WSON’S ESSENTIALS OF RAL PATHOLOGY ::::. oma eonee w NO VAHL | ieee eee PTE Pte lic tats peal] pron bop owe 5) pe ares | CHURCHILL Liv ONEMOSBY ELSEVIER = aap hms ee arpa adie semgnment wh Rhee of The Bubetrd, Seat ng ne eng OH ye i 9 ya ny Une aon tpt ois bn may ih on i ant ei dina asd Bd ant Tinie Sevens nag “Does ect scene Fo da ita tt bape ath pS a ain ie An inp nia a Ba ar jana meand cago oe Por 5 ag ay el ca theft eet tthe rer ne Puen the Ere 9 ot mn on ald aa dl ae ine iia niteioy ocd be anetlentanel wtb enh Ph Working together to grow libraries in developing countries sroaleviercom | winchookaidong | wevenbreong Eee eee aac ia ay PRY occ hncio i www.elsevierhealth.com oetanteets Printed in ChinaProfessor Roderick A. Cawson OS, ISHS MSA, MBBS, MD, FCPath 1921-2007 For Elsevier Commissioning Editor: Michel Parkinson/Alison Taylor Development Editor: Clive Hewat Project Manager: Kerrie-Anne Jarvis Design Direction: Erik Bigland Itustrator: David Gardner lusmaror Manager: Merlyn Harvey api os sas opal ered Plu ae spans waneCAWSON’S ESSENTIALS OF ORAL PATHOLOGY ~ AND ORAL EDICINE R. A. Cawson iio rosecs rosacrsicies Frovat FaaoMP Emeritus Professor of Oral Medicine and Pathology, Guy's, King’s and St Thomas Dental Institute, King’s College London Visiting Professor in Oral Pathology, Baylor College of Dentistry, Texas A & M University System, Dallas, Texas and E. W. Odell rossesiuse eno roan Professor of Oral Pathology and Medicine, King’s College London Honorary Consultant in Oral Pathology, Guy’ and St Thomas’ NHS Foundation Trust, London eens fearon ELSEVIER EDINBURGHLONDONNEWYORKO) FORDPHILADELPHIASTLOUISSYDNEYTORONTO20085 CAWSON’S sale a S9-eAN pcoyl Tp sist) iJ) att ubs tied 2 es Lasadlly al) ppl cystic 78 ol giSag ptannle Geko delay gw Gb ad 76 gly eal po sN cy dit) St) yg) ole aldl 78 lily ald ppl up shcl 58 pla steal ‘ cane soli pol; ghey eld opll Capabill y§ ptaoleContents Preface 2 1. Principles of investigation and diagnosis 1 Taking ahistery 1 Demegraptic details 2 History ofthe present complaint 2 The medical history 2 The dental history 3 The family and socal history 3 Gonsent 3 Clinical examination 4 Extraral 4 Oral examhation 5 Medicalexamination 6 Making a cinical dtferential diagnosis and investigation plan 7 ‘Specalnvesigatlons 7 Imaging 8 Histopathology 8 Laboratory procedures 11 Molecular biological tasts 12 Haematology clinical chemistry and serology 13, Micrbiology 13, Other ctnical tests. 16 Interpreting special irvestigations ané making a diagnosis. and beatment pan 16 Normal haematological values 17 HARD TISSUE PATHOLOGY 19 2, Disorders of development ofthe teeth and related tissues 20, ‘Abnormalities in the number ef teeth 20 loolatsd hypodonta or anodontia 20, Hypodonta or anodontia with systemic defects. 20 Other conditions associated with hypodontia 21 ‘Additonal eeth:hyperdonta 21 Syndiomes associated with hyperdoniia 22 Disorders of eruption 28, Delayed eruption associated wilh skeletal disorders 23, Localfacters affecting eruption of deciduous teeth 24 Localfactrsaftectng erution of permanent teeth 2¢ Changes aiTecting buried teth 2 Defects of structure: hypoplasia and hypocalctication 24 Defects of decieuous teeth 24 Defects of permanent teeth 24 Amelogenesis imperfecta 24 Dentinagenesis (adontogeresis)imperfecta 27, Shell teeth (dentinogenesis impericta ype I) 26 Dentinal dyspasi (rocless'teeth) 28 Regional odentodrsplasia (ghost teeth) 28 SSogmental edontemaxilary dyeplaeia 20 Mutisystem disorders afectng the teeth 30 Epidermolyss bulosa 30 Infection 30 Metabolic disturbances 31 Drugs 31 Fuuorosis 99 ther acquired developmental anemalies. 34 Treatment of hypoplastc detects 35 Odontomas. 35 Genetic disorders ofthe jaws 37 Herediary prognathism 37 Clefis ofthe lip and palate 37 Develonmerial disorders associated wih cltting 37 ‘Submucous cet palate 39 Developmental defects ofthe oral soft tissues 39 Other genetic diseases relevant to dentistry 39 Dental caries 40 Aetiology 40 Microbiology 40 Bacteral poleaccharcos 41 Bacterial plaque 42 Stages of formation of bacterial plaque 43 ‘cid production in plaque 43 Plaque minerals 44 Sucrose as a piaque substrate 44 Efocts of aurroas on paque polysaccharide production 44 Etects of sucrose on the orl microbial flora 44 Eiperinenta studies ov humans 46 Susceptiltyofteth to caries 46 fects of fuorides 47 Saliva and dental cates 47 Effects of desalivation 47, Rate of flow and tutferng power 47 Other factors: 48 Pathology of enamel caries 49 The early lesion 49 Cavity formation 51 Pattology of dentine caries 53, Protective reactions of dentine and pulp unde cates. §3, Root surface caries $4 rested cares and emineralisaon 53 Ault and childhood caries 56 Ginical aspects of reactions to cates. 59begs XV dead ee B A yelandaut galee TA Lo ga eal! 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OF geal» JLLLM a OM pS a LSM day gel Vapi! aad} Fits desta andl gy Stas dll na acca ea P dueLese gut Lol Adal! £ gpl gan fgets eae 8 gyal yon! 1 ell pal Velanitanl Aas 9 pipet pasta ang Apes A peel pl apa 1) edt cleat Vapi aged gop VY cleat 9 pal ela ilg dupa hang We Achat pee Mabe 1 SY ypu papel Bas ya ntl iy Sal gop pas vi ua W dapat dugaal el pres) V8 att geet Znatpal Shap ey tL yp tat Te Tha ph pant eligi F ALeS Aged ape JS Gla one yas 1 dhe one meg go AIL ge J bat ane yas . 1) oa padi Aditya gps] o¥Le aay laa aL lt 11 Mane a a ea 17 ill hal alec Soe tal fo 16 Sel eM Ge he bog acyl Joga 12 dal ga gay he ip ill oat ota Speed a eens yl atl 1 galt gad gust JEN jad ga pga 164554 Lead pee 16 cast tial pee 14 pt Jeet ypae WV (gat JS pa gh Sepacones 4 Pulpitis, apical periodontitis, resorption and hhypercementosis 60 Pups 60 Pub caltications 65 Pulp stones 65 Diffuse caletfiation 65 Periapical periodontitis 65 ‘ete apical periodontitis. 68 Chronic apical perndonttis 68 Resorption ofteeth 70 Resorption of deciducus teeth 70 Resorption of permanent teeth 71 Idiopathic resorption 71 Hypercementsis 72 Concrescence 73 ‘Chronic non-carious) iniresto teeth 74 ‘triton 74 Bruxism 74 Abrasion 75 Erosion 76 5. Gingivits and periodontitis 77 ‘The normal periodontal issues. 77 Gingival and periodontal tares 78 Gingial crevicularfid (exudate) 78 Nomenclature and casstication of periodontal disease 78 Chronic gingivitis 76 Pregnancy gingitis 80 Down's syndrome 80 Diabetoe mollitus £0 Chronicadultpercdontiis 80 Complications o chronic peiodentiis 87 Petodontal(aterab abscess 88 Juvenile peredonttis 88 Other causes of early-onset perodontal destructon £0 ‘ate pericoronitis 91 Act necrotsng ulcerative gingivitis 92 HWV-asseciated gingivitis 02 HWV-assacated periodontitis 93 Hespetic gingvostomatits. 94 Miscellaneous peradontal disorders 94 Gingival sweling 94 Herecttary gingival fitromatosis 94 Drug-induced hyperplasia 95 Inflammatory gingival swelings 95 Wegener's granulometosis 95 Sarccidosis and orofacial granulomatosis 95 Acute leukaemia 95 Scuryy 96 Gingival recession 96 Gingwal abrasion 96 6. Major infections ofthe mouth, aves and perioral issues 99 ‘cate osteomyelitis ofthe Jans. 98 Chronic osteemyeltis 101 Chroniclow-cradeosteomyeltis and osteitis 102 Bisphosphonate-induced osteonecrosis. 102 Osteoradonecrosis 104 Alveolar coteitis 104 Scleotic bone slands 106, Fascial space infections (cericofactl celts) 106 Necrotisina fascitis 108 Cavernous sinus trambosis 108, Maxillofacial gangrene (nema, ancram ors) 108, ‘Actnoniycosis 109 The systemic mycoses 110 Systemicinfectons by orl bacteria 111 Infective endocarditis 111 Ling and brain atscesses 111 Immunodeficiency states 111 Norial healing ofan extraction socket 113 7 ysis ofthe jaws 115 “Typieal features of ew cysts. 115 Other cysic or oyst-he lesions 113 Radicular cysts 116 Residual and lateral radicular cysts 119 Paradontal cysts 120 Denigercus cysts 121 Eruption eyst 123 keratinising odontogenic cysts 4128 Odontogeni Keratooyst. 124 The basal cell naevus smnrome (Gortn-Got syndrome) 127 Orthokereinised odantogenic cist (athokeratrised dontogenickeratocyst) 129 Gingival sts 129 Dental lamira cysts of the newbom (Botn’s nodules) 129, Gingival cysts of adults 129 Lateral periodental sts 120 Botryod odentogenic ests 130 Glandular odontogenic cyst (salo-odontogenic cyst) 130 Nasopataiine duct cysts 130 Nasolabial cysts 132 (Gyste nevplasms 192 Unicystic ameloblastoma 132 Calefyng odontogenic cyst 132 Neoplastic change within cysts 132 So-called globulomaiary cysts 132 Cyst of he sot tissues 132 Sublingual dermoid. 132 8, Odontogenie tumours and tumour-like losions of the jaws 136 ‘Ameloblastomes 136 Unicysic ameloblastoma 129 Netastasising ameloblestora and ameloblastic carcinoma 140 ‘Adenomatoid odontogenic tumour 141 Calctying eptretat odontogenic tumour 142 Clear cell odontogenic carcinoma 142 Calctying (ghost cel) odontogenic cyst 143, Squamous odontogenic tumour 144 ‘Amedoblatc fibroma 144ef lI iba 58 yatiall gas 18 peel abba cpus Vb eal gal Fast kale VN pga gal gg wigati a st data 1A pipe AdLN lg NA ppt ads 1h Goad AS] Lops) aggegth Saat ypasas! 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Sage gl $1 geil Lact $0 gill Jol SN edt Joe a Sg el gh as SULT 99 SS bly gat Vs} ail gaily as gt fe bat slgily de pabsie pill Ll gealwi cones Amelobastc sarcoma (amlobestic fibrosarcoma) 145 Odontogenic myxoma 145 Odontogenic fibroma 146 ‘Tumours and dysplasias of cementum 146 Cementoblastoma 146 Cemento-ossityng fibroma 147 Psammomatoidossiiing froma 149, Juvenile ossifying fibroma 149 Non-necplaste odontogenic lesions 149 Cemento-osseous dysplasias 150 Periapical comental dysplasia 150 Florié cemento-osseous dysplasia 150 Focal cemento-asseous dysplasia 160 Gigantform comentoma 151 Odontomas (dontomes) 151 Comgound odortomas. 151 Complex odontema 152 Other types of odontomas 152 Wii classification of dantogenic tumours 2005 154 9. Non-odontogenic tumours ofthe jaws 156 ‘Osteoma and other bony ovorgrowhhs. 156 Compact and cancellous osteoma 156 Gardner's syndrome 187 Osteochondrema (artlage-capped osteoma) 187 Cemento-ossiying fibroma. 157 Giant cell granuloma. 187 Other giant cell esions of the jaws. 159 Hasmargioma of tone 159 Melanote neuroectodermal tumour of irfancy(proconora) 180 Malignant neoplasms ofbone 161 Osteosarcoma 161 ‘chondrama zd ctonarasarcoma 162 CChondrosarcoma 162 Ewing’ssarcoma 163, Nyeloma 103 Soitary extramedullary) plasmacyioma 165 Amybidosss 165 Langerhans cll histioytoss histiocytosis X) 165, Solty eosinophilic oranuioma 166, Multiocal zosiophilc granuloma 167 Letteer-Sive syndrome 167 Lymphomas 167, Metastatic tumours 167 10, Genetic, metabolic and other non-neoplastic bone ‘seases 172 Genetic diseases of bone 172 Osteogenesis imperfecta (rite bone syndrome) 172 Osteopetrsis -marbe bone disease 173, Achondropasia 174 Cleidocranial dyspasia 174 Chonubism 175 Hypophosphatasia 17 Sickle cel anaemia and thatasszemia major 177 Hypergarathyoidism-jaw tunoursyndrome 177 Ggantsm and acromegaly 177 Fuorosie 178 Metabolic bone disease. 178 Fickets 178 Vitamin D-esistant rickets 178 Scurvy 179 Hypergarathyoidsm 179 Other bone diseases. 181 Paget's disease of bone (osteitis deformans) 181 Fibre-osseous isiors 183, Fhrous dysplasia 183 onosttic fbrous dysplasia. 184 Palyostotic flrous dysplasia 185 Abrigi’s syndrome 185, (Cemento-osseous dysplasias 188 Solitary bone ‘cyt (solitary bone cavity) 188, Osteogortic bone marow defect 187 ‘Aneurysmal bone ‘cyst (avi) 107 Pathology of osseointegration 189 114, Disorders of the temporomandibular joints and periarticular tissues. 192 ‘Temporary limitation of mavement(tismus) 192 Infection ang inflammation in or near the jot. 192 Injuries 193 Tetanus and tetany 198 Temporomancibuar pan dystuncton smdrome. 193, Hysterical tismus 188 Drugs 193, Distecatien 198 Recurrant dislocation 103 Enlers-Danis syndrome 194 Persisten limitation of movement 194 Iradiaton 194 Oral submucous fibrosis 195 Progressive systomic sclerosis (sclerodrma) 195 Arthtis and otter causes of pain in or arcund fe ont 195 Rheuratoidarthris. 196 Ostooarthris. 198 Other ypes of artis 197 Granial giant cell artes. 197 Pain dysfunction syndrome 198 ‘costen's syndrome’ 199 CCondylar hyperpesia. 199 Neoplasms 199 Loose bodies inthe temporomaneibula joints 199 Selt-assessment questions and learning guides 202 SOFT TISSUE DISEASE 205 12, Diseases ofthe oral mucos Infections 206 Primary herpete stomatits. 205, introduction and mucosalWV Sil ppl aie * all le BLA bod WW olga dala g dies! 