microorganisms of low virulence. 3 —Chronic pulpitis May arise from previous acute pulpitis, but may arise as chronic type from the onset. The signs & symptoms are milder than those of acute pulpitis. It is classified as open & closed pulpitis. A special form of chronic pulpitis is recognized and presents such characteristic features that its separation is deemed unwarranted.This is known as ( chronic hyperplastic pulpitis). Clinical features Pain is not prominent feature of chronic pulpitis. The pain is mild, dull ache, which is often intermittent than continuous. The reaction to thermal changes is reduced in comparison to that in acute pulpitis. The-threshold of stimulation by electric pulp tester is increased in contrast to cases of acute pulpitis because of the degeneration of the nerve tissue in the affected pulp. Pulp may be totally necrotic without pain. Histopathologic features Mononuclear cells, chiefly lymphocytes & plasma cells are usually prominent. Capillaries are usually prominent. Fibroblastic activity is evident & collagen fibers are seen, often gathered in bundles. There is sometimes an attempt by the pulp to wall off the infection through deposition of collagen about the inflamed area. -21- The tissue reaction may resemble the on the surface of the pulp, in a wide formation of granulation tissue, when this occur open exposure, the term "ulcerative pulpitis" has been applied. Microorganismsmay be found in the pulp tissue, especiallyin the area of a carious exposure. Treatment Root canal therapy, or extraction of the tooth. Chronic hyperplastic pulpitis (pulp polyp) : This form of chronic pulp disease is uncommon& occurs either as a chronic lesion from the onset or as a chronic stage of a previously acute pulpitis. Clinical features: Chronic hyperplastic pulpitis is essentially an excessive, exuberant proliferation of chronically inflamed dental pulp tissue. In children or young adult, it involves tooth with large open carious lesion. Appears as pinkish-red globule of tissue protractingfrom the pulp chamber &often filling the entire cavity. It is relatevely insensitive to manipulationbecausethe hyperplastic tissue contain few nerves. May or may not bleed, depending on the degree of vascularity of the tissue. The most commonly affected teeth are deciduousmolar & first permanent molars. They have excellent blood supply because of the large root opening,and this coupled with the high tissue resistance and reactivity in young persons.accountsfor the unusual proliferative property of the pulp. On occasions,thegingival tissue adjacent to a brokencarioustooth may proliferate into the carious lesion and superficially resemble an example of hyperplastic pulpitis. In such cases, the distinction can be made by careful examination ofthe tissue mass to determine whether the connection is with pulp or gingival. Histöpathologic features The hyperplastic tissue is basicallj granulationtissue made up of delicate CT fibres, interspersed with variable number of small capillaries. Inf. Cell infiltration, chiefly lymphocytes &plasma cells, sometimes admixed with PMLs, fibroblasts & endothelial cell proliferation is prominent. The granulation tissue commonly becomes epithelized (st.sq.epith closely resembles the oral mucosa) as a result of ; -4 implantation of epithelial cell on its surface, The grafted epithelial cells are normally desquametedcells carried by saliva to the surface of the pulp -22- --4 transplantion of epith. Cells from the bucall mucosa which may rub against the hyperplastic tissue mass and the epithelial cell become transplanted directly. Treatment: It may persist for many months or even several days. The condition is not reversible, so it may treated by extraction of tooth or pulp extirpation. 4-pulp calcification Pulp stones (or denticles) are calcified bodies with an organic matrix. It occurs mostly frequently in the coronalpulp. True pulp stones contain tubules, & may have an outer layer of predentine & adjacent odontoblasts. False pulp stones are concentric layers of calcified material with no tubular structure. According to their location in the pulp, stones may be described as free or adherent. Calcification may be either diffuse (linear) or nodular (pulp stones). Pulp stones increase in number & size with age. They don't cause symptoms, althoughneuralgicpain has sometimes been attributed to their presence. They may be problematic during endodontic therapy. 5-Gangrenous necrosis of the pulp: Untreated pulpitis, either acute or chronic, will result in complete necrosis of the pulp tissue. Since this is generally associated with bacterial infection so termed pulp gangrene, Gangrene: is necrosis of tissue due to ischemia with superimposed bacterial infection. Pulp gangrene is consideredas end result of pulpitis in which there is total necrosis of tissue. Dry gangrene: is a type of gangene occurs when the pulp dies for some unexplained reason.the nonvital pulp maintains its general histologic characteristics, being nonpurulent. This condition may be due to traumatic injur or infarct. 6- Age changes in the pulp: The volume of the pulp gradually decrease with age due to the continued production of secondary dentine. Decreased vascularity, reduction in cellularity, increase in collagen fiber content, have also been reported, and these changes may impair the response of the tissue to injury & its healig potential. The prevalence of pulp stones increases with age, but the evidence for this is inconclusive. -23-

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