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The Warning Signs of Pulpal Insult   A New Diagnostic Perspective on Pulpal Insults and Early Warning Signs of PathologyAs...
showed a 17.7% incidence of pulpal                                     Over-restored tooth   morbidity. They further repor...
the chamber space, increasing fibrosis,                     pathognomonic indicator of chroniccellular density and inducin...
Loss of Lamina Dura: When the apical orperiradicular lamina dura begins to                                                ...
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The warning signs of pulpal insult


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  1. 1. The Warning Signs of Pulpal Insult A New Diagnostic Perspective on Pulpal Insults and Early Warning Signs of PathologyAs patients gain a better understanding of euphemistically stated that, “after the 20rejuvenative and reconstructive dentistry, insults of crown preparation, there has to beour diagnostic skill set will need to expand to an element of suspicion about the viability ofanticipate unexpected problems. the pulp. We must comb bite wings for signsConceptually, there is little difference of pathology, not just decay, recurrent orbetween appreciating that a poor diet and virgin and then pursue an evaluation oflack of exercise causes atherosclerotic pulpal health”.problems and the fact that restorative insultand resultant degenerative pulpal pathosis The following warning signs of pulpalcan exist in the absence of symptoms. The insult offer a new diagnostic paradigm:description “stressed pulp” carries with it abiologic understanding of the daily insults Deep restorations: The placement of gold,and iatrogenic vectors visited upon our alloy, porcelain and resin restorations neardentition throughout a lifetime. the pulp precipitate irreversible inflammatory changes. It is relatively simple to un-We examine our adolescent patients, find knowingly nick a pulp horn in a deep pre-tooth decay, drill it out, scrape the dentine to paration and unless there is hemorrhage, itremove all carious tooth structure, place a may never be realized. It is the bitewingbase, acid etch the enamel, the dentine, radiography that reveals this potentialexpose the dentinal tubuli, place a primer, pathologic vector most dramatically.thoroughly air dry the preparation, place anunfilled resin adhesive, condense the finalmaterial into the preparation, then heat it up Pulp test, notadjusting the occlusion and contouring it, crown prep;then again polishing it to luster. The patient historical impact onthen goes through 600,000 chewing cycles, pulp must be factored into thepounding away all night, bruxing and equationclenching, then we do it all again, eight toten years later.At age 35, we drill out the old filling material,for the second time, heat up the pulp once Large/Multiple Restorations: Theagain, scrape the decay, place anotherrestoration, shave all the enamel off with a larger the restoration, the greater therough diamond bur spinning at 500,000 rpm, ratio of filling material to tooth, thecreate a significant amount of heat within the greater the number of dentinal tubuli cutpulp, place an acrylic transitional, allow it to and the greater the number of odonto-get hot, take it on and off the tooth 8 or 10 blastic processes exposed and availabletimes, then exert significant pressures for contamination. An adult pulp or oneseating the restoration and finally insulting induced to age by large/multiplethe pulp with an irritating luting material. It’s restorations lacks the resistance ofnot altogether a pretty picture. “younger” tissue. As the reparative potential of pulp in a pre-viously filledIt was Abou-Rass who defined the stressed tooth is dramatically reduced, care mustpulp as one that over the years has beencompromised by caries and periodontitis, be exercised in crown preparation.trauma – impact, occlusal and iatral, and he 1
  2. 2. showed a 17.7% incidence of pulpal Over-restored tooth morbidity. They further reported that pulpal – pulpal viability? insult can continue undetected for many Fractures are years. Among restored teeth that became occlusally induced endodontically involved for no know reason only 12% deteriorated in the first three years after restorative treatment. That necrosis rate increased to 38% in years 3 to 7 and 50% by years 7 to 12.Crowns, Inlays and Onlays: The firstquestion to be asked in regard to assessing Deep Bases: Bases rather than protectingpulpal status is why are you crowning the the pulp are irritants designed to stimulatetooth in the first place. Usually, the tooth has secondary reparative dentine formation.a failing restoration greater in size than two- They cause atrophy, pulposis and prematurethirds the intercuspal distance or perhaps a aging of the pulp. The combined insult offractured cusp. The tooth probably has a chasing deep decay toward the pulp, thedeep base and has been restored once or iatrogenic trauma of scraping the dentinaltwice in the past. It is not an infrequent walls with decay and the irritative propertiesoccurrence to prepare a tooth, have the of the base itself as well as the pulpalpatient indicate thermal sensitivity for a inflammation that ensues that causesperiod of 7 to 10 days only to have it irreversible pulpal changes and inflam-disappear. Sadly, this does not reflect matory reactions leading to pulpal Endodontic involvement increases inproportion to the degree of dentaldestruction and the complexity of therestoration. Pulp cap Direct or indirect Deep Base Rx for trouble 50% of crowns within 7 to 12 years will have Canal Constriction: This reflects increased necrotic pulps fibrosis in