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EFT dt chat rt aap bd) 2 ATF all eS oil ATT yall pays ad oth SPP dep ah PF etl llimage not availableimage not availableimage not availablePreface Undergraduate students will never see many of the conditions discussed in this book. Despite this. on «qualification they are expected to not only diagnose them, but also institute appropriate referral or treatment. This. the eighth edition of Cawson's Essentials sth only updated, but also designed to make elinical relevance immediately accessible to the learner. We have used more colour illustrations ang have introduced symbols to link the vextto the dis The text has been updated with many new sections on. cancer, premalignaney, ossecintegration, sinusitis and Aistucbances of taste, as well as novr diseases euch as bisphosphonate-induced osteonecrosis, There is a new section on normal healing of tooth sockets, an important topic hardly covered elsowher changed relatively little, such as that on earies, but the amportunce of understanding the disease process i8 wow more clearly linked to clinical practice in tables. nostic summary charts Some chapters have Sell-dirscted learning iscritical to devslop understanding. New learning guides now follow each section, an attempt to help students direct their own learning from other sources, Because no book cin he comprehensive. References have updated but remain largely unchanged. Often the older classic papers ate those of most use co undergraduates and the retention of these older papers is deliberate, (Our thanks are due to Clive Hewat, Alison Taylor, Kerrie ‘Anne Jarvis, Erk Bigland, Mike Parkinson and all the teum at Elsevier for maintaining the excellent production standards and rescuing many of the older, now almost ineplaccable, photomicrographs, ‘This edition of Caneson's Essentials is, sadly, the last 19 which Professor Cawson will contiibute, He died shortly alter the manuscript was completed. A dedicated teacher, he understood low students were often baled by the complexity of our subjecis. He was a master of succinet text and ruthless in editing out ideas without an ‘evidence base’ long before the expression iid been invented. Canson's Essentials has been published continuously since 1962 and it as the first textbook to integrate oral medicine, pathology and suns orientated fashion, The many students who have relied ‘on it over the last nearly half-century give testimony to his breadth of knowledse, inellectual authority and the clarity ‘of bis wrt ry in a practical, stadent- E.WO. London 2008image not availableimage not availableimage not availablePAIRS OF VESTIGATION AIO OAGWOSS Iodes youself nd greet the pabt by name Pat patents at thor ease ‘Sart win an open queston oc open anc closes questions ‘vcd dln goss ‘Avoid eon Expat the neo fer spocie uostrs ‘Assess the paints eri sae ‘Assos the paint xpectatins from wostmont During history-taking, the mental ord emotional state of the patient should be assessed. This may have a bearing on psychosomatic disease and will also suggest what the patient teepects to gain from the coneultaion and treatment. I the ptien's expectations are unreasonable, itis important tty to modify them during the consultation, otherwise 0 treatment say be satisfactory, Demographic details “The age, gender, ethnic group and occupation of the patient should be noted, Such information is occasionally critical. For instance, an elderly woman with arthritis and a dey mouth is likely to have Sjogren's syndrome (Ch. 18), but a young man ‘with a parotid swelling due to similar lymptoproliferation is far more likely to have HIV infection (Ch. 24). Some diseases such as oral submucous fibrosis (Ch, 16) have a restricted eth- ic distribution History of the present complaint Frequently, a complaint, sich as toothache, siggests the disg- nosis. In many cases, a detailed history (Box 1.3) is required ‘and scmetimes, as in aphihous ulceratica, a provisional diag nosis can be made on the history without examination or investigation, BOx1.3 Misty of e pres complart “= Racord the disortion ol he compl tho pation own sors ‘ict the oxaet meaning ot these wees Facord the dation and ihe tne couse f any changes ‘Simpions o sane Irlude any fever facts inthe patent's rascal sory Note any temporal relationship beteon them ard tho present ‘compart ‘Conse any provi stent an the ecventas If earlier treatment has been ineffective, the diagnosis should be reconsidered. Many patients’ lives have been short- feted by ving malignant wumours teated with repeated courses of antibiotics Pain is completely subjective and, when physical signs are absent, special care must be taken to detail all ks features (Toble 1.3). Especially important ave features suggesting dental cause. A fractured tooth or cusp, dentinal hypersensitiv- ity or pain on occlusion are easily misdiagnosed. Factors triggering different causes of pain are discussed in dowil in Chapter 34, The medi history ‘A medical history is imporaant as it aids the diagnosis of oral ‘manifestations of systemic disease. It also ensures that medi- cal conditions and medication which affect dental or surgical treatment are identified To ensure that nothing significant is forgotten, a printed {questionaire for patients co complete is valuable and saves time. I also helps to avoid medicolegal problems by provid- ing a written record that the patient's medical background has been considered. However, a questionnaire does not constitute a medical history and the information must be checked verbally, verified and augmented as necessary. It is important to assess whether the patient's reading ability and Table 1.3. takings panier, formate fates we ‘che, tenderness ul pan, throbbing, stabbing, ok shock Thowo toms {0 of tes uso sn tho constany of ans more ues Severity id -rmanaged wih mi erdgescs fe9. esprinioractar) deste umesponsie tor snaigesce Severe ~ dubs soon uraten Time dno erst. Duration ofpain sacle ‘Sontrous, poise orparonsta {Trot eortruous, pan prose betwoon atc? nating factors dey potenti inating fctore ‘socaton wth cnalvetant ox lack ots especialy meortant in saminating dot causes raowaty and reed lacbrs Recor al na now espace Not nd od east or pa en eating which Icaleston The patent shoulé map out the Aaa 0 LEP pty ay Legale al SURE Lia pi eM 3 et okey hall Ls Lig sees gl ial opine g sls ga Lath ealyapt is ad il al agatha oll) 1M ple pas 9 nel Getbaly hantge SI dil go Leb pi ull odd Lasse CI eat ga) La lS Jo} omy ad pA!) pee hey deel eh iyo le Lag pent at praind SueS 90 Magee pie Lidge S83! a ye el Sige eid se Rakes cb deal aces Lb gull Ail Ad Lene 906 ple fo Gt ol sal) QSL deed Spt gal pti Aa abe aL Yell apactny Bae phe I GY ig Je gh post le goed 8 OT MaPl) TLS) dela ofa tia he agoy edimage not availableoh ie Jeb all AE ud Uy ht SL Jue) ole Go ad Sol) a yp 3! Lal) Sai Gholtt Gb Staal Anephly gual! Glee ose IPP LSI dase AaHLdbgh Sgt! 9 duals Ayogh Hl SiS! ofaywe fol Cpbasall pS gall Le byillad aba 5nd wots ole Lghad te Skeid) ngUl ge eS oles Js Tedipe Sight OLS pSICu chasse gl jaySaull (Az) Spal, Les (FF jeg GlSeLe) QheSaaall gee ish! gill cole dsy5ii) Sitbll clade oe Sad gle Cd aetaly HL jab Spl GS OLICAGN ge BS oles JSSs stl bee pte bgt ae Eat lS gal yA se adap Re ac le + SAAAAtpM ate ph ned i yh Joana al he * mttaer Conc 5 uPA a le Eyes AAs SLC eae pod JAS sleigh * Ghainy tyes flashy clade ULLAN gens Taya gy diols egies Job ge TM ile -gul pSetly ghatL BOGYL (gills SAU) olazal Lig ASL CL ay nig pe Bplay Bye JES aS no Shia! eWDLe dad go oul! paby geld lty cdl poco! gle giyad an tg gL Silat Bat ALA phe Rall ed jy Sell Sead ages dae JSG Gens yilly Sb “Sele al) yi BULA ps} jaca gl agin ip SGLANT JU Alaasly SLC! PSUS whaad LelaNN BeS pan jap! Sd 1! lepaig igh Jal aya alyab gl Slay Seall cllezy ain ene) WASH Lag LE JL gh ell) diane pSFOISLe ST glags Shai wtIl geld is ethi! (gated gill dangly SIC oluyse gal Sat a a aly yl pol date gal Golo IS ple Logae SACU plADy SLC algae ne pHa plat pf ALB SS legisgagll od po Se ag) GUS SISA clagae yo LLSaLas! FSAI ya Spal yy Saly NT HG pa fily ALS La po ELS AST LYST LeS i) pee JS! (paso Spl! Aaysa) ctype gan Hy pI yb dyes SSMS Le Soli Uns ob SIS Sloe JEU Y ally Sas) Sana ony shoal dgiaalt Zolaall i ps! lost jas ysis clays JEG ga) aa otal go opi SiSaal lass alu dys) Gilad os Lgl gad ¥ SURDU Laghin daoagl ALES JS sy Glatt ye ae leat gh Wyk aad eh bgie gt a at leu AL gut aia, Lente tht oo Sah biped gal pial pai) glass ¥ Iyghatlofilgadl ga) aaa sillyig Sau Latics Foilasal! deans Gn cigh daetall dipedl Fipene Lin yo ban Sid oul psatholatnd Ll dss ing) Sits Lgaellaccals iy yan polis io luau pate BAAN chyna capes Yass 685 eb ead Gols JS hag dalla pb dog Mal Sy) thea gy Saal! po gayi! SAI Jy call i aa Joo yo Algal! yaa call gay (FT LS) hylaledl gal gay ate dandy sical Pau allyl Agu dyapaall ah) gh J Cegltl g abagllg dascStll cyl) Leal Soul IN bc¥ly abigail gb Znsoly yh FoF JS PLAN gpg Sigh Jy fo pall on ne Vente phase Lint bay gi Sasi) has rr Jct Gan SL ge SWIG bigs) le ane yale po) ToS alee a) peg a alinal poops gins aahimage not availableas pe Ale tpl Sogn pes Ha Makai So anal gt ablaeiy Sod “be Shave 9 doseage gil lpee dezasl G8 hey) gi Stet) dpb glo! ge Gide Yes SptnbpHl aUoba! doped SEM pl z bby) Lakins Sapdll dosh Hh yeS3 a duel Lad g} EUs asap dl dug pi leans Al peal eg SA 2 Add gold Jy Laid dyogiy> led conaly Ub ty pL oi Set gel an le abgb dapat! Ant ¥l yoibes JLiGS! was as Easy eal asl co TLR ySall AS go Lplhe Tela) cay BLL sacl aegt LgiSy eed wy le 5, pall Bla pag ptm al neg Laas AisoiaiohdadlatuaalysS. i Dela GAS ple Jy Sal Jil Adal doll JSS yg, Graal yeaa bdsyype deel cls daily yyS gle Abas casey aallasad yiiealusailgiSy. teal Ube 8p Aanegl ob p81 gual 30 aaa! ange ad HL ess LoS Hygne dd! JIS 50 wall ys gant GS! Ipshabe Sill py Laaie ols Gal oes Ab dy hd! Cplesall cll lant le Spld ges Lgl GB peed ASKS ge Sohal yo elt! 3 wey Byes pot SLOG Goons (ET LSU dog S} Suightl plead! ope aL gay big gL ty ola! gle aie Aidesl! dogtl LUG 5). deog! Sh olen JUAN pat PP UbY yb Seas pill pal Sigel lg, Abaya ie Sty dl gal * prey OA Ait gel gunboat pat = aga ga pst ashing ihc neg gts * suaahga gear inna apopaticaa etal © I a ie Sata en cole pS) SS ke Sy ola) Gb as LY byl gd de ul jail! mela att nen * gis ana a gh et * ab sa Al ge td pg al abate pnd de © Se es ey i ga Agegid| doug Cra gle JEG ddetley dsj) claws go dnugl 8 JE SH phe seins syne lb ge tly Guu! (Or ge TEP 30 JSAM lb Lge FLke Sida) GLAM) ole go dngltl as Las pod os eet Gy pb oo dyed aed! lly lH aos dephl GUS SUS! basa alled os Of PAS LSS ad 5aSIs) SEM ake gb aqua $45 ab LoS ated ed Jitaall yyls gh Spngll ts isles bts geet! auhe¥) 2b Laud alld! sry ro Tsou rarHaLo6y Fig. 3.6 This scarcing secrenmicograch at her pomer shows ‘rangement sometimes seen in pace. (Bj kind permission of Or Shei “linically, bacterial plague is @ tenaciously adherent deposit ‘nthe teeth It resists the fiction of food during can only be readily removed by toothbrushing. However, neither toothbrushing nor fibrous foods will remove plague from inac- cexssible surfaces or pits (stagnation areas ~ see Fig. 3.3) Plague becontes visible, particularly on the labial surfaces ff the incisors, when toothbrushing is stopped for 12-24 hhours, I appears as «translucent film with a matt surface that dulls the otherwise enooth and shiny cnamel. It can be made ‘obvious when stained with disclosing agewis, Little plaque forms under conditions of starvation, but it forms rapidly and abundantly on shigh-sucrose dist In stagnation areas where they are undisturbed, plague be- teria can form acid from sugars over suificienly long periods as to attack tooth surfaces. Adbesion of bacteria to the teeth from which they wo oherwise be washed away is an esseatial requirement for the colonisation of enamel. Atachment depends on complex mechanisms and depends on such molecules ss glucans andior slucosyliransferase. Components of plaque, which act as adhe sion receptors, include a group of proline-rich proteins (PRP) from the saliva mastication and Stages of formation of bacterial plaque 1 teeth are thoroughly cleaned by polishing with an abrasive, plague quickly re-forms (Box 35). 108% GLUCOSE RINSE fan sof ie ee niNtres Flg.3.7_steptancuves. This ih tal frm ofcurves obtanad when | {hopl fos blow the cia lol, ens Patents wih active cries end o show a cane. Neteworhyfeatuosare he very rap fl in pH and th ‘recovery othe normal lave in spits of he vay shert ime the suger sin themou. Catahyerates which a etainod onthe toch ave @ rere prolonged fet sth * Depostion of aruclusesscol-ie,palcle ol sakary @ysonr=n Furr dopostonofpelicy entre by bested ate Freipaing salivary poten Caicroaton ofthe el roe layorby basta partly by 'S eangus and. rans sain vstin 28 Fours Preyesove bul of pags substance by bacteal poresocharces Protferaon of laontous and ctr tater a he sae ‘Acid production in plaque Sucrose diffuses rapidly into plague and acid production quickly follows. These changes have been measured directly in the human mouth asing microelectrodes in direct contact with plaque. It hes been shown by this means that, after rins- Ing the mouth with a 10% glucose solution, the pH falls within 2-5 minutes, often to a level sufficient to decaleify enamel Even though no more suctose may be taken and the surplus is washed away by. the saliva, the pll level remains at a tow level for about 15-20 minutes; it returns only gradually to the resting level after about an hour. These changes (the so-called Stephan curve) are shown diagramatically in Figure 3.7. The rapidity with which the pH falls is a reflection of the speed ‘with which suerese can diffuse into plague and the activity Of the concentration of enzymes produced by the great num bers of bacteria in the plaque. The slow rate of recovery to the resting pll ~ a ciitical factor in caties production ~ depends mainly on fastors summarised in Box 3.6wo ae Shai pa cal SMa gt ohne VF cat Wagga sible Jy Sota mel Lal a gb cb is pe agai a gad Gab Ep spay ens Sp a ge Oe i eg et a ‘obal bel gh eral neal pa platy pd! al! 1a eg St ge al Sa a pga pal! is ok Gop ghae gle SAH! hag BI ae Spal ay pl gasp + ge pH LG Sel pa iy eit anlm ta ce J ya Lt yaa at Ll # ELD E ALI Lge Ang UIb A dL ag A Stata * et gaa a AS + Anaghit pi aod csi} q1S| depen Legace doigh ans dep jgySaal) ps PED algal gb pbs Slpabstl ke old aly yen! Pile gla le pf Allan day gS lla) placuly Jplone pill ad aay a) Ldgy hal aise hay dneplll go col) Gils OT JUS PH oN days aks N+ jy Syke 99 (2s hey eel yal GU GAS: ALM gd spine stabil, dL Janes japSaul! go ial ay ageg ane Las digds T+-10 dal Lede chs pH I days old eM I I eet Lenya dapat ae od ey lass nae jal Legh obpall ska 5 cL! lg Lipo dep yaSas Sem VF JSAM gb binge alle Silay eg jg Saat) Lt Lep pH gysne Oh pd eal a Ube Skea bynes Gall ole itl ph ete ggtaall ll Sigel gi pla Joell LA) dona! Cones pat SoS gb ule Jolt gay pH ot ye