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Explore Further: Topics Discussed in This Paper Book Endodontic procedure sentence Aspartate Transaminase 6 Citations Fields of Study Fields of Study All Fields Art Biology Business Computer Science Chemistry Economics Engineering Environmental Science Geography Geology History Materials Science Mathematics Medicine Philosophy Physics Political Science Psychology Sociology Citation Type Citation Type All Types Cites Results Cites Methods Cites Background Has PDF More Filters More Filters Filters Sort by Relevance Sort by Most Influenced Papers Sort by Citation Count Sort by Recency Internal Tooth Anatomy and Root Canal Instrumentation J. F. Siqueira, I. N. Rocas, D. Ricucci Medicine 2019 6 Save Alert Research Feed Clinical and radiographic success of vital pulp therapy using marginal regression model A. Akbarzadeh-baghban, M. Safari, S. Asgari, F. Zayeri Medicine 2011 Save Alert Research Feed An in vitro comparison between the apical sealing abilities of resilon with Epiphany sealer and gutta-percha with AH plus sealer. Rajan Lambor, I. D. de Ataide, P. Chalakkal, F. Akkara, S. A. Shariff, K. S. Fernandes Medicine 2012 1 View 1 excerpt, cites background Save Alert Research Feed Review of pulp sensibility tests. Part I: general information and thermal tests. H. Jafarzadeh, P. Abbott Medicine 2010 76 Save Alert Research Feed Evaluation of Apical Sealing Ability of Three Different Root Canal Sealers Anita Kale, Kunal Walkar, Sunanda Gaddalay 2018 View 1 excerpt, cites background Save Alert Research Feed Pour une determination rationnelle de la longueur de travail en endodontie. Maria Fennich, Majid Sakout, Faiza Abdallaoui Philosophy 2012 1 Save Alert Research Feed Related Papers Abstract Topics 6 Citations Related Papers The Allen Institute for AI Proudly built by AI2 with the help of our Collaborators using these Sources. To browse Academia.edu and the wider internet faster and more securely, please take a few seconds to upgrade your browser.
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You can download the paper by clicking the button above. The 13-digit and 10-digit formats both work. Please try again.Please try again.Please try again. They offer a guide to diagnosing reversible pulpitis, irreversible pulpitis, and necrotic pulp; defining and achieving success; clinical procedure; and treatment outcome and prognosis. Color photographs and drawings illustrate the text on nearly every page.Then you can start reading Kindle books on your smartphone, tablet, or computer - no Kindle device required. Register a free business account To calculate the overall star rating and percentage breakdown by star, we don’t use a simple average. Instead, our system considers things like how recent a review is and if the reviewer bought the item on Amazon. It also analyzes reviews to verify trustworthiness. Note the adhesive biofi lm (BF) in the root canal. The AC and the biofi lm are magnifi ed in (c) and (d), respectively.He grew up in Philadelphia and completed his high school education at South Philadelphia High School in 1919. He earned a doctorate in dental surgery at the University of Pennsylvania in 1923 and a doctorate in medical dentistry (Dr. Med Dent) at the University of Rostock in Germany in 1928. On December 21, 1928, he married Emma May MacIntyre and the y had two children, a daughter Clara Ruth Gros sma n i n 19 39 and a s on Ric hard Ala n Gr ossm an in 1943. Dr. Grossman began his teaching career as an Instructor in Operative Dentistry at the University of Pennsylvania in 1927, in addition to being appoint ed as a Fellow in Research at the American Dental Association. In 1941 he was an Associate in Oral M edicine; he became Assistant Professor of Oral Medicine in 1947, Associate P rofessor of Oral Medicine in 1950, and Pr ofessor in 1954. His achievements and honors were ext ensive in many sectors of dentistry with a pr ime focus in endodontics.
