2011 Diagnosis and Treatment in Prosthodontics [PDF]

  • 0 0 0
  • Suka dengan makalah ini dan mengunduhnya? Anda bisa menerbitkan file PDF Anda sendiri secara online secara gratis dalam beberapa menit saja! Sign Up
File loading please wait...
Citation preview

......,.,



Diagnosis and Treatment in Prosthodontics Second Edition



DIAGNOSIS AND TREATMENT IN Second Edition PROSTHODONTICS Edited by



William R. laney,



DMD, MS



Professor Emeritus Department of Dental Specialties Mayo Clinic College of Medicine Rochester, Minnesota



Thomas J. Salinas,



DDS



Associate Professor of Dentistry Department of Dental Specialties Mayo Clinic College of Medicine Rochester, Minnesota



Alan B. Carr,



DMD, MS



Professor of Dentistry Department of Dental Specialties Mayo Clinic College of Medicine Rochester, Minnesota



Sreenivas Koka,



DDS, MS, PhD



Professor of Dentistry Department of Dental Specialties Mayo Clinic College of Medicine Rochester, Minnesota



Steven E. Eckert,



DDS, MS



Professor Emeritus Department of Dental Specialties Mayo Clinic College of Medicine Rochester, Minnesota



Quintessence Publishing Co, Inc Chicago, Berlin, Tokyo, London, Paris, Milan, Barcelona, Istanbul, boollt Sao Paulo, New Delhi, Moscow, Prague, and Warsaw



..,..__



Library of Congress Cataloging-in-Publication Data Diagnosis and treatment in prosthcxlontics I ediled by William R. Laney ... (et ai.J. -· 2nd ed. p.; em.



Rev. ed of: Diagnosis and treatment in prosthooontics I William R. L aney Joseph A. Gibilisco . 1983. Includes bibl iographical references and index. ,



ISBN g78-0-86715-404-7 (hardcover) 1. Prosthodontics. I. Laney, William R., 1928· II. Laney, William R., 1928· Diagnosis and treatment in prosthodont ics. [DNLM: 1. Prosthodontics--methods. 2. Oral Surgical Procedures, Preprosll1etic--methods. WU 500) RK651.D5 2011 617.6'9--dc22 2011006322



... � boolu



© 2011 Quintessence Publis h ing Co, Inc All ri ghts reserved. This book or any part thereof may not be reproduced, stored in a retrieval system, or transmitted in any form any means, electronic, mechanical, photocopying, or otherwise. without prior written permission of the publisher.



Quintessence Publ ishi ng Co, Inc



4350 Chandler Drive Hanover Park, IL 60133 www.quintpub.com Editor: Leah Huffman Design: Ted Pereda Production: Angelina Sanchez Printed in China



or



by



Contributors



Mayo Clinic College of Medi cine



Brent E. Larson, DDS. MS Professor Department of Diagnostic/S urgical Orthodontics University of Minnesota



Rochester, Minnesota



Minneapolis, Minnesota



Dusica Babovic-Vuksanovic, M D Chair and Associate Professor



Charles L. Loprinzi, M D Professor of Oncology



Department of Medical Genetics



Mayo Clinic College of Medicine



Mayo Clinic College of MediCine



Rochester, Minnesota



David J. Archibald, MD



Resident Otolaryngology



Rochester. Minnesota



David MacDonal d BDS. BSc(Hons). LLB(Hons). MSc. ,



Charles R. Carlson, PhD. MA. ABPP Professor of Psychology and Dentistry



DDS(Edin). FDSRCPS (Giasg). DDRACA (UK), FRCD (Can) Asso ciate Professor



College of Dentistry



Faculty of DentiStry



University of Kentucky



University of British Columbia



Lexington, Kentucky



Vancouver, British Columbia



Alan B. Carr, DMO, MS Professor of Dentistry Departmen t of Dental Specialties Mayo Clinic College of Medi ci ne Rochester. Minnesota



Canada



Kevin I. Reid, DMD Assistant Professor of Dentistry



Department of Dental Specialties Mayo Clinic College of Medicine Rochester. Minnesota



Mijin Choi, DDS. MS Clinical Assistant Professor Department of Prosthodontics



New York Universi ty College of Dentistry New York, New York Steven E. Eckert, DDS. MS



Kevin L. Rieck, DDS. MD Instructo r in Surgery Section of Oral and Maxillofacial S urgery Mayo Clinic College of Medicine Rochester. Minnesota



Department of Dental Specialties



Jana M. Rieger, PhD Associate Professor



Mayo Clinic College of Medicine



Institute for Reconstructive Sciences in Medicine



Professor Emeritus



Rochester. Minnesota



Department of Speech and Language Pathology



Robert L. Foote M D Professor ,



and Audiology Faculty of Rehabilitation Medi ci ne



Radiation Oncology Mayo Clinic College of Med icine Rochester. Minnesota



Canada



Rochester, Minnesota



Thomas J. Salinas, DDS Associate Professor of Dentistry Department of Dental Specialties Mayo Clinic College of Medicine



Sreenivas Koka, Dos. MS PhD Professor o f Dentistry D epartment of Dental S pecial ti es Mayo Clinic College of Medicine ,



Rochester, Minnesota



William R. Laney DMD. MS Professor Emeritus Department of Dental Specialties Mayo Clinic College of Medicine Rochester, Minnesota



University of Alberta Edmonton Albert a ,



Jan L. Kasperbauer, MD Professor of Oto laryngology Mayo Clinic College of Medicine



,



Misericordia Community Hospital



Rochester, Minnesota



John E. Schmidt, PhD Assi stant Professor of Psychiatry Mayo Clinic College of Medicine Rochester, Minnesota Kostandinos Sideras, MD Assistant Professor of O ncology Mayo Clinic College of Medicine Rochester. Minnesota



IX



Preface S ince publication of the first edition, many changes have occurred



8ectronic t echnology has provided for an improved diagnostic and



in the clinical practice of prosthodontics. While the human patient



treatment-planning capability. Imaging techniques and equipment



and related oraVperioral problems remain physically unchanged.



have evolved that provide more extensive and accurate information,



psychosocial attitudes toward dentistry and care deliverers have



which assist the clinician in decsion i making prior to and during



been altered as a result of shifts in societa l values and priorities.



treatment. COmpared to two -dimensional or flat-screen ima ges,



An enlightened and enti tled generation now places more e mp hasis



newer three-dimensional imaging and modeling have s ignificantly



on personal appearance, early relief from pain and inconvenience



enhanced the planning and delivery of surgical r estorative treatmen



in a timel y manner, as well as cost and cost sharing by third p arty -



contributors.



t.



In response to these developments, this second edition r equired the so lic itation of additional knowledge and expertise from experienced



Hard and soft tissue substance continues to be altered by disease



prosthodontic specialists and competent representatives from re·



and traumatic injury with genetic overlay imposed occasionally by



lated contributing disciplines. These relevant additions have provided



racial commingling and natural evolutionary processes. However,



a n enhanced scope and depth of subject matter on topics pertinent



the clinical management of tooth and bone loss and acquired and



to pr osthodontics.



congenital oral and peri oral defects has changed dramatically as a result of improved technical and procedural modalities and materials. The intro d uctiOn of BrAnemark's concept of osseointegration in



Acknowledgments



1982. with its accompanying biocompatible titanium hardware. has resulted in re ma rkable developments and ap proaches to restorative treatment with versatility of application



The authors would like to acknowledge their colleagues in oral and



and predictable outcomes.



and neck surgery for their dedication in helping compile the sub·



North America in



maxillofacial surgery, radiation oncology. and otolaryngolo gy/hea d



In addition to implant-support opportunities, probab ly more than



ject matter. Additional thanks are extended to the secretarial support



any other phase of restorative dentistry, the advances in ceramic



section o f the Department of Dental Sp ecialties at Mayo Clinic for



options and materials have contrib uted to satisfying pat ient demands



helping wi1h portions of the manuscript. Further acknowledgments



for more esthetic treatment outcomes. These applications relate



are extended to the authors wives and families for their understand·



primarily to fixed restoratio ns which now have more durability and a



ing of the time needed to accomplish this important project.