NP LM ob Se alge he Ll AL gut aia, A) posh Laake yl) dyggne e VS SSI Sere Yel Spd wlypael pie in typ gs (DF Shella J Jones ye git) anil! ga unl saul Spat ole ppd Lede lias Legh tl Sept Sal Lye Seg fell ektl alae!) SISSS! yl Wgil Lis glut Bekil 9Se ¥ 9S ola syd zd depen JI ol gall call pw Soap Jak gf dell Lele gh it (FF JS lh ao -igS 9 Ls) Ang Lgall wos! ge dapat pplasall gle old Shy Aye UoagD cae Seay EL SEstT ack ofa EN hagas psa aaa’ cuaigats PLuuLll call lney gilly wolS qubawy a9 SLE cLiLE JS, oF ail LS Sell gh! Ga jo Lal bg Le Arepbl oot Sola Shiny GAGLS olga Lgeegl Serle ef Bite dep J Jy vagal fod! cin SapSoull ll Sa pla ee Y Lae sapSM jlalie yb Leagll retlpe glans Aipb olh gas cle SISA ye yaed! JE GI gales! pal Conall Leos pgs! LS planet gabe) Clase ghd! ye gail $ Gla! 5f ota he Lah aes if dig gany lines LG Bp «Lill 20s SS aT foe Sige le La) wees LoS Sadza asi pill dneplll cpSo Joss ip Splisl 8 te elaell HD hicgpall 9a Regen bhi! oNlgdi eS LL 59 PRPS) Teed Spt HS tops Hib Sele dha Jol Jit ga cal! Ly uy (0.7 Usd de yauy douglt JES shes arNTL CaS “Rapid production al aigh concentration of acd within he ‘plague erperariy overcomes cal buierng + scape taco mote sata ojea by he amuse ming ropes of planus ands thickness + Ditinon of slvory butler nto plage Harpore by the ‘dBuson-ming propartes of aque and = themes + Continuad acd protien Kom Gocli iracoh a rag povvescheres afar deny sugar existed ‘As discussed in relation to the pathology of dental cares, itis| lear that acid produetion is responsible for the carious attack, Lact avid is mainly responsible. When plaque is sampled after exposure to sucrose, lactic ac is the quantitatively predomi- rant acid daring plague activity, particularly during the trough of the Stephan curve. Lactic acid has a lower pK constant and ‘cuusesa greater fll ia pH than equimolar solutions of azetie or propionic acids that may also be detected in plaque. Plaque minerals In addition to bacteria and their polysaccharides, salivary com- ponents also contribate to the plaque matrix. Calcium, phos- phorus and, often, rides are present insignificant amounts. There is some evidence of aa inverse relationship between calcium and phosphate levels in plague and caries activity o suerose intake, The ability of plague to concentrate calcium fad phosphorus is used in mineralising mouthwashes. ‘The level of fluoride in plaque may be high, ranging from 15 to “TSppm or more, and is largely dependent on the fuorige level, in the drinking water and diet. This luorde is prokably mosily bound to organic material in the plaque but, at low pH levels, ‘may become available and aetive in ionie for SUCROSE AS A PLAQUE SUBSTRATE Dirset measurement of pIT changes in the mouth shows that there is intermittent acid production on the surface of the teeth end this follows the pattern shown earlier in the Stephan carves, Ingestion of suctese leads to a burst of activity in the plague so that the pil may fall low encugh so attack enamel ‘before slowly returning to the resting level. The Frequency with ‘which substrate is made available to the plaque is therefore Jmportant. When sucrose is taken asa sweet drink, any surplus beyond the capacity of the organisms in the plague to metabo lise at the time is washed away. If suerose-containing drinks are taken repeatedly at short intervals, the supply of substrate to the bacteria can be sufficiently frequently renewed to ea acid in the plague to remain persistently ata destructive level. ‘A smmilar effect may be caused by carboayarete in sticky form, such asa caramel, which clings tothe tecth and is slowly dissolved, eleasing substrate over a long period. The effects of ng plague activity by repeated administration of smal ‘quantities of suerose have been demonstrated by the use of animal feeding devices to dispense metered quanities of suerose in diets at fixed intervals. These show that a given amount of sucrose is more eariogenie whea fed in small increments, but at intervals to maintain maximal plague activity, than the Same amount fed asa single dose. Effects of sucrose on plaque polysaccharide production As discussed earlier, the cariogenicity of plaque depends on its ability t adhere t the tecth, to resist dissolution by saliva and its protection of bacterial asids from salivary buffering. These properties depend on the formation of insoluble polysaccha: ie ppc aria carcgene: traiacol Scant Effects of sucrose on the oral microbial flora Covonisation by cariogenic bacieria, especially S. mutans, is highly dependent on the sucrose content of the diet. In the absence of sacrose, . mutans cannot usually be made to colo- nise the mouths of experimental animals. In hurans, the plague ‘counts of S. mutans also appese to depend on the sucrose eon tent of the diet. Severe reduction in dietary sucrose eauses ‘mutans o destine in numbers oF éisappear fom plague. Experimental evidence for the essential contribution of ‘sucrose to caries actviy is summarised in Box 3.7 Box S.7 Experimental evidence forthe erica cantintion ef suerese tears acy Incas suscentbiarimals a sxrose rich diet promos canoe reduction Cats sot inducedin suscepti anal aucose ieted cn by merc seis ot etey Sueroao scl frm cigs to he tech and remans alae {0 bocora for alongs pore ar is nav carlogs Suerose-cotahing ful ere quckl Care rom the mouth nd oes carzgerse Froquont foods of srl quarts of sucrose are moe caronerie ihe iy erie i eect ret one we ere DDocalvaton, by detaing ceararco of sugar, enhances caroe tty ‘The importance of sucrose in human eaties Jepeads rmainly ‘on epidemiological studies and a few interventional studies. “The findings of epidersiological studies are surnmarised in Box 38 * Low cafes prolencoin papuaions wih low aucose hakos 1 The deco in caves province dra wartine sutose shortage {Theres of canes proaoncs wthinoreaing avaiable sctess + Arcisctgicaleviden oaw cares prealenea eras befor Surose became reay valerie + Low cares preaenca in deorcrs of aicros metabotim (rove rocise lore)qigSaull 4 dbpuine oleeS gigi! obi d ahs ge! 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In the past particularly, there have been many studies of poor cormuni- ties living on traditional diets with little or no sucrose content ‘A low prevalence of caries has been shown (For example) in purts of China and of Africa, the Seychelles, Tristan da Cunha, ‘Alaska and Greenland. Many studies were cariied out on [skimp races who were earies-free when consuming their tr ltional die: of seal or whale meat, and fish. Similarly, in South African races, despite a bigh-starch carbohydrate diet, caries ‘was found in fewer than 9% of those examined, but greatly increased when there was access 104 modern suerose-rich diet In sich studies, no association has been found between mal- nutrition and caries. Generally, the reverse is true and, when nutrition is poor, caries is infrequent. These dies also vary ‘widely in contest, from rice as the staple in China oF coutsely aground cereals in Africa to 4 mainly mest and fish diet among, Eskimos, The common Feature of these diets, and one diffeten- tinting them sharply from westernised diets is low or negligi- ble consumption of refined sugar, particulary suerose, Britin is an example of a couniry where consumption of sucrose is exceptionally high and where the rest ct the diet is more than adequate. A survey in England and Wales in 1973 showed, for example, that (in spite ofthe benefits cf a National Health Service) 78% of 8-year-old children had active decay ‘and many teeth which had been filled oF lost from this cause. A survey in 1978 showed thst dentate adults had on average orly 13 sound and unfilled teeth. Though there has boon dramatic improvement nationally, such consequences are sill found in some populations In Britain and other countries, the incidence of cavies has riken roughly parallel with rising consumption of sucrose. The Zn TO3YEAR.OLO CHLOREN oq (1 ero sveanowcanonen [610 7.vear-o1o cHioReN incidence of caries has risen in spite of the much greater con- sumption of so-called ‘protective’ foods, namely dairy prod: ucts, meat and Feit, ix recent years. As a consequence of this ‘more varied diet, carbohydrates overall have formed a smaller proportion of the diet. Nevertheless, sucrose forms a higher ‘proportion ofthe carbohydrate component Where there has been a change from simple natwal diets to a Westerised die, as in Alaska, caries hus increased starply and Inuit children now have a caries incidence at least as high as other American children. A similar state of affairs is develop- ing in Africa as sweet cating and sweet berweer-meals ‘snacks! hhaxe become popular. In Nigeria, many of the older adults are stil totally caries-ftee, but the prevalence of dental caries among children and young people who have picked up sweet- ceaing habits is rising rapicly. This effect has also been strik- ingly Well documented in she population of Tristan da Cunha ‘who, up to the late 1930s, lived on a simple meat, fish and veg- table diet with @ minimal suerose content and had a very low saries prevalence, With the adoption of wesernised diet, the eat= ies prevalence had risen up to eightfold in some age groups by the mid+1960s. Even in Europe, in the 1930s and 1940s there ‘wore isolated communities, such at the Outer Hebrides or the Loischeatal in Switzerland, where dental caries. prevalence ros 20:fold or more when sucrose and sweets became widely ccorsuimed, ‘The effect of limiting sucrose consumption was shown ‘on avast scale during the Second World War. Those coun tries which suffered food shortages during the 1939-45 War had severe restrictions, mainly of meat, fats and sucrose, To maintain an adequate calorie intake, over all coasumption of strchy carbohydrates 10se con Siderably. In occupicd Norway, where shortages were paticularly severe, the pattern of dental caries during and after the war is shown diagrammatically in Figure 3.8 As suerose became more plentiful at dhe end of the wat, caries prevalence progressively rose. 109 00 Fig. 2:8. Thewartine resco on et andar i Howey. The coinuous Ine shows anextimats fe chal ty ugar concurpion surg ane ator he war Tho highs of tho-colamns show tw ence of cea chien of fr ta he nadenee of cares decid sony ad coined fora ser ime after sugar became tel alae. The grt ct rodution i canse was the youngest group of chikzen home sth vere exposed othe warm ai forthe shorast petods: the motors ofthese citer, on the oor Par. ad ben oxsosesto the wate dt ughou presnaney and foralong povod bate rat. Manly ater ToverucG 1989 euro! the Amerean Osta Assocation 29 127) GMs SUGAR PER BAYaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.NTA cS In Japan also, rising caries prevalence has been associated with rising sucrese consumption. Towards the end of the Second ‘World War, sugar consumption and caries levela were very low. ‘More recently, Japan is one of the few countries where sucrose consumption, from 16.5ke per head in 1961, aearly doubled in 1070, Caries prevalence has risen in parallel. Unlike most other countries, this picture has not been significantly masked by use of fluoride toothpastes where the market share of Muoride tooth pastesis only 15%. ‘Cares has become epidemic only in elatively recent years 1s sucrose became cheaper and widely available, In Britain, there was « sudden, widespread rise in suerose consumption in the middle of the 19th century. This resulted both from the falling cost of production and, in 1861. the abolition of a tax fon sugar. Evidence from exhumed skulls confirms the low prevalence oF caries berore sucrose became Widely available and the steady rise in prevalence theceafter. Patients unable to metabolise fructose a a result ofan enzyme Aeficieney cannot tolerate frustose-vontaning fools including disaccharides such as sucmse where fruciose forms part of the molecule. Tse children therefore learn to avoid all suerose-cen- taining foods and have an unusually low incidence of caries, Experimental studies on humans In the Vipebolm study, over 400 adult patients were studied in 4 closed institution, They recsived a hasie low-carbohyadrate diet t0 establish a baseline of caries activity for each group. a+ 24-TORFEE (GROUP (FEMALE) al x SUCROSE GROUP CONTROL GROUP (= SWEETENED, BREAD GROUP IFEMALE) Te Tae as Fig. 38_ TheVoetnin dental ears sity. {sired slg showin the resus somect he groups of satois and in pati, the sth inact on cas act of sticky ewes eaten betnsen meas hen compared wih thosalng of weet shits 2 meatrmes The broken es Ineate those who consumed sugar ony et meds, the conthuous ne Sows hose who consuned sigar toh at ana betwoon meal. (| Gistafson ta 1054 Acta Osontloica Scandinavia 11232) ‘They were then divided into seven groups which were each allocated different diets, A control group received the basie dit made up to an adequate calorie intake with margarine. ‘Two groups received supplements of sucrose at mealtimes, either in solution ot as sweetened bread. The four remining ruups received sweets (offees, caramels, or chocolate) which ‘were eaten between meals, ‘The effects of suerose in diferent quantities and of eitTer- ent degrees of adhesiveness, and of eating sucrose at different limes were thus tested over a period of 5 years. Cares activity ‘was greatly enhaseed by the eating, between meals, of sticky ‘sweets itoffees and caramels) that were retained on the teeth ‘Sucrose at mealtimes only had litle effect (Fig. 3.9). The inci- desce of cares fell to its original low level when toffees or ear- amels were no longer given and caries activity was very slight in the contro! group having the