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H e was an honorary member of the Asso ciation of Lic entiate s in Dental Surge ry and Uni versity of Dentists of Belgium; Montreal Endodontia Society; V ancouve r Endodontic Study Club, Brazilian Dental Association; Dental Association of Medellin (Colombia); and the Japanese Endodontic Association. He received an honorary Doctor of Science (ScD) from the Univ ersity of Pennsylvania. His major publication and crowning achievement was his textbook Root Canal Therapy published in 1940 (now known as Endodontic P ractice ) with multiple editions appearing worldwide. Subsequently trans- lated into eight languages, the book has served as a benchmark for the development of modern endodontic philosophy and practice. Dr. Grossman also authored Dental Formulas and Aids to Dental Practice,.He was a chairman of the American Board of Endodontics, was a charter member of the American Association of Endodontists (AAE) and served as its President from 1948 to 1949. He was a Fellow of the American Association for the A dvancement of Science. Dr. Grossman passed away at the age of 86 in 1988. The University of Pennsylvania has honored Dr. Grossman with an endow ed Professorship, usually given to the depar tment chairperson. The AAE has honored him w ith the Louis I. Grossman Award that recognizes an author for cumulative publication of signi.This award is given at the AAE meeting when warranted. A study club was for med in Philadelphia in the honor of Dr. Louis I. Grossman for his unyielding dedication and commitment towards facilitating the recognition of endodontics as a specialt y in the.I t w as e st ab l is he d in 1 93 9 i n Philadelphia, P ennsylvania, at a time when the Focal Infection Theory threatened the future of endodontics. The purpose of the Root Canal Study Club as stated in the original letter compiled by Dr.
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Grossman was “ to study pr oblems connected with root canal therapy and to pr esent clinics so as to help others in practic- ing this important phase of dentistry more adequately.” Endodontists from as far away as Massachusetts chose Philadelphia as the hub for scienti.It t ru ly de se rv es th e t i tl e “B ib le of En do do nt ic s ” as it ha d con s is te nt ly se t a be nc hmar k of excellence in the teaching and understanding of the art and science of endodontics. The last edition of E ndodontic P ractice (eleventh edition) was published in 1987 and tremendous changes have occurred since then, both in our understanding as well as in our practice of endodontic therapy. The focus of this current twelfth, edition is twofold; primarily, it is to update this classic book and incorporate all the advances in materials, instruments, and techniques which have revolutionized endodontics in the past two decades. The other objective is to highlight the gradual shift in the philosophy of endodontics from being chemo-mechanically ce ntered t o a more biologically centered and biocompatible approac h. This approach, coupled with a better appr eciation of the microbial dynamics and c omplex root canal variations, has made endodontic prognosis more predictable. In this edition, we ha ve included three new chapters: Chapter 18, P rosthodontic Considerations of Endodontically T reated T eeth; Chapter 19, Lasers in Endodontics; and Chapter 20, Procedural Errors and Their Management. This edition contains over 1100 new.W e have tried t o keep the spirit of Grossman alive by retaining most of the line illust rations which were the hallmark of the earlier editions.I have toiled for several months along with Dr. Gopi Krishna to br ing out this updated edition.
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I would like this edition to be my t ribute to Thai Universal mother god almighty, my spir itual guru Sri Swami Narendranath Kotekar, and Amma Shakuntala Kotekar for all their blessings, inspiration, and guidance for this project. I am grateful to my teachers as well as my beloved students and colleagues for all that they have taught me. They have truly made me what I am today. A special note of gratitude to Sir Prof. A. Parameshwaran and his belov ed wife Mrs. Seetha P arameshwaran who have continued t o be everything for me in my professional and personal life. In Dr. Parameshwaran, I have always found a teacher par excellence and a friend, philosopher, and guide. Thanks t o Mr. A.J. Shetty and Mr. Prashanth Shetty, President and Vice President, respecti vely, A.J. Institute of Dental Sciences, Mangalor e, for all their encouragement. I would like to express m y gratitude to my coeditor Dr. Gopi Krishna for all his efforts, dedication, and perseverance. I would also like to appreciate the efforts of my postgraduate students Roma, Naveen, Arun, Meeta, Saurav, and Gautam signi.A t t h e s a m e t i m e, I w o u l d n o t h a v e b e e n p a r t o f t h i s b o o k but for the kind permission granted by Dr. Anil Kohli, President, DCI, and Ritu Sharma, Reed Elsevier. I would like to take this opportunity to thank each one of my teachers who have helped in my growth as an endodontist. My pranams to my Guru s Dr. A. Pa ra me swa ra n, D r. B. Su res h C ha ndr a, Dr. E. Mun ir at hn am Naidu, Dr. D. Kandaswam y, and Dr. L. Lakshmi N arayanan. I would like to specially thank two people who ha ve been instrumental in my growth as an academician and as a clinician: James “Jim” Gutmann, for being a perennial source of inspiration, motivation, and support in m y academic endeavors; Dr. Vijailakshmi Acharya, for motivating me to give the very best to our patients and inspiring me to be a quality conscious clinician.