,



more li felike appearance.



1



viii



'



Robert Stewart, ODS. MS



Julian B. Woelfel, DDS



Clinical Assistant Professor of Dentistry



Professor Emeritus



University of Detroit Mercy



School of Dentistry



Detroit, Michigan



The Ohio State University



James M. Van Ess, oos. MD



Columbus. Ol1io



Assistant Professor of Surgery



John F. Wolfaardt , eos, MOent. PhD



Section of Oral and Maxillofacial Surgery



Institute for Reconstructive Sciences in Medicine



Mayo Clinic College of Medicine



Misericordia Community Hospital



Rochester, Minnesota



Professor



Christopher F. Viozzi,



DOS. MD



Assistant Professor of Surgery Section of Oral and Maxillofacial Surgery Mayo Clinic College of Medicine Rochester, Minnesota



Jonathan P. Wiens, oos. MSD Clinical Associate Professor School of Dentistry University of Detroit Mercy Detroit, Michigan



Faculty of Medicine and Dentistry University o i Alberta Edmonton. Alberta Canada



Table of Contents Foreword by George A Zarb Preface



vii



viii



Contributors



ix



1



Basic Concepts of Genetics



2



The Orthodontic-Prosthodontic Relationship



3



History, Laboratory, and Examination



4 5 6



1



Dusica Babovic-Vuksanovic



9



Brent E. Larson 17



William R. Laney and Sreenivas Koka



Oral-Systemic Interactions



39



Sreenivas Koka, William R. Laney, and Thomas J. Salinas



Oral and Maxillofacial Radiology



51



David MacDonald



Psychologic Aspects of Diagnosis and Treatment in Advanced Dental Care



71



John E. Schmidt and Charles R. Carlson



7



Temporomandibular Disorders and Orofacial Pain



8



Considerations in Treatment Planning



9 10



83



Kevin I. Reid



97



Alan B. Carr, Steven E. Eckert, and William R. Laney



Preprosthetic Surgery



115



Christopher F Viozzi



Bone Grafting and Ridge Augmentation Considerations Prior to Endosseous Implant Reconstruction James M. Van Ess and Kevin L. Rieck



129



11 12 13 14



Osseointegrated Implants and Implant Site Development



141



Kevin L. Rieck, Thomas J. Salinas, and James M. Van Ess



Surgical Defects of the Mandible and Maxilla



149



David J. Archibald and Jan L. Kasperbauer



Oral Complications of Chemotherapy and Radiation Therapy



163



Kostandinos Sideras, Charles L. Loprinzi, and Robert L. Foote



Radiation Therapy and Chemotherapy for Head and Neck Cancer



183



Mijin Choi



15



Restoration of Congenital, Developmental, and Acquired Oral and Perioral Defects



197



Thomas J. Salinas, Alan B. Carr, and William R. Laney



16



Contemporary Dental Materials and Their Application to Prosthodontics



233



Thomas J. Salinas and Julian B. Woelfel



17



Diagnosis and Management of Inadequate Denture Prostheses Steven E. Eckert



The Mutually Protective Complex: Occlusion and Fixed



18



Prosthodontics



263



Jonathan P. Wiens and Robert Stewart



19 20



Speech Pathology and Prosthodontic Applications Thomas J. Salinas, William R. Laney, Jana M. Rieger, and John F. Wolfaardt



Management of Patients with New Prostheses Steven E. Eckert



Index



333



318



293



249



Foreword Twenty-eight years have elapsed since I came across the first edition



it also preceded the osseointegration era; and the intervening



o f this superb text. I had al the time already made my personally



years between the two editions were overtaken by the remarkable



decisive journeys to two renowned US institutions of graduate edu­



speed and excitement of the relevant scientific changes-biologic,



cation in my chosen field of interest. And just like many other would­



behavioral, social, technologic-that have now come to dominate



be clinical academics-both then and now-1 benefrted enormously



the discipline.



from my extraordinary teachers' experience and their commitment



The editors are therefore readily forgiven for making us wait so



to clinical excellence. However, my acquired and presumed ability



long for this very welcome second editiOn. It significantly expands



to address the bigger picture of diagnosis



the original book's scope by its recruitment of those essential topics



as



well as treatment in



the discipline of prosthodontics had to be acknowledged as an in­



sucl1



complete one. I had gradually realized that the rigor and focus that



concerns, imaging techniques. etc, that have informed and revised



underscored the era's guidance in specialized dental education was



the entire profession. It also makes it far clearer than ever before that



not automatically reconcilable with patients' systemic determinants



the discipline has not only benefited from the infomnation explosion but



and individualized needs. Dental treatment planning tended to be



that it has also convincingly embraced it. The net result is a renewed



hegemonic because handicraft and anecdotal traditions in



and elegant confimnation of the conviction that good prosthodontics



the discipline were dominant. Moreover. the additional objective of



is simply not reducible to tidy formulas or rigidly ordered credos, that



treatment interventions t o restore orofacial function was rarely de­



i t demands scrupulous and eclectic observational skills, and that this



temnined by the exacting standards today's treatment outcome de­



approach remains a wise and essential strategy to avoid what might



mands.



very well be unnecessary and misguided interventions.



overtly



as



genetics, adjunctive laborato1y examinations, psychologic



It was inarguably an opportune time tor a text that sought to proVide



This text makes a compelling case tor prosthodontics as a clinical



a synthesis of what was even more essential and comprehensive



dental specialty in the best scholarly tradition. I cannot think of a



for optimal management of the prosthodontic patient. and this



better one to make the profession appreciate what the discipline is



book's first edition addressed that big picture need in the scholarly



really all about.



manner that admirably reflected the Mayo Clinic's distinguished authorship pedigree. It quickly became a de rigeur assignment



George A. Zarb



for graduate students in the specialty



Professor Emeritus, University of Toronto



who were considering prosthodontics



as as



well as new graduates their career pursuit. But



Editor-in-Chief. International Journal or Prosthodontics



vii



Chapter



Basic Concepts of Genetics Dusica Babovic-Vuksanovic,



T:



e field of genetics has undergone rapid growth in recent



ears and greatly affected all areas of medicine. The compte­



MD



• Does this patient have a hereditary disorder? o



on of the Human Genome Project. which identified the three



Does this patient have a simple condition or a complex disorder underlying the symptoms?



billion base pairs of DNA that compose a human genome, was a



o



Is there a need for evaluation of other family members?



landmark event of the end of the 20th century. Genetic information is







What is the risk that the patient's children or siblings will inheri t the condition?



now being incorporated into all areas of clinical medicine. changing even basic concepts in evaluation of and therapy for patients. While science has yet to reach full comprehension of all gene functions and







Could the disease be managed or stopped in its early stages i f a timely diagnosis is made?



protein interactions we remain optimistic that opportunities soon will ,



be developed to p redict. prevent, and cure human diseases through



The answers to these questions



can



significantly affect a pa·



methods such as personal genetic fingerprinting and routine gene



tient's life. For example. if



therapy. Staying up to date on recent genetic developments and



ents with dental irregularities (eg, crowding) recognition of a gen·



applying this knowledge to patient care will become a necessary skill



eralized connective tissue abnormality would typically lead to a



for most clinicians.



series of p reventive measures including screening f o r aortic root



a



patient with Marian syndrome pres· ,



dilatation. In this patient, early diagnosis and appropriate treatment might be life-saving. Another example is a patient with osteomata



Genetics in Clinical Medicine



of facial bones, dentigerous cysts, or supernumerary teeth-pos· sible signs of familial adenomatous polyposis. Early identification of this hereditary disorder in the patient and his or her family would



The role or genetics in human disease is well-known. Some condi· lions are caused by single genes and inherited in a Mendelian pat·



live colectomy, thereby transforming a uniformly malignant and le­



tern; the diagnosis. risk assessment, and counseling for the family



thal condition into a manageable one. The dental specialist often



usually simple for these conditions. 1·2 In other cases, recognition



may be the first t o see a patient with an unrecognized. complex



of an underlying genetic trail may be a challenge. and multidisci·



medical problem; a high index of suspicion and appropriate refer·



plinary evaluations and complex diagnostic testing are often needed.



rat may dramatically influence the well-being oi a patient and his or



Common quest1ons that general clinicians should ask include the



her relatives.



are



lead to necessary surveillance for colon cancers or even preven·



following:



1



1



i



B as ic Concepts of Gen eti cs



I



> a



J



J



)



LEGEND



1(1 )



1·)t)) 2



I



u 6



1(' 13



Ji 19



Fig 1·1



((' )f



3



)f IJ 7



?I )) )) 8



1(



.