low-carbohyaraie dict, In another large-scale clinical experiment in Turku (Finland), ‘an experimental group was allowed a wide range of foods ‘sweetened with aylitol (4 sugar ales) but no sucrose, The ‘control group was allowed as much sugary (Suetose-containing) foods as desired. After? years, the experimental group showed 190% less caries than those who had been allowed sucrose, Essential features of suerose incriminating it as the most ccaiogenie substrate are summarised in Box 3.9. + Sucrose brmsun toa thre of ha carzohydata content many dots + Tepemotss cobnsaten ottestnby Sueptocaccut mitane + Its disaccharide bor alone contains enough enory 10 act hac enya 0 on extasr dota at + its smal molecular seo alows to tse ready fo plqu0 * Bact! metatciomo sucrose opis Use of sugar substitutes (artificial sweeteners) in place of sucrose greatly reduces caries activity. The cariogenicity of sugars and atificial sweeteners are summarised in Table 3.1 ‘SUSCEPTIBILITY OF TEETH TO CARIES Teeth may te redistant to decay because of ractors arfeeting the strecture of the oth during formation. Serious elforts Were made in the past to confirm the misguided belie" that dlcatal cities was due to hypocaleiication of the teeth and wat essentially a vitamin deficieney disease. This simplistic view ‘of course ignored the extensive epidemiological findings that the best nourished populations had the worst record for dental disease, while poverty-stricken communities on deficient diets had a low caries prevalence, as discussed earlit Hereditary hypoplasia o hypocaleification of the teeth, in ‘which there are severe disturbances of structure, are also not pat the degree of calcification of the teeth affects their resistance ularly susceptible to caries and there is no evidence thatLet Lge elf legos ee oll reall he tl aig pov fi Saal degedl w - Sleegane city Bayly atl go aie Jpna le gt! VUplne gi ld ching ad) 5g) Su 0 AGL sll oe lydia MI lege dl iliy Sl pas pd (85S) Jest SI pigs phen Es eS Saullo dal oF ay He LiLo lid pb jypSaall Js LS Gla ye Silo op iss eS pA All Sal ay lg gua LS cole ose eal Sly gpI) oli Le 5s 731 AiLen! Sit pct Jabd LSS Laid clang high yi jgyS all al Se aA poo Lapis pS ds ah AT pb ing Liga gy BiB at oLSy -Jeoly Sg pigs iL! 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S50 dljakll voll ou dege de TD opey BD ols pe Lage Ele ypSi gall dts glial Gl yet sal! ily gael ask St ad ey gas Ld ‘tall gia Ssareihgal Mags ‘odgll ange GN peas (ebsiel a Lo pun) Saggy Sls pial joy spsll cla ga phi duulSatl gual seb Y dgaaiy jolly pli gpny Leaicy Layglas JMS psi Ph ol Se ophall ps pS JS a ob Shi stg) BE.0-7 AbxN beasts obull 550) SLOG he jptall olka ake dup ole tll plas ell jp ALS yepatl 3 gill hall JUS ya aisha gSe Le hay Sf! Sih Sly aad gly gill go Slat) olypeall sey opts anaes gS pled) LU Ob GL yo Ja) ay ST AeA Mast goa LoL gla he petal gta ib go Leal AS! ofpStul obs gant! site} pubs cael! slid! ass le jp Lil fp al enes Aa Sa JE SM gh an a in an ony ee es ta te Rl pad hye bl abrad Aigo pi oye cad gill agogl LA yaaa LANA High La gual Lyla dns pad gh egal pl eg oe ceed AAU pate Gintly nal le igh Hl Bah WU aS Las pF LEG Le pS pls gL 5) gull 3 WAN Ege pple galas ageg chil Yims gay wvCry NTA CaS ance of foodstuTs from the mouth, other physical properties of diffrent salivas have not been shown to have a significant ‘lationship to cares ativiy. Other factors ‘Inorganic components and enamel maturation Radiosctive isotope studies suggest that there is some exchange fof calcium and phosphate ions between enamel surface and saliva, In particular, enamel undergoes post-eruptive Clinical observations suggest that newly erupted teeth are mere susceptible to caries than adult teeth and radiosetive tracer studies show that newly erupted teeth ean incorporate 10 t0 20, times as mach inorgenic material in ionic form as adult tect, ‘More importants that saliva isa Vehicle for Muoride which can cater plague from the saliva and affect caries activi Enzymic activity Salivary armylase breaks down polysaccharides such as starch ‘This conteidution to digestion s small and its main value isto rmake food residues on the teeth more soluble to assist their clearance. The breakiown of polysaccharides leads to produe- tion of sugars, but the amounts and their contribetion 10 ear- ies are small and are only likely to be seen with experimental suerose-deficient dies. Usually, the amount of suevose present in the dict overwhelms that produced by amylase activity, In general, therefore, amylase activity and caries prevaleace are not closely relate. Antibacterial activities Saliva contains thioeyanates, a lysozyme-like substance and folter dheorelcally antibacterial substances ruouth terms with bacteria and there is a0 evidence that nen- specific antibacterial subsiances in saliva have any significant fect on caries sotvity. Nevertheless, the Immunological defences IgA jis secreted in saliva but small amounts of IgG enter the mouth from the gingival crevice. Persons who suffer frem defects in non-specitic host defences (complement and neu tuophils) or specific immunological defences (Ig deficiency, Down’ syndrome or AIDS) do not appear to suffer an excess ‘of dental caries. Nevertheless, an immunological host resist- ance to dental caries is detestable experimentally in man. and appears to act by reducing the number of S. musans in plague ‘The effect does not appeat to be very potent and iseasiy over- ‘helmed ifthe diet is high in sucrose or if low levels of the relevant antibody are produced Immmunologies! defences against 3. mutans could be medi- ated by salivary IgA or serum IgG from the creviculsr fluid “Although salivary IgA is capable of preventing caries in experi- mental animals, it appears o play ne significant role in humans. Immunisation of motkeys against S. muians generates specific serum IgG which protects them against caries. Serum IgG also appears to protect against $. mutans in humans, bat the response varies widely between individuals, Te has been shown that dripping 4 solution of monoclonal antibody against 5, muzans onto the teeth prevents recolonisa tion by S. muans in humans, For this to be effective, plague rust be removed before treatment by using chlorhexidine and effective oral hygiene. This effest of antibody lasts for several ‘months after applications and this “passive immunisation’ has the potential to reduce caries activity significantly. The effects are prokably not mediated by traditional immune mechanisms ‘but rather by binding to the bacteria and preventing adhesion to the forming new plaque. Once new plague is established ‘without S. mans, the stable biofilm ecosystem prevents colo- nisation long after the antibody has been washed avi. Key facts about the effects of saliva on plague activity are summarised in Box 3.11 + Salary compenents contre’ plaque oration anton rush of te marx Sueroan ssotes in sla and is actly takon up by plague {The bullsingpowor af sara ay tte fal caused by ‘eis formas in age +The butaing power fsaliais rated the rate of secretion. Hig few rates may be associated wih loner caries actly + Gress eduction Fy sary secreon lands toncreaseg cars actly wien acaregenc dt iseaton + gals present isan but hos eet on cares aty, ‘may pretent bec specs ram cobnizng planus PLAQUE BACTERIAL ENZYMES, ENAMEL SUGARS 1751 veACCHARIDES PLAQUE eieine BUFFERS SALTS ‘\ sauwany | _,.__acios. BUFFERS N caLcUM ‘Sars -— PLAQUE BUPFERS, POLYSACCHARIDES Susans, BACTERIAL Fig. 3.10. Diagrammatic oprsantatin of he main iochemal evans In onia plague, eating cares, rom McCracken AW, Cason Ra 1963 (Clrial and aa mcrebiclogy MeGra-HiL)ph asl MES Sia Sy lilt gal ila ladda 9 pp gob tM ge dns Epa ag aad ple gt ple poles Gl ang ad Los esto dole! aie glad! gle Silla claball Lae SIE) Sb MIRA cls yg, Soy pall gal clad ns phat ly pete Sangh ON plains Ube Jad mgd bg als yo gtd Sa a ch ld pig, LEE dnd GEolloes GAT LLL golpatS dled della Js Ae Je dangled peli I AlaLngy fois ¥ pslut La Sf Kael JLe¥! ghey ail SL LLY JUS oe oS) JS cAgaball gpuy Sagadl dogll) Ss atzy LSI Saad! Sphad gaghydl jlesiat! ALI! Aged! digi! B27 flail shus¥l Jos aes dsb oe dat! 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Ghagegil yal cleldall gb cfs dane) Age a) dell eli eLéall Jing Jie Si he gat 5 25 35 yo osiles el gate 8 Gate! ted aks Se tl pil) Apel in daglde old Bpilad cadad lad para J2e2; lg’ gee 9 glad gb p88 Jaaall 0g Lae lS poll Lk J gay Ho done Slip atl Ff jap] ge gad pile lad gL gldall Lal otal ga Ande 1A aboLingy SMa cabal oS dgalill celal! (es3 gpl alyetl Jelaal! gpa geal! IgG deLange gf glad Slee ok A ge ole lh GLAU IQA gl go ell 9 gages guid i Lele bp Gal ¥ al gand dpll fp gett 0G alps iN cad ab byl ai? 5] deal 196 gh Lin) gingg LoS yal! ue glial yes Jal n« wo Tissue rarHaLooy ‘The main biochemical fens in dental plague in the devel- ‘opment of dental caries are summarised diagrammatically in F PATHOLOGY OF ENAMEL CARIES Enamel is ceementum becomes exposed by site of the intial lesion unless dentine or ssion. Enamel, the hardest and densest tissue in the body. consists almost cetirely of calcium apatite with only a minute er Aen, I therefore forms a formidable barrier to bacieral attack, en breached, infection of dentine File obstruction, Preventive meus- ned primarily at stopping the attack ‘rat making enamel more resistant. ‘The essential nature of the carious attack on enamel is per- reation of acid into its substince. The crystallite latice of calcium apatite crystals is relatively impermeable, but part of te organic mausix of enamel which tals hus a relatively high water content and is permeable 10 hhydrogen ions. Permeation of enamel by acid causes a series However, once enamel has b can spread with relaive ‘urs must therefore be a fenvelops the apatite crys. of submieroscopie changes. This process of enamel caries is a dynamic one and, initially at least, consists of alternating phases of demineralisation and remineralisation, rather than a continaows process of dissolution E stages of enamel caries are distingushable microscopically and aa also clinically significant. In particular, the early (white spot) lesion is potentially reversible, but cavity formation is ireve ible and requires restorative measures © subsite for the lost mel caries develops in four main phases (Box 3.12). These Phase of non-bnctea! ramet cysts dostton Biacteral son ef enare The early lesion ‘The earls. visible changes are sesn as a white opaque spot ‘at forms just adjacent fo a contac: point. Despite the chalky ‘appearance, the enartel is hard and smooth to the probe (Fig 311). The microscopic changes under this early white spot lesion may be scen in undcealcified seetions but more readily ‘when polarised light is used. Microradingraphy indicates the degree of demnineralisation seen inthe diferent zones The inital lesion is conical in shape with its apex towards the deatine and a series of four zones of differing translucency tan be discerned. Working. back from the despest, advancing edge of the lesion, these zones consist frst of a translucent zone most deeply; immediately within this is a second dark zone; the third consists of the body of the lesion and the fourth ceonsisis of the surface zone (Fig. 3.12) ‘These initial ckanges are not due to bacterial invasion, but due to bacterial lactic or other acids causing varying degrees of demineralisation and. temin features of these zones are summarised in Table 3.2. ‘The translucent zose is the first observable ctange. The appearance of the translucent zone results from formation of sulbmicroscopie spaces or pores apparently Iceated at prism boundaries and other junctional sites such as the sire o Revius, When the section is mounted in quinoline, it fills the pores atd, since it has the same refractive index as enamel, the normal structural features disappear ond the appearance of the pores is enhanced (Fig, 3.13). Microradiography confirms that the changes inthe translucent zone are due 1 deminerlisation, alisition in the enamel The Fig 3.11 ary enanet cas, ite sot son, a deduous mola. Tho len forms bow tre cortact pont anim consquence feu gee thon an irerprerallesion na permanent oath eo Fi, 3.1 Fig 3.12 Ea inteproxinal cares. ound section n water vowed by pcisediht. The icy Delon sid hota staceyRS de eshedl git i] Saat obyasill oka spas ¥ ed gill 593 8 galee¥ ye 4 pesipdl oulll uae oe fellae © Ainll yb gameall dstely Qh) oo Aalne cles FF Jyabl gb duaSLS goal oka ety dbgall) chats Jy) ge SUG Last! SB plane ) chile YSts Jy asks aatatl gine sesiel sue ole abyss Lal cualall 50 anSs cas dane AL gut ia, AbheSH Glo et yaaa Yok yabtly WHS GM gobs gly Aaa dal gd dashed dyed! el pl il pL ty ca alt OU clad gS pl Le 9 AU seat! LSU tat La Eby Losics gugesy Hoglas ie GSM MALLGM gills andl gay vole! silly jpil! Laan . dT Ley cla ihe gy Ld get ps ginal 1) po Leys pls aks Loud oud! i Jal! dpa allel! g sliced) ln Sitt pith Leyio bels JEL Ly Jin guine gps 22 peal fl adgiat ana Spy Ur yeu) cbatatl gla Gy Qussell Jyj sua ad ADL asl doable os ght hing py I ee ype 9s NAD SBA Tne Sgt Gey test EE BT es aa US Jets! 