The Etiology and Pathogenesis of Tooth Wear

PRO S T H .0 DON TIC S
The Etiology and Pathogenesis of Tooth Wear PART 1 by Effrat Habsha, DDS
istorically, the most common
reason for tooth loss and
dental hard tissue loss has
been dental caries. Since the intro­
duction of fluoride, the prevalence,
incidence and severity of caries has
declined and the dental life
expectancy has increased. One of
the most common problems associ­
ated with this prolonged dental life
expectancy is tooth wear. Tooth
wear is an irreversible, non carious,
destructive process, which results
in a functional loss of dental hard
tissue. It can manifest as abrasion,
attrition, abfraction and erosion. l
This article will describe the etiol­
ogy of pathogenesis of tooth wear.
H
ETIOLOGY
Tooth wear can manifest as abra­
sion, attrition, abfraction and ero­
sion. The distinct definitions of the
patterns of dental wear tend to
reinforce the traditional view that
these processes occur indepen­
dently. However, a combination of
etiologies probably reflects the true
clinical situation. 2 Identification of
the etiology of tooth wear is essen­
tial for its successful management.
ABRASION
The term abrasion is derived from
the Latin verb abradere (to scrape
ofD. I It describes the pathological
wearing away of dental hard tissue
through abnormal mechanical
processes involving foreign objects
or substances repeatedly intro­
duced in the mouth. Abrasion pat­
terns can be diffuse or localized,
depending on the etiology. Exten­
sive oral hygiene has been incrimi­
nated as a main etiologic factor in
dental abrasion. Both patient and
material factors influence the
prevalence of abrasion. Patient fac­
tors include brushing technique,
frequency of brushing, time and
force applied while brushing.
Material factors refer to type of
material , stiffness of toothbrush
bristles, abrasiveness, pH and
FIGURE 1 Dental abrasion due to horizontal brushing technique
ORAL HEALTH· OCTOBER 1999
Ell
PRO ST HODONTI CS
amount of dentifrice used .3 The
most commonly cited effect of abra­
sion is the V-shaped defect, which
usually is ascribed to the use of an
intensive horizontal brushing tech­
nique (Figure 1). Cervical areas
are susceptible to toothbrush abra­
sion, particularly cuspids and first
premolars, where thin buccal
plates, gingival recession and
exposed root surfaces predispose
cervical notching. Habits involving
other intraoral objects (e.g., pipe
smoking, toothpick use, threadbit­
ing) can cause defects on the
incisal and occlusal surfaces. 4
Dietary abrasion is not very promi­
nent in modern days, as the typical
western diet tends to be very soft,
as opposed to primitive man's diet
which was more abrasive, and thus
contributed greatly to tooth wear.
ABFRACllON
The term abfraction, derived from
the Latin verb frangere (to break),
describes a wedge shaped defect
at the cementoenamel junction of
a tooth. 5 These lesions are some­
times
located subgingivally,
beyond the influence of tooth­
brush abrasion and are hypothe­
sized to be the result of eccentri­
cally applied occlusal forces
leading to tooth flexure, rather
than to be the result of abrasion
alone. According to the tooth flex­
ure theory, masticatory or para­
functional forces in areas of hyper
or malocclusion expose one or sev­
eral teeth to strong tensile, com­
pressive or shearing stress. These
forces are focused at the CEJ
where they provoke microfrac­
tures in enamel and dentine. The
microfractures are thought to
slowly propagate perpendicular to
the long axis of the stressed teeth
until enamel and dentine break
away resulting in wedge shaped
defects with sharp rims. The sci­
entific basis of the tooth flexure
theory has not yet sufficiently
been explored and it is often diffi­
cult to differentiate between abra­
sion and abfraction lesions. l
The term abfraction, derived
from the Latin verb frangere
(to break), describes a wedge
shaped defect at the cemento­
enamel junction of a tooth.