14



0



9



' -'W ""'



10



II



n



16



Bt.



·-�



20



21



A normal, male, G·banded kal)'otype. (Courtesy of



5



J(



(



12



i(



IS







l( 17



u 22



0 Healll>y female



)



• Affected male e Affected lemale



()



b



1J



0 Female carrier of X-linked



.



eondrtion



'}



u



(J



18



)



('}



I



Or Gopalrao Velagaleti, Ried



Hete10zygote carri0< male



f) Hete10zygo1e carrier female



X



y



Healthy male



c







;>







()



)



Fig 1-2 Family trees demoostratill(J autosomal dominant (a), autosomal recessive (II).



Meyer. Daniel Kuffel. and Or Eric lhorland. Cytogenetic Laboratory, Mayo Clinic, Aoch· ester, MN.)



and X·finked (c) lraits.



Inheritance Patterns



drome), and some forms of ectodermal dysplasia. Disease expres­



sion may vary significantly in affected people even within the same



Some examples of autosomal dominant conditions include Marian syndrome, von Hippel-lindau disease tuberous sclerosis, Gorlin



family, res ulti ng in different severity of disease in different individuals. Carriers of an autosomal dominant gene may not develop the p he notyp e at all. because some genetic traits have reduced penetrance. Alternatively, development of symptoms may be limited to late age, as is seen in so me neurodegenerative disorders that manifest in adul thood (eg, Huntington disease. spinocerebellar ataxias , or Alz· heimer disease). This behavior sometimes may give the impression that the disease is skipping generatiOns. In contrast to autosomal dominant conditions, for which one abnormal gene (or allele) is sufficient to produce disease, autosomal recessive conditions occur only in individual s who inherit two abnormal copies of a gene (FIQ 1-21:>). Usually. each parent iS a carrier of one abnormal copy or the gene. but they are a y s mptomatic because they also have a normal copy that prevents expression of the phenotype . The aut oso mal recessive t rait is often suspected when a disease occurs in several siblings or in consanguineous families. The risk for carrier parents to have an affected child is 25% in e ach pregnancy.



syndro me, some chromosomal



Examples of conditions that follow t his inheritance pattern include



Despite the availability of many sophisticated diagnostic tests, basic genetic prinCiples and the tra d�ional evaluation of the patient (medi· cal history, family h is tory and physical examination) remain essentia l. Genes can be d ominant or recessive and are located on one of the ,



autosomes (chromosomes 1 thro ug h 22)



or sex



chromosomes (X



orY)'"' (Fig 1-1). Careful analy si s of the family tree often provides a clue t o t h e di ag· no sis or suggests whether further investigation is warranted. When a genetic cause of the co ndit ion is unknown (le, diagnostic testing is not available). the family analysis becomes the p rimary tool used in g enet ic co u nseling. Autosomal dominant conditions are transmitted through multiple



generations of families. An affected individual has a 50% risk of passing the abnormal gene to each of his or her children (Fig 1·2a). ,



disorders (eg, velo-cardio-faeial syn-



·



J



Genetic Screening and Counseling



Table 1-1



'



_



Example



Inheritance pattern



Autosomal dominant



Recurrence risk"



Most craniosynostoses



Siblings: 50%



Sex differences None



Children: 50%



Autosomal recessive X-linked recessive



Most dysmo.phlc syndromes



None



Siblings: 25% Chlldren: 1 100



0.2-1.3



0..10d



7.6-10.4



10d-24



100



9.0..11.0



24 mo-12 y



8.8-10.8



> 12y



8.4-10.2



Carbondioxide (CO,) (mmolll)



22-32



Chloride (C� (mmot/L)



98-107



Creatinine (mgid�



Glucose (mgi1 mo



65-110



0..12 mo



3.5-6.0



> 12 mo



3.5-5.0



Protein. total (g/dL)



6.o-8.0



SOdu i m (Na) (miOOIIL)



135-14 4



Urea ntrogen i (UN) (mgldL)



Q-7d



3-12



>7d



8-20



21



3



History, Laboratory, and Examination



spected for ulceratrons, crusts. fissures, or other surface changes. No physical examtnati on IS complete without digrtal palpatron. Lat­ eral surfaces of Ihe face and temporal areas are palpated as the pa­ tient opens and closes the mouth to ascertain the extent of lemporal.



pterygoid, and masseteric function. Asking lhe patient to purse the lips gives an indication of the perioral muscular vigor and integr ity. To assess the smoothness and range of motion of the TMJs, the clini­



cian should place t he Index fingers bilaterally over the preauricular areas as the palient opens from a closed position and moves the mandible anteropostenorly and laterally. Tenderness, onep1tus, and deviation are noted. The condyles can be further examined by plac­ ing the fiOQBf wi thin the external auditory meatus and palpat.ng the Cervical lymph nodes



anterior wan below the tragus. This examination often can suggest



Thyroid gland examined



potential problems 1n record•ng rnaxillomandibular relations. lnspecllng the neck and cerv�cal lymp h nodes is an Important part of the extraoral examination of the head and neck and logically fol­



Fig 3·1 Left, Bimanual palpalioo of the neck should include examination of the cervical lymph nodes. Right, Clinician should palpale along the larynx tor Immobility and enlarge­ men! Examination of the U1yroid glancl includes palpatioll olllle lobe, which Is facilitated by !laving the patient swallow to e!evale the gland.



lows digital palpation {Rg 3- 1). A suggested routine includes pal­ pation for enlarged nodes In the jugular chain and in the parotid. submandibular, and submaxillary groups.



Salivary glands The lateral structures of the face and the penrnand!bular area are



Physical Examination



best examined wrth bimanual manipulation {Fig 3-2). Nodular or indurated surfaces



1n



the V1Cin1ty of the mandtbufar angle are sug­



gestive of parotid leSions. Lesions deep in the cheek are difficult to



The face and mouth are relatively s.mple to examtne because their component structure s are readily accessible to visual inspect ion ,



by means of a forefinger placed intraorally and the opposite hand



digital palpation, percuss1on, and radiographic record1ng. Any ap­



placed extraorally, should be a routine procedure. Obviously, the



proach to the actual examination should be systematic and routine



purpose of the examination is to distinguish the normal from the



for each examining cli n ician. Printed forms may be helpful to record



abnormal. The parotid duct {Stensen's duel) i s usually clearly iden­



findings because they provide an ouUine that minimizes oversight



tifiable in trao r a lly, and manipulation of the gland should elicit a flow



and encourages thoroughness.



of watery ftuid. Diagnostically, it is advantageous to locate nodes or



detect: therefore, careful palpation of the buccal mucosa and skin.



The common tendency when conducting an i ni tia l examination is



swelling relative to the musculature of the area. Circumscrrbed Ia·



to proceed with the intraoral phase without givi ng much consider­



sions are readily movable whereas inflamed tissues or structures ag­



ation to the body as a whole. In preliminary deliberato i ns, an astute



gressively 1nvolved by neoplastiC disease are relatively fixed. The pa­



observer notes the patiSnt's relative body proportiOnS. weight. pos­ ture, gait, degree of functional coordination, and any obvious abner·



tient may provide subjecllve Information by reacting to patnful st1mu�



malit1es or deform1Ues. A closer look at the head and neck should



early indiCation of Inflammation. but 1t is also associated with tater



reveal signifiCant aspects of facial compositiOn. asyrTllmelries, sk1n



stages of malgnant diSease.



texture, complexion, expression in the eyes, breathing, functional



The submandibular gland is readily identified by intraoral and ex­ traoral palpation. It can be examined by gently rolling the glandular



habits of teeth clenching . twti ching, and other neuromuscular invol· un tary manipulations.