The true soul of this edition has been the numerous images and clinical contributions by eminent researchers and clinicians from across the world. I thank each one for ac cepting my invitation to contribute and for their kindness and generosity in sharing their knowledge and expertise. I would like to compliment the w onderful team at W olters Kluwer Health for showing genuine passion and professionalism in giving life and bod y to this edition. Thank y ou Rajiv Banerji, P. Sangeetha, Eti Dinesh, M unish Khanna, and Honey P al for your support. Many thanks t o Dr. H arini Swaminathan for her meticulous editing of the manuscript. A special thanks to Siju Jacob and Vivek Hegde for being m y friends. My sincere thanks to each one of the follo wing people at the places of my work for helping me in various ways during the genesis of this edition. Your favors, big and small, assistance and support made this possible. Meena kshi Amma l D enta l Co lleg e —Dr. P. Ja yakum ar, D r. Krithika Datta, Dr. A baraji than, Dr. Rub en Joseph, Dr. Vij ayalak shmi, Dr. Kris hnamurthi, Dr. Santosh, Dr. Sm ita Sur endran, Dr. Anusha, Dr. T arun, and Dr. Denzil. Root Canal Centre —Dr. Fazila, Dr. Krithika, and Bose. Acharya Dental —Dr. Aby John, Dr. Ramesh, Am utha, Chiranjib, Poonkuzhali, and J ayalakshmi.Geoff Young, BDS (Syd), DCD (M el b), Uni- versity of Melbourne Brazil. Ale ssa ndr a Sver ber i Ca rva lho, Sao Paulo State University ? Prof. C arl os Estrel a, DDS, MSc, PhD, Fed eral University of Goias ? Prof. Carlos Jose Soares, Federal University of Uberlandia Canada. Anil Kis hen, MDS, PhD, University of T oronto China ? Prof. Bing Fan, DDS, PhD, Univ ersit y o f Wuh an England. Juli an W eb ber, BDS, MSc DGDP FICD, The Harley Street Centre For Endodontics France ? Wilhem J. P ertot, DDS, Endodontie Exclusive Contributors Germany. Sebastian Horvath, Dr. Med. Dent, University Hospital Freiburg. Domonkos Hor vath, Dr. Me d. D ent, Uni versi ty Hospita l Frei burg India.