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Ges AALS 5) GLO aul AM deaatall JRaciy 3) 2n3L) olla Syght) ASN Sp elnald pal! on geld gc lll iim GSI Lae Bigds pab tht Baki Spay alll le gyn cS gly soll SLs! ge ents eegarall uledb B05 ol oSe9 Sy Aall Aueall obs oS gd) ob clyaball yo dlawl Sebl go JM! gle gions Je ofp ULES Gilet! cpatth JAM SLs pa ay Sahel yume Sl coe Lglita SUT MM eas Lolo es) ae Si gS js 8s i Lal 9G LS sp gane eit) pad gs Jol aha at dingSe (tay deny Laks 2401 2IM gS a5 dyop AR ene Siofpel lly ape pad ERI LS GT Sosbillinadt pesca cara poeta etait eat ge His pai lat a at pe Sl al Le JE cing dhl dees 5.5 2 oles phe (opt eps ae Ly aa ill Sip yulZAlad jane Spek sala gh ghe ONE LSIN gypcatall pall! ga Alaa pad able pd5,Sall clined Andon iygdl poe poly laduall sgl She pdgs gBslgESic MN BAL Slate ph Sal Jyh dy ball pel Lal po Lp ey JEL Saga Sl GM ops lly abl alee gle ay ga Ada al 5 LoS a8 pall pL! Line j25Y) dita fea gall! aie il See Saka eH) ahh datas yo alls GUL aka 3 tn oe SU Etsy te St aa (1 JS gba Lada ye 8NTA CaS Table 3.2. Key eaues oF e enamel oes prcesng cavity romaton tone oy atures Comments Tranducert zone 186 mineral los Eavlest and despestGorieratsaton Broader progressing carlos, narow or absent in arrested or omnealzed lesions Devkzone: 2-4% mineral los oval but a zene oremineratation Broader arostd or reminealisa sions, narow ust bone the aduaneng Ft bh achancig lsons Boa) 5-25% moral ss ‘Broader progressing caro, replaced by a bread ‘ark zone naresieg oe emiroased ears ‘Surlce 208 {Seine los A Zone of eminwrasation resting Reately constr with ato tiekor fromthe tain barre and mineral corte of anu siesta of amneateny ese Cavtatonis bs of th ayer, aloning Eacora Fig. 3.13. Eay nbrproximal ers. drow econ vowed ay pasrsed rl ‘the five deta the body of tholesion to dean Fig a the dark zone wh ts smalr pers is acoortuate ‘The dark zone is fractionally superficial to the translucent ‘zone. Polansed light microscopy shows that the volume of the pores in this zone has increased to 2-4% of the enamel vol ume. This change is due mainly 10 formation of additional small pores. Two different-size pores thas coexist in the dak ‘zone. The small ones are #9 minute that molecules of quinoline are unable to enter ard the tissue has become transformed into ‘molecular sieve. The small pores therefore remain flled with air ~ this appears to produce the zone’s dark appearance. Miczoradiogrephy confirms that the dark zone has sutfered a seater degree of deminerslisation. However, when the lesion is ecposed to saliva or synthetic ealeifying soluions in vir, the ‘dark zone actually extends further. This may indicate that the formation of the dark zone may be due not merely t9 creation Fig. 3.14 The same eson Figs 3.12 and 5.18) vowetcry under solar Isodlightto shaw the ful cent of dorineralaatier. Figs 3. 12-3.74by ‘aha perizate of Prveser Laon Storetons and he eater f Dol Update 1289; 10:262) ‘of new porosities but possibly slso 40 remineralisaiion of the large pores ofthe wanslucent zone so that tey become micropo- resimpermeable to quinoline. Its widely believed therefore that these changes in the dark zone are evidence of remineralisation, as discussed later The body of the lesion forms the bulk of the lesion and ‘extends from just beneath the surface zone to the dark zone. By transmitted light, the body of the lesion is comparatively trans- lucent compared with normal enamel and sharply demarcated from the dark zone, Within the body of the lesion, the sthae of Reizius appear enhanced, particularly when mounted in quino- line and viewed under polarised light, Polarised light examina tioa (Fig. 3.14) also shows thatthe pore volume is 5% at the periphery but increases to a leas! 25% in the centreimage not availableoo a ao Tsu rarHoLogY 9.215 _exty neni ene A micro ott se eo {kn past ot Pres A Crag) Microradiography, which will detect demineralisation in excess ‘of 5%, shows thatthe area of radiohicency coresponds closely with the size and shape of the body of the lesion, in contrast to the surface zone which appears relatively radiopaque (Fig. 3.15) ‘Alternating radicpaque and radiolucent ines, about 30mm apeet, ‘an also be seen passig obliquely though he substeface region ‘The radiolucent nes show an appareatly preferential deminerali. sation and probably represen the striae of Retzius, Athighee mag nifications, still finer lines running aright angles to the enamel, surface, and others parallel to the surface, may be discerned ‘These lines may represent preferential demmineralsation along the junetional sts mentioned earlier and represent the prism bounda- ries and the crose striations respoctvey, The surlace zone represenis one of the mos. important changes in enamel caries in terms of prevention and manage rent of the disease. It shows the paradoxical feature that it has not merely remained intact during this stage of the attack, ‘but remains more heavily mineralised and radiopaque than the deeper zones. Ithas 2 pore volume of only 1% When the surface zone is removed and the el is exposed tw an acid buffer, the more highly mineralised surface zone reep- pears over the deeper changes described earlier. The surface zone therefore appears to form party by remineralsation. The remineralisng salts may come either from those corcentrated in the plague or from precipiation of calcium and phosphate fons sitfusing outwards asthe deeper zones are demineralised Fig. 3.16 Urdocoltegsaction showing sty erametosons inthe In pit and rissure cares, the same chianges take place ut as acid diffuses oat from the pit, the esion forms a ring round it. However, in a two-dimensional view, the same zones as in smooth surfave eaies ate seen on either side ofthe fissure (Fig 3.19). [As noted earlier, the inital attack on enamel appears to be by highiy mobile hydrogen ions permeating the organic ‘enabling them to attack the surface of the apatite crystals. The apatite erystals become progressively smaller. Microdissection Of the translucent zone his shown that the apatice crystals hare declined in diameter from the normal of 35-40nm to 25: datk zene, by contrast, enamel crystals appeared. to have ‘grown 10 50-10Gnm and in the surface zone to 35-40am, ‘These findings also suggest that deminerlisation snd remin. cralisation are alternating processes. However, as the lesion progresses and cavitation develeps, demineralisation comes t0 dominate the process, In broad. general terms, therefore, enamel erysiallites are progressively dissolved until disintegration becomes visible ‘microscopically, Defects eventually become large enough to allow bacterin to enter, ‘There is evidence of preferential destuction of the prism ‘cores and, experimentally, a similar effect is Seen when enamel is exposed to dilute acid (Figs 3.17 and 3.18), Whatever the precise nature ofthese changes. bacteria donot physically pen trate enamel until acid destruction of the tissue has provided pathways laige enough for them to enter, he stage oF cava toa (Figs 3.19 and 3.20, nm and in the body of the lesion to 10-30am, In the Cavity formation ‘Once bacteria have penetrated the enamel they reach the ame. Jodeatinal junction and spread laterally to undermine the examel ). This as three major effects. Fast, the enamel loses the support of the dentine and is therefore greatly weakened Second, itis attacked from beneath (Fig. 322). Third, spread of bacteria along the amelodertinal junction allows them to attack the dentine over a wide area (Fig. 3.23), Thus, the primary lesionSoS! St UN gl OLY dyna yad gas MAP Sa LD 0 ja gy il aan yh £5 GSI5 -Sebily akegtt yas ot peaall guts a Ugtge dle Jats cai Sb ag) CAs Geel Lal I pelle gle Ladle pyle aL! gil ai Gj) ne SSI gala qual) ps gb Sapesll ly dgiltce or $05 plall Sle 2g¥1 dengit Gb .Lakw 453 Les) ALAN 85 gilly ASH 5S eee ala oe ABU AL uae) SUM ipl Cola donlge Mgt Gemmy Ue spans GaN sali cai) aie’ ge shinl aight oun cused jo SaGl¥l hgh lad gels AULLI adksal gd! 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Jig ge Lyle baka!NTA ca provides the bridgehead for the attack on enamel, but under ing of the enamel determires the area of a cavity. Clinically, his is frequently evident when there is no more thaa a pinhole lesion in an occlusal pit, but cutting awey the surrounding enamel shows itto be widely undesmined, ‘As undermining ofthe enamel continues, it starts to collapse ‘under the stress of mastication and to fragment around the edge of the (clinically obsious) cavity. By ths s Box 313 Process ot namelcaies The warty damage f submcroscope and sen as seis of 2ores of fenrgtaesicency racograpny cons nt fees changes preset arcs of Iremasirg domneralaton The surface zone is gel formed by eminealssion Thee fattening daminursaon ard remeron, but Clomneraetion pedomnant as cay fomaton progresses Bacteria canal invade enamel ut demerateation peices patty rg enough tor themto ora ena) 1 nat by trogen ons causa bacterial damage to the dentine is extensive. ‘The process of enamel caries is summarised in Box 3.13. Fig. 3.17 clay mamot An clochonphstsmirearah of hay enamel produoed by he acon el very cute aci, The cystalkes ofa sal ieorpeamatic substances nave en destroyed. The same acpasrance ‘ston chal enamel caused by ony cabs, By Kec permease of rk utie) Fig. 3.19. Diega summarising the main features of th prosenitaton ‘hese ofsrarat caries as ened here sal tage of sd attack ‘The roa/A) wuld be radlucert in a ite-wng fin But he aca cous ‘graphy Circa, enamel would appear sll ana act Et the ue {nce woud be marked by an opscin white soot ce the nen as aenn in que 3.11 Fem MeCrackon AW, Ganson PA 1953 Circa ra micoblooay. NeGraw sg —_Tematixtobemae corse n heregen othe pram steaths than nthe Fg. 3.20 Ear caviation m enanel cates. Th ssface yer tho write ism cores orintrorismatic substance, (8rd pomissn Or K Lite} spleen hastbrekan down, albwing plague baci to the eratedail ga Aetna Lay Angra d nhs nah Ut opepecl apie dhist sat * a8 SoU pals all ogee LIMA gS * ea ene pA jhe Je oe J Ada aR A + eae oS J a SE Sing ge ul 5p ape) elas gn # . att teehee iSite gk eee iLe ab piece maidens enepssgtad vr yet ARABI kL gh tt al le pn ee se a ane pages aa Lik Lie gal el SULLA Ral 34s Je. LA gl lg papi! gl Sob al el cll oD glade AY lB Al Sly dnd A este ab phat 5p Lacing Ln eal pg lr die at 9) FremMocrahon AW) (V7) SSA pb Lal A Sill iy Ay igen »* Aah Adah ah pla pl kee ke Fo JSST lod Jpoas Del t Svan eangel yadl A 9 ait 1 aege T Le ate Le by sll! gad ySly LLL! ines gd gupsall ysly ones ine danbe Lgl] pyle dlagt! see SB segith a Lele elit peed Lpata! gy ‘ay siyjipin tacalyy 448) as Jpg ecasy Gast dessly Glall paSlsdl ail gp St alo, 20 ode glial pS glee VT Uf yas, amt YI a Hitt Sat denene ee teeth att Ta yet Sige ie My eS Goole Las! ope pb ge BLT dt Phen yet Ca Rpg La yen deck peat a ap Gong lk ay 2 dy al) ce aghl ay apcelt a Lenbns bp Pi ina) gyal MA VAP Sat SS I ot ALS JOP pps dope ae gat Loy! we ge TSI go he asl yng tae chee go as oCry ‘ano T38UE maTHoLoGy Fg. 3:21. Low-power vw ot carespreadngakeng te ameldential [nnn Note ow tsprends ony a nat detanca hr acvance of ales In denine, Te amledernal urcion sony lle mere suscepini tS Fig. 3.22_ Caries spoad along th ameledontna junction at higher ower ehonieg how enamoie utdered andere blow. Th ferminaions of he centr tubas ae eae ected but deaructn, at ‘tie atage, ain athe expen othe ena eat fs hoe ineralonien. Fig. 38.28. Bto-viegraiorech showing tempos cas below my ofthe contac! por PATHOLOGY OF DENTINE CARIES “The iniial (p0n-bucteral) lesion forms deep 10 carious enamel before s cavity has formed. Ditiusion of acid into the dentine leaves its collagenous matrix intact at this stage. However, ‘once bacteria have penetrated the eramel, they spread along the amelodestinal junction to attack the dentine over a wide area. The lesion is therefore conical with its apex towards the pulp ig, 3.24), Infection of the lesion is facilitated by the dentinal tubules \which form a pathway open to tactera (Fig. 325). Atter dem ineralistion, the dentine matrix is progressively destroyed by proteolysis Streptococei phy the major role in the attack on enamel, ‘but lactobacilli may be as important in dentine caries. As the lesion progresses, the bacterial population becomes increas: ingly mixed and their relative contributions to dentine destruc: toa become more difficult w disentangle. AM ist, the decaleited dentine retains its normal moxphol- ‘ony and no bacteria can be seen. Once bacteria have reached the amelodentinal junction they extend down the tubules, soon fil them and spread along any lateral branches, ‘The tubules ‘become distended into spindle shapes by the expanding masses ‘of bacteria and their products, which the softened matrix ean- nol confine, AS a result, adjacent less heavily infected tbulee become bent. Later still, the intervening. tubule walls are destroyed and collections of bacteria in aljacent tubules coa- lesce to form irregular liquefaction foci. These. in turn, coa lesce to form progressively more widespread tissue destruction (Figs 3.26 and 3.27), In some areas, bacteria also spread laterally and. ocession- ally, large bacters-filled clefts form at right angles 'o the gen- eral direction of the tubules. Clinically, these clefts may allow carious dentine sometimes o be excavated in flakes in a plane parallel to the surface (Fig. 3.28). ‘The main events in dentine caries are summarised in Box 3.14 10x 14. Key events nthe development of denne cares ‘Nor-bacii. recantation, ac softening of mati Ween utues by dr iereiston Migration of ener acta along Tubes Dorion of tutes by expan masoos of bactra rakdoun of erring naticorming lefacton foc Proyosee diononton ef remaining mat wu Protective reactions of dentine and pulp under caries ‘The reactions in dentine are mainly due to odontoblast activity. so that dentine and pulp should be considered as one tissue, “These reactions axe not specific and may be provoked by other irviants such as attrition, erosion, abrasion and restorative procedures. Reactionary changes in dentine start even before ‘cavity formation in enamel, but are more likely to develop sig nificantly under slowly progressing caries.Pb SAU yl CeypsatT Mia ga aad Gat gh Weagipdl pat) dust asin YS iss Lal hall gi ved LA og BAS JG ad 5s el Gas UL Shy LeU ake yi Lake ets! eek) prbetisLiall paibe Jobo gle Lit ash Lgile. sli Any Sy te AM oyS5 IAS daely dddae le cla! 