Extraoral examination



or



by failing to respond to palpation ol the tissue. Pain 1s usuaJy an



substance belween the fingers, and its patency can be noted by the salivary flow. Irregular or firm structures within the duct or possible at· a t ched lymph nodes should be examined. Inflammation, purulence, a hard mass within the duct, and pa in suggest the presence of a salivary stone



(calcification) and the need for further eval uat i on by Imaging.



Regardless of the examination seque nce . the perioral structures



A quantitative and qualitative evaluation of the saliva is very Im­



should be assessed first. A general evaluation is made of the fa·



portant t o prognos1s, partiCularly for the patient with complete den·



ciaJ contours and support provided by the denlillon. Characteristcs i



tures. Salivary flow from the parotid duct is primarily serous, the flow



such as abnormal swellings. deformities, tes.ons. discolorahons. and



from the sublingual and submandibular glands is mixed ITlUCillOUS·



general bony contours are noted. The tips, ears. and nose are in-



serous, and the products o f the palatine glands are purely mUCinous.



j



Physical Examination



a Fig 3-2 (a) lntra01a1 and exuooral palpation of the salivary glands torpatMiogic change. The tollSillar area should also be inspected visually. (b) SubmaxiUary gland examinalioo with bimanual digital palpatioo. (Courtesy of Dr Dan E. Tolnl A. Fenton A. Mericske·Stern R Prosthodontoc Treatment for the Partially Edentulous Patient. St Louts: Mosby, 2004. 6. Zarb GA Or



Pharmacologic Interactions in the Oral Cavity Medications inducing hyposalivation



Interferon-a iS a cytokine with a wide range of systemic effects that particularly affect the immune system. RCTs appear to have reached a reasonable consensus that interferon-a improves patients' subjective assessment of xerostomia; however, conflicting data have been published regarding benefits on reducing hyposalivation.42 Current dosage recommendations for patients with primary SS who are looking for relief from xerostomia are 150 IU of interferon-alpha



A dry mouth



seem s



to be one of the most common side effects



to be taken in lozenge form three times a day.



of medication use; over 400 medications depress function of the salivary glands.m� Different medications induce hyposalivation by different mechanisms that interfere with parasympathetic signaling.



Drug-induced intrinsic discoloration of teeth



Some do this by inhib�ing adrenergic neuroeffector junction activ­ ity, others by lowering central connection activity of the autonomic



Teeth are especially prone to drug-induced changes from birth to



nervous system, and still others through anticholinergic effects.



approximately 8 years old. Effects of drugs on tooth development



The clinician must stay aware of new and existing medications and



include discoloration that can be difficult to reverse by noninvasive



possible medication interactions. Currently, the following families of



means such as vital bleaching.70 Depending on the teeth and tissues



medications have representatives that interfere with salivary gland



affected, direct or indirect restorations may be necessary.



function: antidepressants, antihistamines. antihypertensives, anti­ psychotics. antiarrhythmics. anticonvulsants . diuretics. antiparkin­ sonians, antiemetics, antiarthritics, anJHnflammatones, and anx­



Fluoride



iolytics. In addition, chemotherapy can lead to hyposalivation and



Optimum fluoride intake results in esthetically unaffected teeth that



changes in the quality of the saliva produced. Fortunately, in most



are



patients, salivary function returns to normal or close to normal after



improved enamel strength. However, excess fluoride exposure dur·



chemotherapy ends. unless doses were exceedingly high or pro­



ing tooth development leads to hypomineralized enamel and chang·



longed use occurred.



es in appearance lhat range from small white flecks at cusp tips lo



relatively resistant to the formation of caries lesions because of



larger opaque areas t o darkly stained pitted areas.



Medications to treat hyposalivation and its effects



Tetracycline Mothers who take tetracycline (or a derivative) during the second or tl1ird trimesters of pregnancy may have children whose teeth are



Pilocarpine is a muscarinic-stimulating cholinergic agonist with para­



significantly discolored and which appear initially as yellow and then



sympathomimetic properties, nesulting in increased muscle tone



turn to gray or gray-brown over time. Parents should avoid giving



o f various tissues o f the gastrointestinal (GQ tract. As a mimic of



tetracycline to children under the age of 8 years to prevent disco!·



acetylcholine, pilocarpine stimulates secretion from the salivary and



oration of the permanent dentition. Tetracycline or oxytetracycline



lacrimal glands.'e Patients should be monitored for sweating or Gl



leads to yellow teeth, whereas chlortetracycline produces gray­



disturbances, and the drug should not be administered t o patients



brown teeth.'6



References



7. Scuty C. Carrozzo M. Oral mucosal disease: l.Jchen planus. Br J Oral Maxil lo fac Surg 2008;46:15-21.



Minocycline Minocycline is a tetracycl1ne denvahVe used to treat a variety Ollnlec­ tious or inflammatory conditions. In contrast to tetracyclrnes. which affect tooth color during development, mil'lOCycine may mfrequently cause tooth discolorallon after tooth development has ceased.80 The mechaniSm for thiS elfect IS unclear. Furthermore, mlflOC:ydlne af­



fects soli tissue pigmentation. causing a1terat1ons in the skin. thyroid gland, naUs, bone. sclera, conjUnctivae, and g1ng1vae.••JO Some re­ ports suggest that g1ngival d•scolorat1011 is a result of changes to the underlying bone. and purple-black discoloration of gingiva has been observed, often in the area covenng the hard palate.83



8. Yaooet



KB. Egan CA. P 40 mm 4. Lateral movements;, 7 mm 5. If S·cUNe deviation is presen t, then joint must be silent



noise



t.



10-intraart iculaf d isorder. (Adapted fromMderson et at �1



increased muscle tenSion were good predictors of jaw pain."' As



tors,31 recognizing that chronic temporomandibular pain. like other



with TMDs in general. the cause of Axis I disorders is not known



musculoskeletal pain syndromes. is frequently identified as a persis­



but has often been attributed to malocclusion, a hypothesis that



tent dull ache'" that i s aggravated by use of the jaw.



contemporary standards of investigation have not supported.2-211



The clinician should ask a standard series of questions to begin to rule out TMD. A jaw disability checklist may be a helpful tool



Axis /, Groups II and J/1 disorders



(Box 7-1 ).1'1 Oth er questions that may assist the c linician include the following:



Axis I. Groups 11 and 111 disorders are related to alteration of soft tiSSLte anatomy within the TMJ or degenerative joint changes (see



1. Are you able to open your mouth as well as you think you



Table 7-1 ). The cardinal signs of internal anatomical alterations of soft tissue in the TMJs include decreased range of mandibular mo­



2. Do you feel your bite has changed?



tion and joint noises w�h mouth opening and closing. Patients may



3. Does your jaw make clicking, grating, or grinding sounds? If so,



report prominent clicking or grinding sounds with jaw use. These



should be able to?



is this noise accompanied by pain?



disorders may not necessarily be associated with pain. so it should



4. Does your jaw lock or catch?



not always be assumed that a patient's clicking TMJ is the source of



5. Have you been told



pain. Symptoms of mandibular dysfunction may also include "catch­



or are you aware of clenching or grinding



your teeth while awake or sleeping?



ing" or locking of tile jaw. Clinicall y reliable criteria (Table 7-2) al­



low the clinician to determine the anatomical status of a par ticular



It any of these questions is answered in the affirmative, the



TMJ with a great degree of accuracy.29 These clinical criteria do not



developing differential diagnosis then should include TMD. A



make reference to pain, which may or may not be present in any of



complete history and clinical examination may then follow, uSing



these diagnostic scenarios. The clinical reliability of the criteria was



criteria presented in the RDC.15 Stohler provides a treatment



tested against radiographic findings, which are not predictive of pain



algorithm based on responses to the Graded Chronic Pain Scale, a



in TMDs. 30 The methods of esta blishing a diagnosis depend in part



seven-item questionnaire assessing pain intensity and impact of pain



on accurate assessment of range of motion (see Rg 7-3).