Anil K ohli, BDS, MDS ( Lko ), FDS, RCS ( Eng ) DLit ( Honoris Causa ), DSc. Siju Jacob, MDS, Root Canal Clinic ? B. Sivapathasundharam, MDS, Meenakshi Ammal Dental College. Viv ek Hegde, MDS, Rang oonw ala Denta l C o l l e g e. Naseem Shah, MDS, All India Institute of Medical Sciences. Arvind Shenoy, MDS, Bapuji Dental College ? K. Manjunat h, MDS, Meenaksh i Ammal Dental College. Krithika Datta, MDS,Meenaks hi A mmal Dental College. Abarajithan, MDS, Meenakshi A mmal Dental College. Ruben Joseph, MDS, Meenaks hi Amm al Dental Coll ege. Priya Ramani, MDS, Meenaks hi A mmal Denta l Coll ege. Jojo K ottoor, MDS, Meenakshi Ammal Dental College. Pra deep Naidu, MDS, Meenakshi Ammal Dental College.Rohee t Khat avkar, M DS, R ang oonwa la De nt al College. Hars h Vyas, MDS, Paediatric Dentist. Sanjay Miglani, MDS, Jamia M illia Islamia. Hemalatha Hiremath, MDS, Loni Institute of Dental Sciences ? S. Karthiga Kannan, MDS, Sree Mookambika Institute of Dental Sciences. Nagesh Bolla, MDS ? R. Prakash, MDS, CSI College of Dental Sciences and Research ? T. Sarumathi, MDS, Adhiparasakthi Dental College and Hospital. T arek Frank Fessali, Rajan Dental Institute Iran. Sae ed As gar y, DDS, MS, Shahid Beheshti U ni- versity of Medical Sciences Italy. Arn ald o C aste llu cci, MD, DDS Jamaica. Sashi Nalapatti, BDS, Cert. Niek Opdam, Radboud University Norway. Mathias No rdvi, University of Oslo ? Randi F. Klinge, University of Oslo Switzerland ? P.N.R. Nair, BVSc, DVM, PhD (H on.), Univ er- sity of Zurich Thailand. Jeer aph at Jan tar at, DDS, MS, PhD, Mahidol University United States of America ? James L. Gutmann, DDS, PhD (Honoris Causa), Cert. Endo, FA CD, FICD, FADI ? Louis H. Berman, DDS, FA CD. Syngcuk Kim, DDS, PhD, MD (H on.), Uni- versity of Pennsylvania.Formation of Dental Lamina T o oth development star ts when st rati.The cuboidal basal layer of the den- tal lamina begins to multiply and to thicken in.Formation of Ectomesenchyme The strati.
T his condens ed area of ectomes enchym e forms the future dental papil la and subsequently the pulp (Figs. 1.2 and 1.3). Bud Stage (Formation of Enamel Organ) The thickened epithelial areas continue to prolifer- ate and to migrate into the ectomesenchyme and in the process forms a bud enlargement called the enamel organ. This point is considered the bud stage of tooth development (Fig. 1.4). Cap Stage (Outer and Inner Enamel Epithelium) The enamel organ continues to proliferate into the ec- tome sench yme with an unev en rhythm ic cell divi sion producing a convex and a concave surface character- istic of the cap stage of tooth development (Fig. 1.5). The conve x surface consists of the cuboidal epithelial cells and is called the outer enamel epith elium.This is a frontal section of the head of a human fetus. You can see the maxilla and the mandible taking shape. You can also see Meckel’s cartilage in the mandible. The mandible also contains two dental buds in this section (stain: Azan). (b) At higher magni.The nasal cavity (Latin cavum nasi ) is divided into two by the nasal cartilage within the nasal septum. At both sides of the septum, you can see the nasal conchae (Latin concha nasalis media et inferior ). They are made up of cartilage at this stage of development.Endodontic infection is the infec- tion of the root canal system and is the major etiologic factor of apical periodontitis. The root ca- nal infection usually develops after pulpal necr osis, which can occur as a sequel of caries, trauma, and periodontal diseases or operative procedures. The role of microbiology in endodontic prac- tice, although clearly important, has remained controversial through most of the twentieth cen- tury. Onderdenk suggested the need for bacterio- logic examination of the root canal in 1901. Shortly thereafter, in 1910, Hunter made his his- toric address in Montreal, in which he condemned the “golden traps of sepsis, ” the ill-.