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Fig. 3.25 tection ofthe dentinal tubules, This cectrorphotomicearaph ‘lagenous matrix the denne, By ke permssion of K Ut Reactionary changes in dentine ae summarised in Table 33. ‘These reactionary changes sart to develop early but at best, can only slow the advance of dental caries. Even sclerotic den- tine is vulnerable to bacterial acid and proteolysis and once ‘ctera have penetrated the normal deatine they can invade any reactionary dentine to reach the pulp (Figs 3.29-3.32) Root surface caries When the neck of the tooth becomes exposed by recession of the gingival margin in later life, a sugnaion area may be formed and the cementum tacked. Cementum is readily 1958, 0727-20). Fig 3.25 cares ot demo. noce! tse ar! elon mans bac te have expanded rio the sofned issue Adjacent ttl i the dom decalcified and presents little barrier to infection. The cemen tum therefore softens beneath the plaque over a wide area, reducing a saucer-shaped cavity and the uncerlying dentine is soon involved. Cementum is invaded along the direetion of Sharpey's fibres. Infection spreads between the lamellae along the incremental lines, with the result chat the dentine becomes split up ané progressively destroyed by a combination ofUdnipa parila A’A A ta mounts ursees (YC) (CD A gb Aaah yeh ppt Jiss agp ant aieveye 8k, GB yaa eal ent glial pss an sab a © « "#4 So Gis; manea "geek ciseatip secunetsity Ciena % 3 ~ i ay puis Ye oa. 2 (mart Deal ral Cite, FX HORS HS = taoerar 38 geass OHH : Aes asd Jat ae! ud pop all gad AP Jt iy ST jan as Cla gulch at) al geen estado te 22 LW od 4 ght pid Wee Fel YE, JS hae Ucks deal Sle Gi anydl qhetal Grog ips Chall lay Le lena gona! OER pny gobble ob Jyh ole Loui! Snell opSiy Ghat bephe Jple Gle glial! oe IS me ates US ety let! JL! aed Apel! oa ghd gel GH gh gta TOF YSU St al Ta aoa Raa abt Sinn WY Syed pb dbode cLal pb ipl 8 ots) Sele pall 9S.) Sh plat dul ohadat obalag Chel ng gael pil pa eye nn Ja gpg posal JEnaly ag dt good ob Lanta oy ¥ Lat! SSS heii eg gab chal edi Hl 85 Uy OF gee RM ga JEM ot Sil J pal che gh 2H gi 9s ua) (tains ip) all gad ity Lae fis gts Gad peat pad ae Gp dee? LO alg dS) erlang of‘ano T38UE maTHoLoGy Fig.3.27_ Aevaned dentine care, The dentine ditngraing (et). Te {tet Isa tege untaction eta and tos packed wh Bnet Fig 3.28 A ransiuent oe. Th dina isos oe sen morose secion. Thosain the cee of to pico hve become bitatod by Califcaon of hei conten; er tho ose oti of Pe us ‘eral vsbieand te ore appears fansucont arsed ght On| ‘tor sd ae patent bib ied with stan, end lent by O: Go ake, ‘Sn repredicel by courtesy f the Honorary Edo, Proosaings othe Rojal Sosa of Meccre 1986;51:678) Arrested caries and remineralisation Precavity (white spot) interstitial cares may become arrested Fig. 3:28 chs incaros denn. rection racking along the tuulos bithasalea spread across the ube, forning eis nected es The appaararenssiggost Pt there ao ras of nostro the date, When the adjacent tooth 4s lost so that the stagnation azea is removed, The lesion may become remineralised by minerals from the saliva bog nic nfsctonspraacs easy, Dentive carles may occasionally be arrested as a result of destruction of so much enamel that a wide area of dentine becomes exposed. If this surface is then subjected to attrition, plaque deposition may be prevented and saliva in contact with demineratisation and proteolysis, The further progress of car ies in the underlying dentine is essentially similar to that in other parts ofthe tooth, “Table 33. feaonry sae nein esses Ker ct Tir ececos Pda dart educa th so ote drial te proving bce parotatin ad gonwalinga rare hoa Tee Ge freislet econ tay ores roa leben omren ae teres cer ‘Namea tons sor ohh ma bin raptor ssbb wh hand ranvmant en een caton Fogler rectory Fora te pdo-dere face nd ae a Wd archueo oirm Fone epore ford ta enn tnd ay saerro ap ore neg te Gen hme Ora Cts an pu. forty Xt Iemsmot oth orn sth up chan whe int ee iene ge cares Ineoisreictory For a eponse to moderator sre by cre nd comparing anges om deine wth ear cone {ile toa dnorgsebone tne mrad tee fours) Danae Pare hon dics ci wl fav adam md opr dr da rraton on ara ble ‘toca dt te doa stay be sles hi acre sca fot, Rnay lw tre ape pomessAL gah ie, oe eg Ligh le) CU ay pte peta hs WE Jha (ib Aaa hay ke et oe SW Blend 2127 EGIL Sl gold MS GAL seep deel! Nonorary Estos Proceedings ga Jit lays atl, D7 GO Blake \ {af the Royal Society of Medicine 1955, 51.578 gatadll Babel aaigilt st (chine dada yb! Jammy ab gi GusSll ps cigs, s ag ay og Ailase JIS See AB gaa adh Lense Sy bal pte py pated Se IA SU AoA oe gl Al gat ot been ep lyn HAP tga gt Uy Uap tga) deeS phd deci Litgel oLell sat! pga Ae at pig all pba Thal oe daly okie GLY Heal) 8 Bree yt) gall eg tga! ally gases Laas aBb cas, Leg Slaw Ghat Ne a8 ly Fish yal ay gall US opaeS Le ll cla yd pall fo aH SLA feoliny Dug SIS ee battoe ee pA ta Tr ph Set gad Seat ang wale yg nl nth A an joo Gal Jy aha rte al Aly a ee hen gt ae Tyke ab fila pais ba ak ge ake del yd sah J al dea A hp gy pola Al ge Jy sie seal seat baaa niga easy any Casas po oth gat ny pay a al gs tae Lah se Ald yelp PAA La Ces a gna all 2 pe sie et pe Cyne dee phn La ESS ALU Mg ny Cpa ae os aia anak enh 9S a yp pada LSA ll Ap Syhee tt i foaereemayere Seite he Fig. 3:31 Seoondry (actions dentine and cats. agar ul, se ‘ny dene sere! unc acre cav Al rai the nto tthe pray and secondary dentine wher he buics charge ection ‘ong th uncon end in tha ubues of fe eactionay er, te lesion can contribute to remineralisation. More frequently ‘ut stil uncommonly, dentine is exposed by sttrtion and remains earies-ree for the same reason. It becomes ssnooih, polished and stained (see Fig. 4.36). Fig. 3.32 A aad tact. Tho omy tuto toiow ho wom incisal ogo ‘ho Bou le wha sa to wn bey are penal om the sree, 0 hat tre whele2ore anpears Back Al the proxmal ond of Pe tubules te dactract ns bean send of iy mera eactenar denne tfecugh whch he stan cannot penetrate. Tre pulp fs us pretactod rom Under favourable conditions, carious demineralisation can be reversed and esr lesions can remineralise. Use of uorides ‘and consumption ofa less cariogenie diet may cause a serface lesion ia enamel to heal entirely. Even under natural condi tions, approximately 50%e of interproximal enamel lesions _may show no radiographic evidence of progression for 3 years. Similarly, in some patients, secondary caries may not neces- sacily develop at the margins of restorations overhanging the enamel Adult and childhood caries, Tm adults, caries usually progresses slowly and a small cavity ‘may take several months to develop. By contrast, childhoodSe pals yale ts Pear pS anton ih Mae Blas ely pa ial Aly dt ae oY AN ph 29 EL ie pak th gL seb 22 uu Laat eee MT Visa cst pe Ug tas 9S all nll Mia ay ast Ha aks NE Aa te ee a J gs (ge ladle) gt! bl gees Yop ak pat clay al “eka AB ge ADL by St gw Hane wll apse gb UB gi gpSill yeseil jfaus lee wan ai LAD lanl goby as 5ySall OLN jue7 ake ay deiga po Hala GY al GL I) Lapis Jal old ably ye fO> HN ili Le GLU damsel gg yi pany clad! pests le poled Job yas Y ab azell ASL otidt oi FAM ats Fads vailbe JSiy g clgiay aL er gal el yb Lect! bap tl Blye ase bay el cettLtly JUAN apg hppa by ggg) pgp psy be la plat 5 GLb cL go yaad leg plas Sasa igi g er got cle Ea ay ti pit cua MP JS ne Al GY CLA i Al ny ab age del By ob galt Dek ale AE et Sl ae tal ga a ql cla yeu al aisty iy AS! fotay ganasll lel gb aM! Fas loan, lal cy add gL SE Jit Yeas, Laat glad aces ae a a (it Jesuit bowitenatay 0eo Tissue rarHo.ogY ‘Table 3.4 The paotogy ot tentalcanies ad is rience cares progressenanareatnent Feature Signiteance Plague tora is table ecosystem “The tactar frais ntuanced by fs entrant bt the acosjtem il est changein the short term Denia of caiogsic substrate by etary contol wl ede the ramber of caronerc scaciesbut Solar change must be martaned tobe elective ‘ho ety carious ioson sa subsurace procses ;Bactra canotentr fo ora unt tho uric lyri destroyed and ur thor can be removed by caning Unileaviston, complete repair by remineralsaton spossbisnd peventon of vation cio Enamels permeable, pores botwoen cystattos account processes extend to th enancl- Earls Foreus acts fuse in aay fo at cares ard aituse to denine toinage pup dence rwaetons exy inthe lesions span, we bee a sion cavaes “The tanshisent zona erat cafisis pasentin ont copexmetely “The wonatvsent 2 oats proyroodn, Many loon we Pet act muh fo tr “Ta dark zn ot enamel care ie sonn dost a tosone “Ta cark zn indicates remnaraantion Theor, amos al ions undergo voce hasas ofremsaiston. fa remirralsed ot arostd lesb te dark zone extort replace mush Of hebody of the lesin (Caria leona undergo rapa paces of dmioralstion and Feminration, Activ oF rost ‘may bee utoome cependeg ‘nite relahe proportion of ach Cais may emireras, arrestor rogess cn very slow so that, inti, cbsenation or prevent intaventon rather than restotions appropri for most nal esions “Tha eros zone ofan enamel loson ety 20m ck an orcas rosa fom probing may cavitat lesions, converting an aesto or slo progestin lesen into an ato son, Daghosis sud ne arp odo ro sure to ce sckhess ort femora plague are fe the autacs texture Fuorde and the remneraiing agents may enter th lesion ealy Prous nana! koe in exogenccs pigments jo tet ion standing lesions become orm spt Fssuo cates areadelatraly into he wal ofa fs, ot Ino i base “The sua lyarf celal arama becomes undead but not ila) clrecty ved may nol facture oF aaa aca! Uri he undeling lion fare (oos cares) “The shape the enlarging cosas leton s guded hwaresanalatraly by tim prism direction ‘an occlsallesionivoves auch gear area of dentine than a comparabiysized oath sce tenon ‘Tho shapso the adncing ont ot atau kaion nr aorne mocth art outed “To conserve tooth tutu, cvs should have erboth rounded cine and ne sharp intoral anges (Cais spread ateralyalora the fmelaenia ston Late extension of a cay 8 ofen determines by daring cars rom the ameledentialfntion (203) However, eres usualy ny prensa to apponsraly fe ene tho fiona to Surface and n urderyng dori. Athough levg casa the uncibn fs undesrable cause it loaves enamel peony pain, romav of ADJ ouroe cn bo inderakon sancontily Caton svete ureredtayn rolaton io he se ancetert ofan fperosimalesen on afacoxraph ‘Some asesement of the patient cainsk nvolira det arava Ror aot factrs a requied bdore deciding that any sion eaures opvatveintenetin Lesions ina gh isk bation Cave ease han in ini patent “The pulp-dontne como sponds tease, Ine denna ut bore the axancing ont ofa caus sion Ieroitwely mpermeatle 98a eau Cf reminereaten an tubul elerosis “Tho pulp-chtine defence reactions shoud be proverved and ths bost achieved by non-aporave intenanton rather thar restoaton Minimal etna shou be removed neat eeparationn esp Tosore, removal ofa sttere! dete vers pulp shoud be woes Denne cas ray bechided nto zones of ceneaacton, panetsion “Tartana caviy prepara Inved moval of fected dentin, Howes, tient mcesary te rorove al nostod cori to provide success estan, Me corto aout Wo raves (eontveaL gute, ba A pi Ley pel pa a) LT Spat San aa ee ee ee ee PALA ADA ce al pl De pal al Sd Sia pS Sg plas 9S Be ligt I ga at alps aig ol orga el ee alent al Jo ose clgadnstt gn ty ee Slag ti lis papper py plana! ah pasta jal oy ca Cia py Eats oner ieee im peat ered Sat a eat EAST ced ctper ov lg A ga St stag YSU ye als eprveereryene Die peta a ss a gana ey aay ant 1 Sy oa IS ee yl Ja dpi an lal A ta iyasciin is nt sph pA ps gh ead Dl and aay au eee ey Hilal para Jott gsdatle ash bbb apaatou eas AUIS AN oe ae cit Jat aby pia ns ag fda it iit 2 on Hebe kn J ad 8 papa ge cy a ling he pl Se deg okey il pa at Lap Jos ans ent TAO peddle yell pane pga? Aslam 2g data phan nad alee Pasha Le ete Joti igi age TELM pschaLs a Sm a J ghd Le bettiteons Bie Stina WW ya playa aga ast gaat pala ct eee Borer pw nal spe blip Dnt gle Bnd wala nla dnd yan enioasl aa BOA Soons pel cla pas pA Ds pa Aghia aa a se abe ste ants ee aay pate peta ne rill ae pn Sgn pl ghey ab Cal Quad yA 38 sa Ee a lh gs eect trae i MN rtp ie Peete rant ey lily SLED el pd Sly gh pe lag pay Jas Se ipa ie UR fy Lee as Sd pl ob gl Satan dae go llc el Jt path Sina sat wet tabi s sca gies wr ele ipa le aaa eUpns Ue alge Jule ye dna cb Ade Ra Seagal pal acne specail ge pal, wD juga Joi) ds neatauiT Ld pA ppl at an GS ass, tpetitea ast aes pri AE gr algn tS ab anaes oe hea ches ey eel Aap ose a jin Smaceyee pa wvTable 3.4 (comnved, Feature Signteance and destaton or intozones of inlet ar afte dente ‘oualy judged by the dogs of sctering. Decloraton isa lass efocive ndcator Discoloured but "Teasenably fet har dentine may 2 let su. These 2ores ae of itl siicarce beyond Understanding he ease process and none an be eal defied nia, Pritula dontno nd rerio forma sclactio zone at was of tholesion ator spread is wos as carlos peretates dont, When reoving soRenod cotine wih hand insane ora sol revohing bu; sek datea maybe fe o harder then acjent dentine and shouldbe prsond Pntubulr dentine oes wy (iy slowly advancing sie ae doled by bie deere reaction. Asclorac zoe vile ragogranh- cally icles a slowly progressing or arestecleson Dental ules mare eth re agit mol than basta osc Bacterial penetraon of dentine towards the pup can ony take place afer ome dentine Domnoraation procedoo batons Invasion in dente bya smal and Not eofaned dentine mua ba removed ung ent prparaion “he edvancig