on usual activities.:!$



Clinical history of TMD



Examination



Diagnosis of TMDs is contingent both on obtaining a comprehensive



The examination should include palpation of the preauricular (TMJ)



history and, t o a lesser extent, on physical examination findings and



areas and the masseter muscles in addition to the anterior, middle,



reproductions of the patient's pain comp la int. It is crucial to ask the



and posterior areas of the temporal muscles. Although much has



patient to highlight the area of discomfort by pointing with one finger



been published to guide clinicians in this technique, no universal



rather than fanning the entire hand over the face. which precludes



technique has emerged as the gold standard."" One useful tech­



the ability to attempt to locate the site of discomfort. It is equally



nique is to palpate the muscles of mastication and the preauricular



important to present the patient with a choice ot verbal pain descrip-



regions with a moderate amount of pressLtre while asking the patient



861



J



Temporomandibular Disorders



Tabl e 7_3 What activities does your present jaw probl&m prevent or llmft yoo from doin g? o Chewing



Considerations



Pain



High



Low Sharp, electric, burning. paroxysmal,



Constant ache/tightness



interm»tent, spontaneous pain



Sharp pa1n with jaw use



o



DrinlOtolac Surg 2008:37:535-541 19. ShahaAR. Preopetauveevaluauon ol the manoo1:>1e n patoents '"'lh carcnoma olthe lloorOI mouth. Head Neck 1991;13:398-402. 20. Ciemo BW. IZ2afd M. � EA. Fwan N. Corlllanson oll!RJone graft. A donocal ex­



lerlSIOular bone �alt. Plast Aeconstr Surg t 988:81: 378-385. 27. Shpitzer T, Neligan PC, Gullane PJ, 01 al. Oromai\OibtA3J reconstructiOn with the fibular free



nap. AnaJysos of 50 consecutive flaps. AICh OtOiaryngol Hood



Neck Surg 1997:123:939-944.



ity



Neligan



Boyd



B. Gullane P. Gur E. Freeman J. Leg onorotd· and functKlfl following fibular free flap h orvesl. Ann Plast Surg 1997:38:



28. Shpotzer T.



P.



dtlQ-464. 29. Wet FC, Seah CS, Tsai YC. IJu SJ, Tsal MS. FltlUia osteoseplocutaneous



flap for reconstruCiion ol composllo mandol:>ular detects. Plasl Reconstr Surg 1994;93:294-304. 30. Futran ND.



Farwel DG. Smith RB. JOhnson PE. Funk GF. Def•�111e manage­



ment d severe faoal trauma ut.t.zing tree tiSSUe transfer OIOiaryngol Head Neck Surg 2005;132:75-85. 31. Futran ND. Retrospectove case seroos 01



� and secondary microvas·



cular rroo tiSsue tr.nsler reconsttuetioro o t mldlaoal defects J Prosthel Dent 2001 ;86:369-376. 32. Muzaffar AR. Adams WP Jr.



Hallog JM. Rohnch RJ, B'yl'd HS. Maxjary re­



constiUCtiOn: FmcbOnal and aeslhehc consideratoons



F'last Reconstr Surg



1999:104:2172-2183. 33. Olsen let These results support further study of pentoxifylline in patients in



The soft tissue necrosis of oral cavity mucosa that occurs after high



whom soft tissue necrosis develops after a course of radiation



doses of radiation therapy may be at1ributed to the obliteration of



therapy.



small blood vessels or to severe mucositis with ulceration. Irradiated



Most bone exposures will heal spontaneously after conservative



epithelium is thinner than normal and appears pale and atrophic. It



treatment. Although small areas of bone exposure Qess than



also has telangiectatic vessels. The irradiated mucosa is more sus­



1 em) generally heal spontaneously after a periocf of weeks



ceptible to mechanical injury and to the noxious effects of alcohol



to months, larger areas of bone exposure may persist and result



and tobacco. Soft tissue necrosis usually begins with breakdown of



in bone necrosis, followed by sequestration. If the bone is rough



damaged mucosa. resulting in a small ulcer. Most soft tissue necro­



or protrudes above the level of the gingiva. an oral surgeon may



ses occur within 2 years after radiation therapy. Occurrence after this



remove it to promote healing. An oral surgeon can also perform local



time is generally preceded by mucosal trauma. The risk of soft tis­



debridement of mocferate- sized necrosis, if indicated. Patients who



sue necrosis increases with larger fraction sizes, higher total doses,



wear dentures should refrain from using them or have them modi·



larger volumes of irradiated mucosa, and the use of an interstitial



lied to provide relief over the site of exposure. Pain is not a common



implant.



symptom; if present, it can usually be controlled with analgesics or



The mandible and maxilla will tolerate rather high doses of



a local anesthetic applied with a cotton-tipped applicator, if needed.



radiation therapy without serious problems, as long as the tissues



Antibiotics frequently reduce infection and discomfort within a few



overlying the bone remain intact. If sott tissue necrosis develops in



days but should be continued for 2 l o 3 weeks. Hyperbaric oxygen,



the mucosa overlying the mandible or maxilla. the underlying bone



along with antibiotic therapy and local debridement, may help



may become exposed. This can lead t o serious injury, resulting



promote healing. Mandibular resection should be reserved as the



in ORN. Patients at highest risk for ORN appear to be those with



last resort for the patient with intractable pain, recurrence of severe



tumors involving the gingiva or bone; those who continue to smoke



infections, fracture. or trismus.



or drink after radiation therapy; and those who receive high doses



Most bone problems develop within 3 to 12 months after radia·



o f radiation therapy, large treatment volumes. large fraction sizes.



lion therapy. but some risk persists for many years, especially if



or interstitial implants. Compared with the maxilla, the gingiva of the



the patient undergoes dental extractions. Necrosis is most likely



mandible has a rather tenuous blood supply, placing the mandible at



to occur after extraction of mandibular teeth, although this is



greater risk of exposure and necrosis. If exposed. necrotic bone may



infrequent i f special precautions are taken. TI1e edentulous patient



become infected. The necrotic process may then extend to involve



has a lower overall risk for bone necrosis compared with the



adjacent bone for a considerable distance. Severe necrosis can then



dentulous patient.



develop and lead to orocutaneous fistulae and pathologic fractures.



175



i



�3



Oral Complications of Chemotherapy and Radiation Thera py



Taste alterations



Malignancy



Loss of taste occurs rapidly and early in the course of radiation ther­



The carcinogenic effect of ionizing radiation 11as long been recog·



a py to the oral cavity. Most patients report that the sense of taste



nized. The latent inteNaJ between radiation therapy and the develop·



is essentially nonexistent by the third or fourth week of treat ment .



ment of cancer varies from several to many years. Kogelnik et al'64



After the completion o f radiation therapy, most patients report some



reviewed the charts of 1, 163 patients from the MD Anderson Can­



t aste improvement within 1 to 2 months. Full recovery of taste usu­



cer Center who had suNived a minimum of 5 years after treatment



ally requires 2 to 4 months. In some patients. taste never returns



for head and neck cancer without recurrence. Follow-up for these



to normal, at least in part because of xerostomia. Allhough some studies have suggested that zinc therapy may be useful in improv­



patients ranged from 7.5 to 25.5 years. Patients were treated with



ing taste acuity. a randomized clinical trial did not show any benefit



(n



for zinc over a placebo.•03 Amifostine may protect against taste loss



cers in the primary tumor site (1.8% vs 2.7%}. within the immediate



caused by irradiation. "4•11•



vicinity of the primary tumor (4.2% vs 3.1 %}, or at sites remote from



surgery alone (n =



826}.