During this period, a few voice s were raised to st em th e h ysterical tide and to r eturn endo- dontic care to its proper role in the healing ar ts. La Roche an d Coolid ge sugg ested th at bact eriol ogic ex - amination be used in treating the root canal. Histo- logic studies of repair were reported by Blayney in 1932, Coolidge in 1931, Kronfeld in 1939, A isenberg in 1931, Hatton and associates in 1928, Orban in 1932, Gottlieb and colleagues in 1928, and others. Another study was published in 1936 by Fish and MacLean, who demonstrated that the pulp and periapical tissues of vital health y teeth are invari- ably free of the evidence of microorganisms when examined histologically. In 1935, Okell and Elliot reported a transient bacteremia following extrac- tion; Appleton suggested that without bacteria no need would exist for endodontic treatment, a h ypo- thesis supported by the classic study of Kakehashi and colleagues, who r eported that exposed pulps in gnotobiotic rats healed without treatment in a germ-free environment. In the last few decades, many reports have been published on the bacterial.Bacterial Pathway s into the Pulp Bacteria enter the pulp in various ways. Through dentinal tubules following carious i n v a s i o n. Through crown or root following traumatic exposure of the pulp.These microbes en- dure periods of nutrient deprivation in a pre- pared canal. However, fewer species are present than primary infections. Higher frequencies of fungi are present than in primary infec- tions. Gram-positive facultative bacteria, par- ticularly, E. faecalis (Fig. 2.3), ar e predominant in such cases. E. faecalis is a persistent organism that, de- spite making up a small proportion of the.It is commonly found in a high percent- age of root canal fail ures and is able to surv ive in the root canal as a single organism or as a major componen t of the ? ora. E. faecalis is also more commonly associated with asy mptomatic cases than with symptomatic ones. Although E.
faeca- lis possesses several virulence fact ors, its ability to cause periradicular disease stems from its ability to survive the effects of root canal treatment and persist as a pathogen in the root canals and dentinal tubules of teeth (Table 2.4). Persistent and secondary infections are clini- cally indistinguishable and are responsible for persistent exudation, persistent symptoms, inter appoint ment exacerbations, and failure of endo dontic treatment characterized by persistent apical periodontitis.Acute alveolar abscess is an example of extra- radicular extension or a sequel to intraradicular infection (Fig. 2.4). Sometimes extraradicular infection can be inde- pendent of intraradicular infection. For example, Survival and Virulence Factors of E. faecalis ? Endures prolonged periods of nutritional deprivation. Binds to dentin and pro.Alters host responses. Suppresses the action of lymphocytes. Possesses lytic enzymes, cytolysin, aggr egation substance, pheromones, and lipoteichoic acid. Utilizes serum as a nutritional source. Resists intracanal medicaments (i.e., Ca(OH) 2 ) Maintains pH homeostasis Properties of dentin lessen the effect of calcium hydroxide. Competes with other cells. Forms a bio? lm TABLE 2.4 apical actinomyc osis caused b y Actinomyces sp. and P. propionicum is a pathological disease which can be treated only by periapical surgery. Other patho- gens implicated in such infections are as follows. T reponema spp. ? T. forsythia ? P. endodontalis ? P. gingivalis ? F. nucleatum Bio? lms (Fig. 2.5) Bio? lm is de ? ned as a community of microc oloni es of micr oorg anisms in an aqueo us so lution tha t is surro unded by a matrix made of glycoc alyx, which also attaches the bacterial cells to a solid substratum. A bio? lm is one of th e basic survival method s em- ploy ed by bac teria in time s of s tarvati on. Accor ding t o Caldwell et al., a bio? l m h as t he fo l lo wi n g at trib ute s. Autopoiesis. Ability to self-organize.