the root canal space and loss of pulpal volume. The pulp is being strangled as secondary reparative dentine deposits and infarction ensues. Atrophied canals found in 1.6, exist in 1.7. As canals calcify coronal apically, access and magnification are key.Teeth treated with a buildup and full veneerbecome necrotic roughly 3 x more frequentlythan those treated with a partial coveragecrown. Cohen and Burns in Pathways of the Chamber Constriction: Irritation fromPulp indicate that research has shown that a trauma, bruxism, deep bases andhigher incidence of pulpal necrosis is restorations induce inflammatoryassociated with full crown preparation responses resulting in chamber(13.3%) as compared to partial veneer constriction. The odontoid layer of therestorations (5.1%). The placement offoundations for full crown restorations pulp deposits secondary reparative dentine precipitating the shrinkage of 2
  3. 3. the chamber space, increasing fibrosis, pathognomonic indicator of chroniccellular density and inducing pulpal inflammation.strangulation and infarction. Simultaneous blastic and Deep restorations - clastic activity at separate pulpal response - apices of same tooth pulpal atrophy Widened Pulp Spaces: In many cases,Often, these take the form of adhesions and trauma can cause widened pulp spacespulp stones. Pulpal atrophy is a normal rather than dystrophic canal obliteration.component of aging as there is a relative They may remain dormant for a con-increase in the amount of collagen as well siderable period of time until one day theyas a decrease in collagen solubility and manifest as an excruciating abscess withchemical reactivity. Chronologic age and associated periapical inflammation andphysiologic age are mutually exclusive. swelling.Aged pulps characterized by densecollagenous fibrous bundles, mineralizationand cellular dystrophy or disappearancemay occur in young individuals with a history Compare coronalof poor hygiene and multiple replacement of canal space inrestorations in the same tooth. decayed 1.3 to comparable level in 1.4 and 1.5Pulp Stones: Dystrophic calcification as aresult direct, idiopathic or iatrogenic insultmanifests within the stroma of the pulpchamber as the pulp calcifies foci of necroticcells. Occlusal disharmony is yet another PDL Widening: Widening of the PDLprimary cause of this problem. The results from incipient pulpal death andexistence of occluding stones should create expression of the exudates from the canala “danger sign” in regard to the vitality of space into the surrounding tissues. Long-that particular tooth prior to initiating further term degeneration leads to pain, swellingrestorative procedures. and diffuse infection. Anticipation of this occurrence through the use of bitewings to predict the impact of large restorations, deep bases and restorations, crowns, inlays, onlays, chamber or canal constriction obviates the patient’s potential for distress. Loss of lamina dura reflects end stage pulpal degenerationFocal Sclerosis/Condensing Osteitis: with extension throughCondensing osteitis is the manner in which portals of exitthe body protects itself from chronic injury,recurring low-grade infection and longstanding periapical infection. Oftenasymptomatic, it is nonetheless a 3
  4. 4. Loss of Lamina Dura: When the apical orperiradicular lamina dura begins to Periodontal disease, moredisappear radiographically, pulpal deleterious to pulp than bothdegeneration is occurring and the exudates caries and restorationsare starting to infiltrate the surrounding combined. The extravascular communication with thestructures. Both the PDL and the lamina intravascular web is adura are being compromised. physiologic continuum that predicates success and failure.Pins: The advent of adhesion systems to agreater degree has obviated the use of pinsin restorations; however, there was an entiregeneration of teeth whose structural integritywas compromised by the placement ofdentinal pins for retention. The trauma of It’s intriguing that many of the warning signspreparation of the pin hole and the insult of are easily identified on a cursory recall examplacement affected an already stressed pulp bitewing film. The nutritional complex thatand in the case where they were serves the pulp is located in the pulp chamber and not specifically at the apical extent of the tooth and as such it is the Pins either cause a significant number control mechanism of health and disease. of pulp exposures Pulpal strangulation is a coronal not an or weaken strategic apical phenomenon. It is this change in parts of the coronal treatment and diagnostic philosophy that will tooth structure. alter the paradigm of rejuvenative and reconstructive dentistry and provide more predictable treatment vistas in the years toinadvertently inserted directly into the pulp, come.the irritation vector was maximized. Ingle,Bakland et al (1994) evaluating extractedteeth with pins in a study showed that eventhe smallest pins caused pulp exposure 40%of the time. If one extrapolates the finding of www.endosolns.coma Chapel Hill study where one regular pin Vol 1(1); 2006placed produced cracks that extended intothe pulp 73% of the time to two pins, theincidence of pulp exposure increases to95% of the time and with three pins 98% ofthe time. Thanks goodness for the adhesionera.Periodontal Disease: The pulpalconsequences of periodontal diseases areoften overlooked. The damage to the pulp interms of atrophy is often catastrophic. Onceperiodontal disease and gingival recessionhave exposed the cemental root surface ofthe tooth, many portals of entry, lateralcanals and tubuli are opened making thetooth vulnerable to the toxins accompanyingperiodontal disease. 4