=



337) or radiation therapy with or without surgery



For these respe ctive groups, the inc i den c es of new can·



the primary tumor but still within the oral cavity or pharynx (4.7% vs 5. 7%) were very similar. It was concluded that moderate-dose or



Trismus



hig h- dose radiation therapy did not produce any new squamous cell carcinomas of the mucous membranes. Similar findings have been



Etiology



reported elsewhere.•65.•60



Causes of trismus include (1) fibrosis of the mas ticatory musculature after high-dose radiatiOn therapy to the oral cavity or oropharynx (2)



before their deve opment, and the difficulty of obtaining reliable l long-term follow-up data make the task of estimating tl1e true risk of



surgical scarring. and (3) advanced carcinomas involving the ptery­



this problem difficult. However. most series include 1 or 2 cases of



goid or masseter musculature. The temporomandibular joint (fMJ}



radiation-induced bone sarcoma per 1 ,000 5-year survivors. If one



is relatiVely resistant to ankylosis caused by radiation therapy, but



were to



the risk of injury increases if the joint is invaded by tumor. The use



term suNivors and an estimated 5-year suNival rate of 40% for all



of large daily treatment fractions also appears t o increase the risk of



patients with head and neck cancer who received radiation therapy,



trismus.



it is calculated that 1 case would be induced per 1 ,250 patients



The rarity of radiatiOn-induced sarcomas, the long latent period



,



assum e



malignant in duction in 1 patient of every 500 long·



treated. A review of lhe Mayo Clinic experience showed no difference in suNival between patients with ra diation-indu ced sarcomas of the



Prevention and treatment High-energy x-ray beams and sophisticated



mandible or maxilla and those with non-radiation-induced sarcomas multiple-field tech­



niques should be used whenever possible to reduce the total dose



of the same site (45% 5-year overall suNivaQ. Because



some



patients



with



radiation-Induced



osteogenic



of radiation to the TMJ and the muscles of masti cation. Patients



sarcomas of the mandible or maxilla can be cured. the risk of death



treated with both surgery and radiation therapy have a greater risk



from a radiation-indu ced sarcoma after a course of radiation therapy



for trismus than patients treated with just one modality. For these



is minimal and is very similar to the risk of death a patient accepts



high-risk patients and those in who m trismus has developed before



when



treat ment daily jaw-stretching exercises may increase the interarch



surgery. or major head and neck cancer surgery.



,



undergoing



chemotherapy,



general



anesthesia.



general



or interincisor distance. A number of devices can be used, includ­



An association also has been noted between radiation therapy and



ing commercially available jaw-stretching tools and less-expensive



thyroid tumors. The latent period is usually I 0 to 30 years. Almost



stacked tongue blades, tapered corks. or clothespins. These devices



all reported cases have followed low doses of radiation therapy



are inserted between the teeth to increase the interincisor distance



(from less than 6 cGy t o 1 ,500 cGy), well below the doses used for



until gradual increases are encountered. The exercises should be



squamous cell carcinomas of the head and neck. In contrast, doses



done for 4 minutes four times daily. Additio nal tongue blades can



greater than 2,000 cGy to 3,000 cGy are associated with a very low



be added or a thicker aspect of the cork can be placed between



risk of induction of thyroid neoplasia. This is likely because higher



the teeth every few days t o increase the interincisor distance and



doses of radiation t11erapy either completely destroy follicular celts or



stretch the muscles of mastication. The rate of advancement should be approximately 1 mm every other day and should be monitored to



at least render the survivi11g cells incapable of division. Not all thyroid l neoplasms that deveOP after radiation therapy are malignant. and



ensure the distance approaches an amount that permits adequate



many of the malignant neoplasms that do develop (papillary and



hygiene measures and reasonable bolus manipulation. Any sudden



follicular carcinomas} are readily curable with surgery. Thus, the



degree ot restri ction In mandibular opening is suspici ous for recur



risk of radiation-induced carcinoma should not be a major factor in



rence or other infratemporal fossa disease.



determining treatment approaches for the typical patient with head



­



and neck cancer.



1



176



j



Oral Complications of Radiation Therapy



Fig 13-4 Tongue depressing stent for balloon catheter. {a) Wax template is fitted to



determine opening and fit to teeth. (b) Maxillary defect is susceptible to mocosltls at the air-tissue Interface. (c) Wax pattern ol the stent shows where the balloon catheter would enter. (d) Wax pattem before processing to acrylic resin. (e) Completed stent and balloon catheter.



Prevention and treatment of radiation-induced



ticiently to the target volume. Historically, this was alded by the use



oral complications



of positioning devices such as stents and shields. The trend toward using computed imaging and IMRT for treatment of head and neck cancer has somewhat decreased the need for shielding devices.



Need for guidelines



However. the use of tissue bolus materials and positioning devices is still required to make the treatment effective.



Investigators surveyed Dutch radiation therapy centers that per­



The target tissue may involve a relatively superficial area, or it may



form irradiation of patients with head and neck cancer to determ•ne



be more centrally and deeply located. As such, the treatment beams



which prevention and treatment regimens are used for oral sequelae



may be projected from multiple directions to mini mize dose to tt1e



resulting from head and neck radiotherapy. •e7 Survey questions in­



superficial areas of the skin and vital structures such as the spinal



cluded queries about screening, care before and during radiation



cord. Movable structures such as the tongue and mandible may b e



therapy, care during postradiation therapy, and the composition of



positioned outside o f the treatment field by the use of a positioning



the dental team who evaluated and treated the patients undergoing



stent (Rg 13-4). These stents often depress both the tongue and



radiation therapy. Unfortunately, these investigators found a great



mandible away from the treatment area to minimize the exposure in



diversity among the institutes' approaches to prevention and treat­



the treatment area and decrease the risk or incidence of radiation­



ment of oral sequelae in patients with head and neck cancer. Dis­



induced mucositis. Further incorporation of gold seed markers



turbing findings included a lack of well-defined guidelines in many



is useful to ensure reproducible treatment orientation between



centers. absence of a dental team at some centers. absence of an



treatment sessions.



oral hygienist on some dental teams, and the observation that many



Superficial lesions requiring radiotherapy can be most efficiently



patients were not referred to the dental team in a timely manner. The



treated by incorporating the use of a tissue bolus material to allow



development of a general standard protocol for the pev r ention of



optimal location of the beam energy at the surface. Often, these



oral complications was recommended tor all head and neck cancer



materials are made of either wax or acrylic resin, permitting delivery



radiation therapy centers.•EB Similar deficiencies are likely present at head and neck cancer



of a focalized and effective dose to the treatment area (Fig 13·5). Shielding devices can be made o t prevent the radiation from af­



radiotherapy centers within the United States. It is strongly recom­



fecting tissues behind the prop osed target tissue . These devices



mended that dedicated teams be assembled to administer aggres­



often are made primarily of acrylic resin surrounding a central core



sive care to pati ents receiving radi ation therapy to the oral mucosa.



of a shielding alloy such as Wood's metal (Fig 13-6). It is critical that



These teams should institute preventive measures and treat symp­



the thickness of acrylic resin be proportional to the planned energy of



toms as early as possible.



the beam. Acrylic resin tt1at sufficiently surrounds \118 alloy minimizes scatter, thereby preventing fonnation of mucositis. Energies used to



Stents, shields, carriers, and positioning devices



treat head and neck tumors are approximately 6-MV photons. and require at least 7 mm of acrylic resin around the alloy to absorb scatter.



One goal of radiation therapy of head and neck tumors is to confine



Brachytherapy is also used occasionally to treat specific areas



the treatment to only the area planned for treatment. This minimizes



ot t118 head and neck and recurrent lesions. Often. radioisotopes



the side effects noted earlier and allows treatment to be directed ef-



are used. which emit gamma radiation from their radioactive decay



177



1 3lOral Comp lic ations of Chemotherapy and Radiation Therapy



Fig 13·5 (a) Bolus of wax used to contrOl deptll of treatment of supe11icial skin lesion of face. The tub­ Ing is used for airway exchange. {band c) CT image shOwing lhe wax bolus alongsi�e lhe skin. Fig 13·6 (a)A wax template is to be created for a shield:ng slenl !hal "nil prolect the longue and other struc­ tures behind the target tissues of basal cell carcinoma of the upper Up. (b) Steo t fabnca"on on casts of max­ lila and mandible. {c) Wood·s metal i s pouree into the stent. (d)Resolution of lesion after 3 weeks of treatmeol wilh stent in place.



Fig 13·7 (a} Brachytherapy



using ce·



slum in tile catheter for treatment of in­ lranasal Kaposi sarcoma. (I>) Computed vault for delivel)' of ra�ioactive isotope. (c) Acrylic resin slenl wilh catheter re· ceptacle.