Correct treatment begins with a correct diagnosis. Arriving at a correct diagnosis requires knowledge, skill, and art: knowledge of the diseases and their symptoms, skill to apply proper test procedures, and the art of synthesizing impressions, facts, and experience into understanding. Diagnostic procedur es should follow a consis- tent, logical order which includes comprehensive medical and dental histor y, radiographic examina- tion, extraor al and intraoral clinical examination including histopathological examination to arrive at the.The process begins with the initial call request- ing an appointment for some speci.Subjective infor mation is supplied by the written history or questionnaire that each patient completes and signs. Further informa- tion is obtained by the clinician, who reviews the questionnaire and asks speci.The clinician should not hesitat e to consult the patient’ s physician whenever the patient appears to be medical ly compromised or when the gained info rmat ion is ina dequ ate or unc lear. M ore of ten tha n not, a patient’ s medical problem affects the course of treatment, especially concerning the use of anesthet - ics, antibi otics, and analge sics. Occas ionally, the pa- tient’s medical status bears a direct relation to the clinical diagnosis. For example, diffuse pain in the mandibul ar l eft molars may be a referr ed pain caused by angi na pecto ris, or bizarre symptom s may be the result o f psych ogenic or neurol ogic di sorders. History and Record Case history is de.Because many diseases have similar symptoms, the clinician must be astute in determining the correct diagnosis. Dif- ferential diagnosis is the most common procedure. This technique distinguishes one disease from sev- eral other similar disorders by identifying their dif- ferences. Diagnosis by ex clusion, on the other hand, eliminates all possible diseases under consideration until one remaining disease correctly explains the patient’s symptoms.
Although proper clinical diag- nosis may appear to be simple, it can tax the most experienced clinician.Obviously, an exposed pulp will require some kind of treatment if the tooth is to be retained. Therefore, pulp exposure, initially rec ognized on the radiograph, should be con.A clearly visible inco mplete fra cture, at a dista nce from the pulp. (b) Sa me too th se ctione d fro m the other appr oximat e surface.One uses one’s eyes,.The patient’s teeth and periodontium should be examined in good lig ht under dry c onditions. For example, a sinus tract (.In fact, a transilluminator may aid in detecting enamel cracks or crown fractures. Visual examination shoul d include the soft tis- sue adjacent t o the in volved tooth, for detection of swelling. The periodontal probe should be used routinely to determine the periodontal status of the suspected tooth and adjacent teeth (Fig. 3.8). Sinus tracts opening into the gingival crevice or deep in- frabony pockets may go undetected because of fail- ure to use the periodontal probe. Periodontal pocket probing depths must be measured and recorded. A signi? cant pocket in the absence of periodontal disease may indicate root fracture (Fig. 3.9). Poor periodontal prognosis may be a contraindication to root canal therapy. Glickman’ s classi? cation for furcation defects is as follows: ? Grade I. Incipient lesion when the pock et is su- prabony inv olving soft tissue and there is slight bone loss. ? Grade II. Bon e is des troy ed on on e o r m ore as - pects of the furcation but probe can only pen- etrate partially into the furcation. ? Grade III. I ntraradicular bone is completely ab- sent but the tissue covers the furcation. ? Grade IV. Through and through furcation defect. The crown of the tooth should be carefully eval- uated to determine whether it can be restored prop- erly after the completion of endodontic treatment. Radiograph ically, the patient has a J-shaped lesion on the mesial root.
The sensa- tion of pain, a warning signal that the pulp is en- dangered, is a protective reaction, as it is elsewhere in the body. The pulp has been described as a highly r esistant organ and as an organ with little resistance or re- cuperating ability. Its resistance depends on cellular activity, nutritional supply, age, and other meta- bolic and physiologic parameters. This variability has led to the remark that “ so me pulps will die if you look crossly at them, while others can’t be killed with an axe.” On the whole, the resistance of the pulp to injur y is slight in cer tain case s, but ev idence of unusual persistence of vitalit y following injury has also been observed. The desirability of maintaining a vital pulp and protecting it from injury was recognized by the ear- liest practitioners of dentistry. The value of the pulp as an integral part of the tooth, both anatomic and functional, should be recognized and every effort made to conserve it. Accurate pulpal diagnosis is the key to all end- odontic treatments. Unfortunately, there has been poor correlation between the clinical sy mptoms and histopathology of the pulp. The endodontist is expected to understand the various causative fac- tors of pulpal diseases, collect information about the presentation and history of symptoms, and conduct many practical tests before formulating the.The enamel has been lost during the preparation of the section.Bacteria and their t oxins, immuno- logic agents, tissue debris, and products of tissue necrosis from the pulp reach the periradicular area through the various foramina of the root canals and give rise to in.Neoplastic disorders, periodontal conditions, developmental factors, and trauma can also cause periradicular diseases. The diseases of per iradicular tissues can be clas- si.The WHO has classi? ed diseases of periradicular tissues into various catego- ries (Table 5.1). Periradicular diseases of pulpal origin may also be classi.