font of bacterial penetration desing ogular Bata miroscopiclvel “The matty vos mechanical natumert used to ros scene dentine wil hay nae some infected dontine bint. However, sabe fective Dol resratns, oso bacteria wi bo rendered et Supercial fectad denineie ‘Send and arnt remem Deopor dentine wl enineaise ven thaugn ft contana bacena Its not necessary to renoveallinacted dentine to place «restrain onthe dentine that cannot romietale sated Gelon the testoraton. Theatre, carbs amtal ay bs mers Sonsevave DoW ‘A Wob-soaled adresverestoion fan below an araigan Dorr mae soon by becteriain the supeical ayors htm zene of destrcton “Ths rng be dont suacepine To crsmoneclanical canes renewal ang propery matures of sodium hypochlte This procedure roves only the most damaged caus deine a conserve pprcach tha reserves Ue dewpe lye tht can enirrane DDontno pio wanevorty along Incremental thes of erourth he DDontno casa nthe our zene of doclrtonseaalyromovedtin largo aoe wih handinatumers| (Cares inceator dyes san satan Adhoing sic © the dye potccl wil mee remheralsable drt that shuld be it stu, fa wel as octal derinw Cros intr dys remota overcuting Reaclonary donno fom sbnly FReacionary donne provide ite protection baow ply progrssing losis and varies maria amour ‘by and perma adie four ‘bel oly al he lesan in perarnt teeth mote Fequert pray eth) oration ot eastonary aerane requtes a good slood suppl and Feat pub {Less tomecin oir nvuls. Once the pup is irate quay of any rectonary dentine | ocr and tis ukaly tbe of ruc beneft ‘Symp of pups donot coeds wal wh cares ect lion size, pulpal nflanmaton aroven dect pulp wovarent ‘Pulp aly ray be toa wi ayo, cr ely mld eprpons An anaes of esas of ‘pulps estab to plan restoration of deep carcus lesion bt base en symptoms is nly Lesins ofroot cares a have @ Sues reneralsed aver ‘Avoid hard probing apparel tact though iscdoured surfaces, a for enamel cae Bactwia penetrate dortine oxy Inet ears lesons but se avcossioto prevrithe measures Removal ofinfectod dentine snot ways racessary to rent Gary root aries Primary teeth have approsiratoly Fa ho teas of eame perranent est larger Puls, longer pulp hers at est italy, ler ental ube Caries progresses fast in pimary teat than permanert testeal eat ereenseres) out! Tae ado 99 aS ta gd ph pA ip De Si dea hyo tle AU Ste Se ace pe deielggpaibaglh anegac}tySpsib aang pep Say apa ae gan bat gilli oe ab pt Lae i pe LR de as gent Je ca bs HE Se a eae peat aioa stay Ae Bu Aiea Rn ‘pb add 9 ib pa ab pl Ca sae geek I Ca Ie sg a agenda lf ge al al sy bd SB Gl ya a ca, ane aan ial yt a at alga tt Ab gt A ll CU Ay pe any patent sens Seattle Soe SD LANG daa do Sa Dal Jon ly J ge yh Cla ne (AA pl nylon esata poll St ga pleat (alka nS CU wea nadlopinn le aca ay sg ES 2 gpa SRS erjaaitay ke hatte pa A IES elt a (ra aii pediine Algerie aap Ent dott aos Tees peal outbid piety ee enh le gears bac cat peat ea pana Ign aang ane al jane eR espe as in cael ta yi et da Jpn par ae etl s a rangi ge Garant See ate at ent a Jo, Aaland gab dy alan cutal Sai ae estes ang al el ped LE SLL tg aad al om pty peed nell sea Sy ga Jl lah acd Agu AL Ae pa ct pe, Ppa a J Dyn LS esther ny ang pe Said Sed or Seba ogo a as aha eM ys ale lpn) agian A ae Ji J Jy iat pS olyie tS pacha aes eerste fer loe dan paici eoee te tee ah aoe al fae aon eee dale ead pep pad De wt Ba a il aeg etic area gaat gl ere prenatal, iin Spat ed AD ppb gla al I pat Peper ety Sp Haig ah gl eta an Sie ati dass eerie) kit lal al eal Migs Sat ha ps gala Hl Shan ns a ge lee LI ead ae Wiles dll aia gas ay eee) onro Tssuerarno.osy caries, particularly of deciduous teeth, may be so rapid thatthe pulp becomes exposed long before the tooth is due to be shed Pulpitis Pulpitis follows penetration of dentine by bacteria or their metabolites and represenis the breakdown of the protective hard dental tissues ard opening of the soft tissues to infection Clinical aspects of reactions to caries ‘The reactive changes described above render the dentine immediately under a carious cavity more or less impermeable, unless caries is advancing very rapidly. ‘A good knowledge of all phases of the carious process is essential to understand the rationale of modern preventive and resorative treatment. The clinical relevance of caries pithol- ‘ogy is shown in Table 3.4 ‘SUGGESTED FURTHER READING Bowen WHI 1999 Wither oF whither ease research Caries Res 331-3 rath D 1992 Cares, views and perspectives, Scand J Dent Res ocs7-s1 Carlson J 1989 Microbial aspect of frequent intake of preduets with higher eoncenteaionn SeandJ Dest Re397.110-114 CCowteton JW et 1987 Bacterial bore in rate ad dsease- Ann Frank MI 1990 Struct events inthe caries process in enamel, ‘emo anddonin. 1 Dent Rox Spo) 550-5 Gibbens RJ 1989 Bactral adhesion to lise: « model for infections disesee 1Dent Rex 8750-160 Fauie JM, Whiley RA 1999 Plaque microbiology of crown caries In ‘NewmanFIN, Wilson M (es), Dell paquerevsie Boline, Card ‘ishinoto D, Hay DL. Gibboas RJ 1989 \ nan svar potela which promotes adhesion of Sreprocozeus mutans serotype Seainsto Fyeroxsapaite Infect Immun 73702-3707 Levine RS 1989 Saliva 2. Saliva and deral civies. Dental Updste THI38165, Liang, Dake B, Doyle RJ 1989 Stailiy of he gucan binding lectin ‘feral septococl | Deut es (Spec Is:1077 “Metlugh WD 1989 Dental plague: hits yearson lz Newman HN, ‘ison N (es). Det ae vised Blin, Cat “Mergenhagen SEt al 1987 Nolecaar bss of bacterial adhesion in the ‘al cai, Res Taft Dis Suppl S).8467 475, Moller H, Serer U 1980 Hany natural subarace caries ASEM sudy tf the enamel surface before snd afer reminealation. Canes Res [Newbun E1989 Frequent sugarintake then ara now ineretation of Rokerts Li SH 1987 Oral ndings in aorexanervost sod bulimia ‘rerout atdy of 17 eaten JADA T1S:407-410 Ruzg-Gunn Al Hachet AF Appleton DR 1587 Relative curogeiciy of arch and tigate n2-yer longi ty of 405 English ‘Shoolsilren, Cues Res 2164-173 Russell MW. Hajshengalis G Childers NK ct a 1999 Secretery ‘murity indefense apa exiogenie mutans sropcoces Cates Res 33-415 ‘ha Ji 1987 Causes and contol of dental cries N Engl) Med 317:996-1003 Shes RE Din GH 1985 Analysis of the biter systems in dental Haque J Dent Res 67318445 Tafuk LA, Bowen Wit 1989 Rok of saliva pelle), dt and mtriton ‘om plague formatin.} Dept Res 68Spes4'1860-1366 ‘YurHowe J 1994 Rule of airoorgatisos caries eulgy. 3 Dent Res 3672-681 ‘idence fom 0 counties, Br De) 176297-302,2p) a SLL IU Lays! UL Gab plat go ab Lipkin dipuagll dgaalS,20 cist Apigild Loglio Jal gl ahi Le} Buble aysatl spd! LGM paw pA! Sy ool Le gare pal ge dy ssil dead Jobe JST od ddpall Sly Siig lio deoeoyilly dilig) Atleol) pabsill pula ogil AN Spat gi phil la gpa DL aL quate, dye tapas gg) ab GERI glut yb Lobsy Alygle B54 gaall dog ange ab ll LS, oa alga Tiel UgiLainnes! fasted Glas! Ab wigs gar GLESilg Seclia! debad) decal) cuit! sales Sire OEM 5g51 pall ‘SUGGESTED FURTHER READING owen Wil 1999 Wither or whither cars resarch’ Cais Res 351-3 Brat D 1992 Caries, views and perspectives, Seand J Dent Res Carlsson J 1989 Microbial aspect of fequen intake of reduc with igh sugar concentrations Seard J Det Res 97:110-114 Ccoseton IW etal 1947 Bacterial biofilns innature and disease. Ane Rev Misbil 1105-464 Frank MJ 1980 Strucarlerents ia the caries process in name, ‘mont nl dentine, J Dent Res 68¢6 poe Lt) $8556 Gibtons Rd 1989 Backerial adhesin to orl tse: mel for infections diseases 1 Dent Rex 6781-760 Hardie IM, Whiley RA 1995 Plage micobiobgy of cam cari. ‘Newmas HN, Wisco M (ed), Dental plague eviste, Bioline. Cait istimoteD, Hy Dl Gibbons RJ 1989 A human svar protein wich [promotes adhsion bf Sirprococeus muta serlypee sans to Fydroxsapaits Infect mun $7-3702-3707 Levine RS 1989 Saliva 2, Saliva tnd deal cries. Dental Update T1si163 [Liat L, Drake D, Doyle RJ 1989 Stablity ofthe phican binding len ‘fora areptecocel, J Dea Res Spee) 1677 Mctlugh WD 1999 Dental plague: thirty yeas on In: Newman HN, ‘son Mt (es), Det age revised. Bilin, Catt “Mergenhagen SE ct l 1987 Molecular basis of bacterial adhesion in he ‘al eit, Rev Tat Dis Spl 467475 ‘of te cnare surface tefore and ater remincrlisation. Caries Res ‘Newhrun E1989 Fioquestsugarintae~ then an now inerpretaon of the ni ceva, Sand) Dea Res? 109-108 Roberts MW, Li 8-1 1987 Oral ndisps i anorexia nervosa. bulimia ‘erho#dy of 47 cases JADA 118407410 Rugg Gan Ni Hacket AR, Appleton DR 1987 Relative cariogenicity chocclden, Caries Res 2164-473 Rassell MW. Hajshenglis G. Childers NK et a 1999 Secretory “iis ia defense agains cariogenic mutans strepocoed, Cates Res B-t5 Staw Ii 1987 Cawes and contol of dental caries. N Eng J Med 31796-1008 Shells RP. Dna GH 1988 Analysis of debate systems i dental plague, J Dent Res 67138 40 Tebuk LA, Ben WHT 1589 Role of salva peti), et and nuetion ‘on plague formation, 3 Dent Res 68(Specss):1560-1366 \anHHote} 199 Kole of mier-ongaisns ners eto. Dent Res HT 68), Woodard M. Waller ARP 1994 Sugar consumpon and det cakes evidence frm 90 counties. Br Dea J 176:297-302 28PULPITIS > summaries pp.66, 448 Pulpitis isthe most common cause of dental pain and loss of teeth in younger persons. The usual cause is caries penetrating the dentine, but there are ether possibilities (Box 4.1). Pulpits, if untreated, is followed by death of the pulp and spread of infection through the apical foramina into the periapical tis ses. This in turn causes periapical periodontitis Box4.1 causes of puts Dental ears * Traumatic exposure of he pu 4 Fractur of town or cus + Gacxea toon snarome ‘Therma or chemical tion Dental caries is by far the most common cause and is usi- ally obvious unless its concealed beneath a restoration Exposure during cavity preparation allows bacteria to enter the pulp and also damages it mechanically (Fag. 4.1), Fracture may either open the pulp chamber or leave so thin a covering of dentine that bacteria ean enter. ‘A woth, pactculaily a restored premolar, may spit, usually niles dsacaney: sess (Fig: 42) These canis cracks ae often invisible, but allow bacteria into the pulp chamber. The affected tooth may somtimes be identised by applying pres sure tothe occlusal fissure witha ball-ended burnisher o open ‘up the crack. Pulp pain usually thea results, Altemaively, the crack may be made visible with obligue trarsillumination of, possibly more exsily, by wetting the crown of the tooth with a dye such as Nuorescein and visaalising it with ultraviolet light. Insufficient cooling during cavity cutting, especially of de=p cewvities, can cause immediate damage to te pulp. Large unlined seta restorations may alse allow continuous low-grade thermal stimuli to damage the pulp over a longer peried, Some restora tions without a protetive lining, particularly in the past, were sufficiently iertant to kill the pulp. Clinical features “The pulps of individual teeth are not precisely represented on the sensory cortex. The pulp pain is therefore poorly Icealised Fig. 4.1. Traumatic posure. Ths puphas toon exposed dug cay Drebaravon and denne chppines anclarge wagrens have Deon aver Info the pu. The toch was extactedbetore a song kfamator reac tients hod ine to deve, baits doar hat sors ntarinstony calls havo aendy localised ecund te dobre which wikhaveintoaied mary acter the pu and may be felt in any of the teeth of the upper or lower juw of the affected side. Rarely, prin may be referred to a more dis lant site such as the ear. Pulp pain is not provoked by pressure ‘on the toth. The patient can chew in comfort unless there is & large open cavity allowing fragments of food t press on the pulp through the softened dentine. Acute pulpitis In the early stages the tooth is lypersensi- tive, Very ccld or hot food eauses a stab of pain which stops as coon as the irtant is removed. As inflammation progresses, ppain becomes. more gersistent and there may be prolonged attacks of toothache, The pain may start sponianecusly, oftea ‘when the patient is trying to gett slep. ‘The pain i partly due to the pressure en the irritated nerve endings by inflammatory infiltate within the rigid pulp cham ‘ber and parily due to release of pain-producing substancesfil pi Hd as yo ane Nt St pat eb ly Lane Sl Wlhy Syren easy dal! GAR hae ol god! ge GAS canal pg lM je ob ad ot sual pst anne AS Le pl! po Says a alg = pit chplia g ggled obi bel 90g pb ae lo tas eee lle GaSe ad Spb Le iy Leal tt) QebaEiy ge al gle ell al METH QMS ay Lagiiog SpeeS pao Clie LS if ¥] Ze JS Gane gh vant QoL Late ll Le sgh plage tao Bpbe BSA Lol gs gull gyS, abl all ga ceeatt ta GLB! gh Te alll plated! of cigoy doled! Gece batt yplasis alll Jigs tiga lll Go Bis So pee alone The ypS Ly dylyetael p35) ll Sinn Le Haley sg iLhbe Jey (aM Nagy ab posal i poll aby ol yall gly Lasts Ke Hee ble ple beet ot Li> atl ga! alll peed ale gg SL eget! PAU dpae alge gS GI] MAS Gye JSiey dba! Hig VW chad! yo badd & Gl! oLgsit leas Lay Saal ofl Lud 28) go Ll Glgall of BAB glia 35 casual ygSs Lo Bley nll ase Leguate Be 0E LH pol Sites! ageg 2 peep! gle clad ERI poe QUIN Lily aig2 ~ gua al hf > Cll olga AGE eats gay Fay aya! Jp Gaal gl} dag AagyAd > Laclede Spaces + Tig eons © feet plage eg oa Se Ue ey Lege a St Jelly go gall gocellana eb gee BY Lely qa pp lo mL LES ey N£JSfNd CAS AE MalaewsleS Rig, Le Ste gh Seb ad ll Lal pt iby a Las yal paid Lgalsleal Sl palais clall sola oS La Lig (Ff JS.) Rall bai ok Bde gl LoL sey etlinld Qed (GIS ayo yd Aa Gyo 00 Dab jerhatyigh ll gaullddpaegeecaiadi aly deeLliynt! eI St ub gS Ahan Alay LEM jg le Easy Le Easel Spa Jdaleg ag Le ls ad re Cag Aha ol ggg J gpl a gman jg ie SMa typaig geal JEafles eb Leaksy iS ad ge gladly gl ySell go Saal Sight! La) Gass ly AL Sables fino apo! Sle ob Geta) pM