Fig 13-8 (a) Trealment of scalp angiosar­ coma. (IIJ Catneter cap used for ra�ioactive isotope delivery.



and can be pl aced a t a specified proximit y to the tumor bed for



invasive in nature. Recent large-scale trials have d emonstrated that



a specific dose based on timed exposure. Positioning stents are



chemotherapy and r adiotherapy in conjunction wi th tumor-ablative



helpful to direct the spatial location of these point sources for



surgery are more effective i n controlling disease than surgery and ra­



repeated exposures. The stents configure the uninvolved tissue at



diotherap y atone. Because of the trends in using this combined ther­



a specific distance from the target tissue and can be automatically



apy and contemporary chemotherapeutic agents. the sequelae of



loaded from a computed vault that contains the radioactive source



common side effects precipitate often within this patient population.



(Figs 13-7 and 13·8).



Several approaches t o h an dling this complex array of treatments and their associated side effects have been presented as guide­ lines. As continued development of radiot herapy techniques move



Summary Combined-modality therapy of head and neck cancers or cancers of other origin is effective in con t rolling tumors that are advanced or



1781



forward, these sequelae may continue to change in their frequency



of occurrence. The goal of disease control with these mod alities is state oi the art and should be approached with the knowledge of management of their accompanying complications.



References



References 1. Peterson DE. Keefe DM. l�-oonlrolled, srudy of iseganan for the IGduction of SlOfi'IIIIIIIS on patients receM>Q stomatoloxoe OhemOlherapy. Leuk Res 2004:28:559-565. 26. Yuen KY. woo PC. Tal JW. Lie AK. LI.Jk J. Liang R. enects of c:ta uthromy · cin



on



oral mucosll1S in bone marrow transplant r�ients. HaematOiogoea



2001;86:554-555. 29. Herrmann RP. Trom M.



CoOr\01' J. Cannell PK InfectiOns in pallents 1nonagod



at home Cfurlng autologous stem coli trOflsplantation lor lymphoma and mul tiple myeloma. Bone Mwow TranspiOI'It 1999;24:1213-1217. 30. Feld R The role ofsurveillance c:uttures ., patoe nts likEly to develop chemolheN. J Cern EdUc: 2002.66:903-91 1. 32.. Mahood OJ. Dose AM. L.oprinzl CL. et a1. lnhlboloo of OU(I(Ot.OliCit·nOOced stomatms byoral CI)'Olt1er8py. JOn Onool1991:9:449-452. 33. Casonu S. F9defl A Fedeli SL Cetalano G Oral COOling (�herap�. an ot· fectl\'11 treatment tor the plll\'eOtoon 01 5·11uorouraoHnduced slOp/iC811ons • Loss oJ seal ((:(eates nasal speech and leakage of loodliq l uids) • lack of retention or looseness • lnabitity to place prosthesis because of contracture Of lateral scar band • Discomfort caused by mucosills (radiolhefapy o r chemotherapy). pros­ thesis pressu re. too-aggressive defect cleafling



Fig 15-16 (a) WebmtXO of 1O·mm sa p c.ng between s and IJle OPPOSing 111e sofl ts ue covering the bone i OCClusion (not the opposing ridge)



Size and shaPe:



Intraoral form



Exhibits a rounded superior surfaoe With nearly parallel buccal and lnguaJ surfaces at least 1 height from vestibule



em n



Provides a minmum bulk for Implants of 10 mm in width and 15 mm In height



Bulk



Provides a 10.mm vestibular depth and distension that allows independent movement of the cheek and toogue relative to the mandible



Ridge coveeations lor proslhellc speech appli­ ances in cleh palate. Plasl Reconstr Sorg Transplant Bull 1962;30:663-669. 39. Gr'ayson BH. Sanuago PE. Brecht LE. Cutling CB. PresUfg,cal nasoal· veotar molding In 1ntan1s wrth Cleft lop end palate. Cteh Palate CIMIOfac J



37. Kuijpened from lOng·term ObServations in tha fleory and Practice of Fored Proslh­ odontiCS. ed 8. & Louis: Medico Dental Media International. 1989. 175. Rosenstief SF, Land MF, Fujimoto J (eds). Contemporary Fi�ed Prosthodon· tics. ed 2 . Stlouis: Mosby. 1995. 176. Mack PJ. A theoretical



and Clinical investigation Into Uie taper aChieved on



crown and Hllay preparations. J Oral Rehabil 1980;7:255-265. 177. Wiskott HWA, Nicholls Jl, Belser UC. The relat10nsh1p betvveen abutment taper and resistance of cemented crowns t o dynamic load111g. fnt J Prostho­



203. McGuire MK. Nunn ME. Prognosis versvs actual outcome Ill. The effective· ness of clinical parameters in accurately predicting tooth survival. J Periodon­ tol1996;67:666-674. 204. Ante 11-1. The fundamental principles or abutments. Mich State Dem Soc Bull 1926:8:14-23. 205.



Nyman S. Lindhe J.Lundgren D. The role of occlusion foeU1e stability of fixed bridges in patients wiUi reduced periodontal tissue SUPPOft. J Clin Periodon·



tol 1975:2:53-66. 206. Stein RS. PontiC-residual ridge relationship: A researc/1 report. J Prosthet Dent 1966:16:251-285. 207. Zitzmann NV. Mannello CP. Berglundh T. The ovate ponitC design: A llisto·



dont1996:9:117-130. 1 78. Dodge ww. Weed RM, ea.,. RJ, BuChanan RN. The effect or convergence angle on retention and resistance form.Quintessen ce lnt 1985:3:191-194. 179. Wiskott HWA. Nicholls Jl. Belser UC. The effect of tooth



cemented zi2G the lateral dimension of the obturator in the various conditions (above, on, and below the area



of posterior pharyngeal wall activity) did not change significantly as the position varied. This finding was contrary to the hypothesis of the



,



follow-up studies showed improved palatopharyngeal



use of a palatal lift include (1J inability to attain adequate retention, (2) presence of a spastic or stiff soft palate that does not tolerate elevation, and (3) lack of cooperation on the Contraindications to the



part of the patient.



inv estigators that the lateral dimension of the nasopharynx wo utd be



Hardy et al compared the use of the p alatal lift in 11 children with



the level where the posterior and lateral pharyngeal wall activ­



cerebral palsy to the results obtained with pharyngeal flap s urgery



less at



ity takes place. compared t o above or below it.



in 6



c hildren with



cerebral palsy.85 Of the 6 chldren treated surgi­ i



cally only 3 made suffiCient speech gains to justify considering the ,



procedure a success; prosthetic management of t 0 of the 11 chil



­



Palatal lift



dren was judged to be successful. Anticipated difficulty i n tolerati ng the lift because of increased gag reflex



was



not experienced. Even



palates related to neurologic



though some of the children displayed gross invol untary head move­



disease or in patients with su rgically repaired clefts where a fairly long



ments, the prosthesis did not irr itate the posterior pharyngeal wall



soft palate remains essentially nonfunctional for closure, a conven­



during head flexion; nor were any instances noted of inflam mation



tional obturator prosthesis may be difficult to fabricate because of



or necrosis of the soft tissue on the inferior velar surface. Improved



the palatal tissue under and behind which the prostl1esis must pass



functioning of the palatopharyngeal valve was noted in one patient



to b e effective. In such cases. a palatal lift has been found to be ef­



after he had worn the palatal lilt for



fective (see chapter 15). Gibbons and Bloomer first reported the use



prosthetic



of such a prosthesis in an adult patient with flaccid velar paralysis resulting from bulbar poliomyelitis.'43 The lift elevated the velum and



palsy is the procedure of choice. Not only is there no surgical risk to



reduced the palatopha1yngeal space, resulting in improved speech.



with the prosthetic program compared with the surgica.l procedure.et.