The root surfac e may show exte rnal root res orpt ion due to cemen toc lasti c activity or h y p e r c e m e n t o s i s d u e t o c e m e n t o b l a s t a c t i v i t y. Treatment Root canal therapy may suf.R emoval of the cause of in.Synonym Chronic suppurative apical periodontitis. Causes The source of the infection is in the root canal.Symptoms A tooth with a chronic alveol ar absce ss is genera lly asymptom atic, or only mil dly pain ful.Note the adhesive bio.Magni? cations: (a) ? 75, (b) ? 70, (c) ? 1 10, and (d) ? 300. (Adapted from Nair, P.N.R., et al.: Intrar a- dicular bacteria and fungi in root-.N oxious stimuli can be ph ysical, chemical, or bacterial. They can produce changes that are either reversibl e or irreversibl e, depending on dura tion, in- tensity, and pathogeni city of the stimu lus and the host’s ability to r esist the stimulus and to repair t i s s u e d a m a g e. On the basis of these premises, we can general- ize that mild-to-moderate no xious stimuli to the pulp may produce sclerosis of the dentinal tubules, formation of reparative dentin, or reversible in? am- mation. Irreversible in? a mm at ory ch an ge s caus e d by severe injury can le ad to nec rosis of the p ulp and subsequent pathologic changes in the periradicular tissues. The in? ammatory response of the connective tissue of the dental pulp is modi.Because the pulp is encased in hard tissues with limited portals of entry, it is an organ of ter- minal and limited circulation with no ef.In? ammation In? ammation is the local ph ysiologic reaction of the body to noxious stimuli or irr itants. Any irri- tant, whether of traumatic, chemical, or bacterial origin, produces a sequence of basic physiologic and morphologic reactions in vascular, lymphatic, and connective tissues. Host-resistance factors and intensity, duration, and virulence of the irritant modify the ultimate character, extent, and severity of the tissue changes and, to some degree, the clini- cal manifestations.
The objective of in.In? ammation brings to the ar ea phagocytic cells t o digest bacteria or cellular debris, anti bodies to recognize, attack, and de stroy foreign matter, edema or.The injurious agent may cause reve rsible or irreversible changes to the tissues. Irreversible damage leads to tissue ne- crosis, whereas reversible damage leads to repair. Repair, or the r eturn of the tissue to normal struc- ture and function, begins as the tissue becomes involved in the in.At the per iphery, Fish noted that the toxin was mild enough to be a stimulant. In response to this stimulation, collagen.This new bone was built in irregular fashion. By analogy, we can apply the knowledge gained in Fish’ s experiment to understand better the reaction of the periradicular tissues to a pulp- less tooth. The root canal is the site of infection (Fig. 6.3). The microorganisms in the root canal are r arely motile and do not move from the root canal to the periradicular tissues; however, they can multiply suf.As the microorganisms gain access to the periradicular area, they are destroyed by the polymorphonu- clear leukocytes. W hen the microorganisms are suf.The polymorphonuclear leukocytes dest roy the microorganisms as rapidly as they gain access to the perir adicular tissues. The result is a chronic abscess. The toxic products of the microorganisms and the necrotic pulp in the root canal are irritat- ing and destructive t o the periradicular tissue and, together with the proteolytic enzymes released by the dead polymorphonuclear leukocytes, help to produce pus. At the periphery of the destroyed area of osse- ous tissue, toxic bacterial products may be diluted Zone of stimulation Zone of irritation Zone of contamination Zone of necrosis Fig. 6.3 Schematic diagram showing bacteria in the root canal and the zones of infection, contamination, irritation, and stimulation.N ot every tooth is suitable for endo- dontic treatment.