olga GU ee hae! Ass AS aid Jy! date ab DS GL gifs ob Ga Se gil) yb Leak dibeall LiL gay anal abiysaials So Sean pte eh ele Joy Ute pad ALB gL Lt 9! Bee ts GA ll gS) aad GUIS aad! a‘ting to the pup trou alayr of eaconary donee. This acute Inrmasonlsaised tthe pu Hors Fig. 4.2_ craked wath Th pup cet beneath ths crack whi a undo- tected citealy but whines cbaned up wer cation of th oath. Fig. 4:3 Pula yperaenia Wis baton aro si somo dsxance rm ho pb, acd alerg the dantnal oles ges ie 1c Fyperaema, Didone and ight cai Inkaratory eiteate in the ul, {rom the damaged tissue, The pain a its worst is exeruciatingly severe, sharp and stabbing in character, Iti litle affested by simple analgesics ‘The outcome of acute pulpits is unpredictable, Acute pulp tis may be deemed irreversible on the besis of constant severe pin oF the persistence of pain after a hot of sok stimulus but, even then, te pulp may’ survive, Though pulp death i the likely Fig. 4.5. acute putts. Soran tho carcus expos (op rift) a cers |nflmmaioy irate acumusting. More deep the pulp intensely hyperacnic outcome, acute pulpitis may progress to chronic pulpitss and treatment can stil preserve pulp vitality: Diagnosis of irre- versible pulptis is corsidered an indication for extirpation of the pulp, but it must be recognized thatthe exteria are poorky defined, Chronic pulpitis Chronic pulpitis may develop with or ‘without episodes of acute palpits. However, many pulps under large carious cavities die painlessly. The first indication is then development of periapical periodontitis, either wich pain or seen by chance in a radiograph. In other eases, there are Bouts ‘of dull pain, brought on by hot or cold simuli or coming on Spomtancously. There are often prolonged remissions and there _may be recurrent acute exacerbations.image not availableimage not availableSD pts Rega Ht) ahh ath wig A SBI el Sede Sylgtl Wb alae bey ately IS) 00 Slate! Saas Lees LY Ga AU Lg A gatig (PE ISM iy B od Eble desyall zlacll yd fersitlpetly cla! Siypane LOLS praaty Seger LOH! clay! ees Sky pail ga game Glia Bs aly ld! Listy VE sae Eo LSM gel Goal pile Byain ¢ Aaegtl dpaal Agel bl wala goo igs iy pl spate (A$ JALIL Se gat Eee deol! lll) Joss atl Gat abl olgait 25 plat geal gb 28h Lally pill ckeey CL! joes JS cealy alll pail Spain Galas Bags gb Geis CLS ISAs peut Le sa llace geese ea ieee pth Lgl a gu piSe eb fal Js Selb ML SF Lgl gags a SB yale gin ole edly Le Jb Sigg LST ISAM pslSM Clall ge Bye SbeaS pata 9) ai ell Syhaks ey Spat obo Sab Le Baley GLEE Jp games Lele als pil) ual SoW) pag JS Le WILE QMS Lge pally gait potas pao JS (Spake Clad oo ALAS dials jolge EtG J oak 0 gL le BSL Cray 2B nol GML yd gyal pul S52) wall Soha AAS JS ef ps USL See gutta Agi dgeQU Sagat! dncilly & BU dba yh adl Sel yo ALY GUT OMe pb [SIT ALLS gli po Pre Spd dul gill Loiglly dig oall dpes¥ oie datas y) BL oha op Soak aig gleg ol Lpaatl ay Lal 3) Aiagll SABI 9 Suyse gb BASS LGM 4 ged! Zayas Pek al) Gye ay Gla a tn wigs To gL Sgt gh Ged Sty ll pnd gS GL ae wh MH) Je ee gy a get De pee eis ISS ae ay ll cel oe eal onl (6 (BYP js) Glad dae ge GUI Olga gon ae geet SL go spill, eal lh Sagal gay pevedl gap! go Lee 9 CU je Ayop!pS! otpaal! cath Sat daued jaa gate aisPILPT, APICAL PENODONTITS RESORPTION AND HYPERCEMENTOSSS Fig. 4.10. Pelpcaping. The prococrs ho allowed ho pulp o urine Lat resctonay sorte hs posi) gaat si he epoatre Faluro of ho proceso i inceated by tho nanmatoy cla sone trates teiow he opening ‘The relatively prolonged survival of chronically inflamed palps is shown by the persistence of symptoms over a long period. However, pulp death is the end result unless treatment is successful ‘Open pubpitis Occasionally the pulp survives but ischroni- cally inflamed, beneath a wide exposure, despite the heavy infection (Fig. 4.11). This is traditionally believed w be assooi- ated with open apices which allow an adequate blood supply Fig.4.9 alate harars Ante ull andfrmation fa thek eb bri but ‘whan atscest meaty elo The rest the pul feed (3) Ti higher bower Vi of enh arb viced by Pulp capping stows he cae baer fond back menses Fig 4.11. opm pups. Baraat tha wise expoair theplp nas sued Inthe ionm of anuation tase uth Wee most ose amity ate ‘ereath the open sutece, CChronle hyperplastic pulpitis (pulp polyp) Rarly, despite Wide exposure and heary infection, the pulp not merely survives, but proliferaes through the opesing. This may even happen in fully formed teeth Clinically, a pulp polyp appears as a dusky red or pinkish soft nodule protruding into the cavity. It is painless but may be tender and Heed on probing. It should be distinguished from proliferating gingival tissue extending over the edge ofthe cav ity by tracing its attachment (Fig. 4.12). Histologically, few odontoblasts survive and the pulp ‘becomes replaced by granulation tissue (Fig. 4.15). As this mass grows out into the cavity thelilised and covered by a lyer of well-formed stratified in the tooth it ean become epi-gs Sankt pag AE JST BOS gis el al eb Bet Ly oats ula GH pak ag jot flay Labs ele GLAST GR Ga) LE goed Gu gat NE Jb Gaede SE dylga Sny ee go ee Jb le cell EU galll Snell apt peel doy abt gat A asa SLMy GLESA ga tt ey Sak ALS (pill pM LESAN ye SSS) Jo ead all gy all JS ALAS (Law fo > ca a LiSl clan deel ede JS le Lan gull ll guar AB LGSly dle pat Basket yg Si BM yaw Syl dys; gb $90 Gest 8 Lnsaal one pall abe Gilg Lae yy Ss IFS JSS Lg lal) gests 5A lyn Gy azo SLU Ee oe chall Spans WLS go UG gs Lae TLGSH oke Quand akg OTE LSI lll gle ase DS LoS Ryall abl agar GLE past Lente Sylg hs AAU ddd, Gti ge dda) pdt ain Eagan ga aa wt pice shee the Gane a Sas Nek YET SURG alone oak JR pets chat! ts gl Bae te Tee eeu alt was Zee leat gill, Shell lll Bla Loans Sayall LUA! pgs 9 pe I ee dbp baad ote¥! ypu! JME ow gepe pol RFLet As of Aslgat ancl ge Gt) whey a bist ur ek gh adeney AVY.6 JEN wpe! gLe¥h HAS gyal taal Geant Le doghta 53 apes yaill iggaas cagegay alan Ebbro TssuerarnoLogr Fig. 4.12 Pulp pote Anita nec ct rerun tsue canbe seen _gowing tome pp chamber of his broken oun fet pormanert mol Fig. 4.13 rap pop. typerlasc nod of hau sowing fit hvough awide xpasure ofthe pup. The masses of nareaory ‘als ard the mary now sesec ane horace of garuaaon squamous epithelium. This protects the mass and. allows inflammation under it to subside and fibrous tissue to ceplace the granulation tissue. This degree of pulpal. prolieration cean occasionally be seen in teeth with fully Formed roots (Fig. 4.14) ‘Management “The chances of survival of an iaflamsed palp aze poor and reat- ment options are limited (Box 4.2). Fig. 4.14 Puppy. ints broten down mol, ganulition tseue prllrang fram tho pulp cay ana ha accuecan optha aoveina ‘ve mc of surice. Note alo theinteral resol fe} a5 ut ‘final lamin 0x42 Teatmetoptons tr pups * atures or eacked, stablae facture and eal pup tempor + Reroval ot cars, obtundent or ster dressing + Removalot cares ara pu capping Pulptony in cuous th + Encore rtmere + Aalgesies ro ago nooctvo ‘Open pulpitis is usually associated with gross cavity forma. toa and it is rarely possible to save the tath, dospite the vital ity of the pulp. Key features of pulpitis are summarised in Box 4.3 and the sequelae of pulpits are shown in Summary chart 4.1 Box 43. voy features et pulps + Pulbis is caused byinfocton oreraton of he pup sal by + Soire story painn a tooth, rigor byhoto cold food or sting sortanooash,lxcates acct reverse pubs + Pulp pains pony located + Ghnt pute ofen sprotomiess * Unteated ulti usualy leads to deat of ho pulp andepreat of Inecton io he penal tsesPES Lagat gael she gh galtl Jatt Mk JST Jeo tang cs sy cA SEI SA oes ged gemll Tae ee) sad! Gelade Lal) yy” andar cael ca a et hg ae iat ToL i EL poh ad BE lant + foo dag ul een * iki + aula re Jpeg pant aa ph ch + 99 BpeS Ben JS Cpl! LT gall jis Le eg se age oo feet rhe al LAY ty) jak) oe Ag gs Lane i igen pelt ceoltt VS peRl dl 55 Sognee ll abgall gy tig Senta lh TK PN gee ge Ble aE a kaa AAS an J pal gh myn * pA Dg he Jag Hiei eae ates * epet at inayat aide + Sette Nt ee neatly * Lay gut ale, Gel ge degile eas get atl IE YSU AnagAt LSI) GW gonN ole gh GA yao sa pel ee uel dlepke take galt Groth Ped geeatT SE pes gu I as tl eat tecaty ana Sgeast anes pe aeaaly Latgltl ast pol cant! wage ob lysd olga Llaes abi gh oSep pesedl gamll Jone Jon of pall genie i ghaM b Bplh Oe gb gall! ISG 0 dpyall ota (044 JS) dest git al CU yl Ab gilt OU BLE Gedo! (8 U8 ) Segara iPULP, APICAL PENODONTITSRESOWPTION AND HYPERCEMENTOSSS Pulp stones Rounded masses of dentine may form within the pulp and ean bbe seen in radiographs as small opacities. In the past, they ‘were thought to cause symptorss but are developmental anow ales, For unknown teasons, they are common in the teeth of patients with Ehlers-Danlos (floppy joint) syndrome, a genetic defect of collagen formation, Histologically, pulp stones consist of deatine which may show complete of incomplete tubale formation (Fig. 4.15). ‘A distintion used w be dravn between free and attached pulp siones. However, this is frequently an illusion caused by ‘ plane of section which fails to pass through the conection ‘between the pulp stone and the pulp wall, Diffuse calcification Amorphous dystrophic eslifications may sometimes be seen histologically in the pulp and are thougtt to be an age-related degenerative change. lp stones and diffuse cakification are of no clinical sig- piffcance except insofar as they may obstruct endodontic treat- :ment, Otherwise they can be ignored PERIAPICAL PERIODONTITIS > summary p.66 Periapical inflammation is usually due to spread of infectien fol. lowing death of the pulp (Box 4.4), It characterstically causes tenderness of the tooth in its socket. Local (periapical) periodon titis must be distinguished from chronic (marginal) periodonti- tis in which infection and destruction of the supporting tissues ‘spread from chron infection ofthe gingival margins (Ch. 5) + Cheatin, Infection is by far the most common cause. The usual ‘sequence of events is cares, pulpits, death of the pulp and ppetiodontits (see Summary chast 4.1) ‘The pulp sometimes dies from a blow which damages the apical vessels, The necrotic pulp prabably becomes ‘infected by bacteria from the gingval margin tits. A high filling orbiting suddenly on a hard object some- times cause an acute but usually transient periodontitis. leading to apie periodon- gaill gyn cigeyay San Ekece Rapes lake hall pe HABA atte gh Jett AOL ana aay dg ll tt Ba gy ld tg ial ge 9 pall I) on gh at in Minded said dg Jpodaclalleuitolentl gil GLEN JLB gl Jp lg a Lo te a Qa piece Bal pha g I UI alge gl Gel Spo) pang Qala gel Algal ad a piel Laake gly MLABD yl dasha id AO Ladd SpA Sly pb o5ll Lil edoclall gail! I ony Lega lM Sh sees a> i ole aad Hash alge gab Ll) gall ph ps RGILS Gls Sat OS APH REST AY) a a tgs Hapaall dye gS dap ena Ugad LT ce ad Spat a edly pal) A ea Jedd ag dag fy aS gy SI dct anal legal Il gate Le dag ete pee te lal! Gal gh SILT Sip as ple gS Le bale a2Sg abe dels gas algal! Lhd ot cabal SS cab lea 68 gb Seg lll Jste Clall go Sygae Jes Joie a adie, ylS DOS Je gle delet jpaals hes tops ott Myst Laie) as tel le gee oliad gh AGILE Ct clad! Lb diye ye Cipla! ye Ble ay Ayal! eal) yugbloryh) dessa PMS Jos gb thy SLAB gan ab Cle oe Hel) clued! yo Lead WS Gall gb (00.1 JSS LIT Leal gba Le bale Sly Adena 9 S51 dell SLad! gy pre! Ph behy AN AU gyn “ass feng ape Ha gas Aol jaseg lh dase guy ak ile a Sa Ae dh ¥ old La bleh sol Smid on Sle lib site ll 9s Joust! pent, Jedye WY dappe dgaal a) hasath ul ScHly GLI cdgaed vege ¥ WISN Lagden yey deed Able lel 1ro Tsu rarHoLoge During endodontic treatment, instruments may be pushed through the apex or side of the root, damaging the periodontal tiembrane and carrying infected debris from the palp chamber into the wound, Irritant antisepties used to seilise a root sanal ean escape through the apex and damage the surrounding tissues. oot-csnal filling may also extend beyond the apex with similar cifect. Very aly pub renal abled intarmatin ese (ny # pup open o ‘mauh aro apices ‘open, esingor ‘ncorplete Palp pl ems ‘son crest Naaseto om adda ae ae | wage Pelgeal yanuona, conic psstet inant, wus asymstomet oth tis of raceoatin ACUTE APIGAL PERIODONTITIS > summaries pp. 66,409 Glinical features “The patient may give a history of paie due to previous pulpitis. When periodontits develops, escape of exudate into the peri- ‘odontal ligament causes the tooth to be extruded by & minute amount and the bite to fall more heavily on it Te tooth is at leading pul necsis inane or mate cans Peiaical abscess resting Yom etbiment ‘via ermism.rascae of earns though tape, of duced ostessnce, leaps smptonatic Drainage ops, Inawaly eexteraly, reduction i symors ads cone ersten nection with pete ol racraton vals eat Inet yt caused by ‘ler! gaan fom pil or carmunicaen asl esi ‘are bat severe campliatons oon ‘vate nlc ifetious ndocris, andorcasenaly death trteonyest Summary chart 44. Saquste of puis Inadegate or inapppt eatrent wanes, penitent nlecsn are bt sovere camplstons of indent lector: Ludi’: sng, cereus snus tronboss sepesemis andoccasonaly deah Fe butsavere Akal pd gS) AE Sui day Ugh he Uhl aig Bhat jiu analy Lgilgo AL ll A Uae te ls 5 oe JS ht] Sey 2AM pene ght Inne valley Jef Gaisé ose BLA Jad y geil! Algal he Sef QUURT daly “dygaall LISly SyeeST catlalyy SlbglieLl, Coen ge ally a Cll deny W’ Shah LMS apy (peer 9 pe ALS JS ple grant (FA g IRA MS ado lat LSS) pla ee ALR HLS a be LE Go atl ley ty cS Haig ay. LL QL pls ign op.09 pola) santey coil yp) ake Saal! Bybe So peel esl! MARANA dle i HEL yo Adlai tag (118 Jt ig St glad) deol ab abet) glatan, ar She ‘iit! Js) gb ancl w