In patients with weak or



paralyzed soft



management of palatal



a time. Based on



these results,



paresis in children with cerebral



the ch ild, but there appears to be a greater probability or success



Gonzalez and Aronson studied the use of palatal lifts in the treatment of 35 patients ranging in age from 4 to 72 years."' Of



311



i



19



Speech Pathology and Prosthodontic Applications



Table 19-5 Age of child 3to4 4 !05



5to6 6to 7 7 to 8



[1 Developmental sequence of speech1. Consonants correctly used in words



/mi. /p/, lbl. /wl, {hi In!. /V,Idl, lf}l.lkl, lgl,ljl Iff. M,lsl,lzJ /j/, ly, !II. !a/.101 /rl, lhwl, Is!, /zJ



production of the phonemes is again possible when the permanent dentition erupts. The developmental sequence of articulation is paralleled in the development o f skill in the use of other features of language. Children advance in orderly increments of language skills such as (1) length of utterance, (2) number of words they understand (recog­ nition vocabulary), (3) number of different words they use (vocabulary of use). (4) grammatic complexity of their sentence structures. (5) accuracy of syntax. (6) fluency and spontaneity of oral expression, and (7) social use of speech to influence listeners' opinions and actions.



Factors Related to the Development of Speech Skills



Intelligence The child's intelligence plays an important role in the rate of mastery



The ability of the child t o communicate depends on more than the



of speech and language skills. The intellectually disabled are typically



condition of the speech structures. Important internal and environ­



delayed in their first use of words and sentences. They present more



mental variables profoundly influence a child's learning and use of



than the average number of articulation errors. most prominently



speech. One must appreciate the patient's social and family history



omissions of phonemes. Complete speechlessness can be attrib­



in addition to medical history to visualize the dynamic relationships



uted to mental deficiency only in extreme cases152•153 (ie, 10 range



between these elements and plan a remedial program comprehen­



of 10 to 25). Mutism is usually attributable to autism or, in an older



sive enough to meet the patient's needs.



child who once spoke but stopped speaking, to hysteria. Altl•ough the level of proficiency in speech and language ultimately attained by intellectually disabled children is below that of normal children. all



Developmental sequence of speech-sound mastery The child is not born able to produce the entire repertoire of pho­



except those with extremely low intelligence demonstrate growth in these skills.



Hearing loss



nemes; the infant has a meager repertoire to which he or she gradually adds. The average child can produce 27 diffe rent phonemes by 2.5



Children who are deaf or profoundly hard of hearing display colos­



years of age.'"" Mastery of the use of these phonemes in words takes



sal delays in acquisition of a symbol system and development of



longer. Cross-sectional studies of children generally a gree that the de­



intelligible speech. Children whose loss of hearing is less severe



velopmental sequence is somewhat as shown in Table



develop a symbol system but miss ce1tain crucial features of the



19-5.1"'·1•1



The rate at which children master phonemes varies greatly. By 3



speech around them and display difficulty in reproducing it. Because



years of age, some children correctly articulate all of the consonants



children who are hard of hearing can monitor their performance to



and all of the vowels (vowels are typically mastered by all children



some degree, they produce voice and speech patterns less bizarre



early and without much difficulty). Other children do not master all of



than !hose of deaf children. Their communication may be lacking



the consonants until they attain the age of 8 years or perhaps even



in vocal melody. and they may demonstrate articulatory distortions,



later. Girls typically master phonemes in context somewhat earlier



particularly of phonemes with high-irequency components (ie. frica­



than boys.



tives and affricates). Also. they may omit final phonemes and may



No single general principle appears to adequately account for



have trouble monitoring the intensity of their speech.



the developmental sequence of speech. Among the factors that



The incidence of hearing loss is higher in children with cleft palate



probably play a role in determining this sequence are (1) frequency of



compared to the general population.154 Incidence of pathologic



occurrence of the phonemes in the child's environment, (2) visibility



conditions of the middle ear also i s higher than in the general



of the phonemes, (3) their auditory distinctiveness, (4) their phonetic



population. 1*1$7 Hearing loss occurs more frequently in children



power. (5) the distinctive tac1ile and proprioceptive characteristics of



with cleft palate only than in cl1itdren with clefts of both lip and



their production. (6) the complexity of muscular adjustment required



palate. 1011 One cannot make a general statement about the incidence



for their production, and (7) the child's changing dental status. With regard to the last factor, although children typically master lsi and



of hearing toss within the cleft palate population because research data indicate that it varies widely with the age of the group tested.



lzl between the ages of 5 and 6 years. these sounds often become



Spriestersbach et al reported that the hearing acuity of children with



distorted when maxillary anterior primary teeth are lost. Correct



cleft palate varies a s a function of age.158 Children who were 6 years



3121



J



Factors Related to the Development of Speech Skills



or older when they were tested had Significantly smaller incidence



severe picture of communication disturbance. Their motor difficulties



and magnnude of toss than did children tested before 6 years of



are often complicated by hearing loss.



age. The research of Goetzinger et at suggested that adults with



Some patients who do not show the weakness, slowness. or



cleft palate do not display more hearing problems than the general



incoordination that causes dysarthria nevertheless may demonstrate



adult population. •so



unusually poor motor-speech performance. Such difficulty in per­



Some clinicians believe that t11e manner in which cleft palate is



fomling skilled motor acts voluntarily is termed apraxia. 162 A patient



managed bears an important relationship to the incidence of hearing



with oral apraxia is unable to follow instructions to wiggle or pro­



toss. Masters et at studied a group of 172 patients."'" They reported



trude and retract the tongue, to whistle, to blow. to click the teeth,



that patients wnh prosthetically repaired clefts had the highest



t o click the tongue, or to cough. Associated with this, or sometimes



incidence of hearing toss, and they attributed this hearing toss to the



occurring independently, is apraxia of speech, demonstrated by



prosthodontist's inability to fabricate



adequate prosthesis prior



difficulty in producing phonemic units of speech. The patient cannot



to 2 years of age and the failure of the prosthesis to restore palatal­



understand where to place the tongue to produce a given phoneme



musculature function.



or how to execute a sequence of movements to produce a word.



an



They considered the preservation of nom1al physiology of the eustachian tube and middle ear to be essential. However, their data did not take into account the age of the children at the time



Specific language disability



they were tested. Spriestersbacll et al also found that the incidence



of hearing loss was greater in children treated prosthetically than



Some children display difficulty in understanding and using language



in children with surgically repaired clefts, but the degree of loss



even though testing reveals no hearing loss. motor defect, intellec­



between the two groups was not significantly different. 1"' Because



tual impairment, or emotional disturbance. Such difficulty in handling



of these findings, they doubted that the higher incidence of hearing



the symbol system is designated specific language disability (devel­



loss in subjects wearing obturators could be explained on the basis



opmental aphasia or congenital aphasia). It is presumed that such



of poorly functioning palatal musculature.



cllildren have tl1is difficulty because of bilateral cerebral lesions or



In another study by Graham et al,161 54 patients were examined



defective crucial neural substrate for language. Such children may



before and after placement of an obturator: no ear infections



express themselves with gestures and indicate considerable under­



developed after initial placement of the obturator. and no patients



standing of their environment, but they are unable to understand the



showed an increase in hearing toss after obturator use. It was



significance of what is said to them or. in milder cases. give the ap­



concluded that an obturator can b e wom with no adverse effect



pearance of mishearing words in a way similar to the hard of hearing.



on the otologic condition of the palatal cleft patient Patients in this



Less severe degrees or specific language disability may account for



study had received otologic care from infancy, and obturators were



some of the persistent articulation and syntactic problems displayed



not fabricated before these children were 4 years of age.



by some children. Examination with the Illinois Test o f Psycholinguistic Abilities may indicate that a child has particular difficulty in the



Impairment of motor control



sequencing and recall of series of auditory units. '60 Although the child may be able to discriminate between and produce individual sounds. he or she may be unable to blend sequences of sounds



Children with cerebral palsy and patients with neuromuscular impair­



and recognize what words they compose. Sentences generated are



ment may display, as a part of their motor difficulties. i mpairment of



often syntactically primitive and reveal a disability in incorporation



control of the speech apparatus with resulting dysarthria. •e. Motor



of implicit syntactic rules from the surrounding auditory language



impairment may range from minimal weakness or incoordination to



environment. The specific reading disability known as dyslexia falls



complete paralysis or severe incoordination: consequently, speech



within the general category of specific language disability.•G