away of dental hard tissue as a
result of tooth to tooth contact with
no foreign substance intervening. It
is derived from the Latin verb
atterere, which is defined as the
action of rubbing against some­
thing. 1 Such contact occurs with
tooth grinding, such as with para­
function, mastication, swallowing
and speech. A typical presentation
of attrition is the presence of exten­
sively demarcated facets which usu­
ally match the opposing arch facets
in excursive contact positions (Fig-
Table 1
Sources of extrinsic acids
Environmental
Diet
atmospheric sulfuric acids
citrus fruit juices
vitamin C
HCL In gas-chlorinated
swimming pools
acidic carbonated
beverages
aspirin
acidic uncarbonated
beverages
acidic oral hygiene
products
wines
acidic saliva
substitutes
citrus fruits
AlTRmON
Attrition is the term used to
describe the physiological wearing
II
ORAL HEALTH· OCTOBER 1.999
RGURE 2 Attrition due to parafunction. Note matching wear facets.
Medicaments
PROSTHODONT I CS
ure 2). Attrition occurs almost
entirely on occlusal and incisal sur­
faces, although it may also affect
the buccal and palatal surfaces of
the maxillary and mandibular ante­
rior teeth in deep vertical overlap
relationships6 (Figures 3A, B, C).
FIGURE 3 Sixty year-old male with advanced tooth wear; A deep vertical overbite .
FIGURE 3 B wear at palatal of maxillary anteriors .
FIGURE 3 C wear of mandibular incisors .
EROSION
The term erosion describes the
process of gradual destruction of
the surface of something, usually by
electrolytic or chemical processes. It
is derived from the Latin verb
eroder (to corrode).1 Dental erosion
is the result of a pathologic, chronic,
painless loss of dental hard tissue
chemically etched away from the
tooth surface by acid and/or chela­
tion without bacterial involvement. 7
The acids responsible for erosion
are not products of the intraoral
flora; they stem from extrinsic or
intrinsic sources.
Extrinsic sources of acid:
Extrinsic acids may stem from
environmental sources, diet and
medication (Table 1).8 Dental ero­
sion has been reported in battery
factory workers exposed to atmos­
pheric sulfuric acids. 9 There have
also been reports of competitive
swimmers suffering dental erosion
from swimming in gas-chlorinated
pools. Large swimming pools gen­
erally use gas chlorination, which
results in the formation of
hydrochloric acid that requires
neutralization and buffering to
maintain the recommended pH
range of 7.2-8.0. Therefore, inade­
quate monitoring of pool pH has
been associated with dental ero­
sion. lO Though extrinsic environ­
mental sources of acids exist,
improved industrial safety regula­
tions have gradually diminished
the extent of environmental dental
health hazards. s
The role of diet in the etiology of
erosion has received the most
attention. II Certain products, espe­
cially citrus fruits, exhibit a low
pH, and when consumed fre­
quently and excessively, may lead
to dental erosion . It appears that
dietary substances with a pH
above 4.5 have a low potential to
ORAL HEALTH· OCTOBER 1999
iii
PR O STHODO N TICS
cause dental erosion. However,
foods and beverages containing
acids with calcium chelating prop­
erties, such as citrate, may cause
tooth damage at higher pH levels.
Several reports have associated
medicaments and oral health prod­
ucts (rinses) with erosion.l2.13.14.15
Many such products exhibit a low
pH and may be erosive when used
frequently. In most cases, the risk
associated with a product could be
reduced by either product modifi­
cation (such as encapsulation of
acidic medicaments), or altering
consumption habits. Special atten­
tion should be given to saliva sub­
stitutes aimed at patients with
reduced salivary secretion or
xerostomia. These substitutes
often have a low pH and may be
detrimental to patients whose lack
of saliva leads to prolonged clear­
ance times. Factors to be consid­
ered with exposure to extrinsic
sources of acid include: the dura­
tion of contact with the teeth
(which is influenced by swallowing
habits, motions of the lips and
cheeks, saliva), frequency of inges­
tion, amount ingested, buffering
capacity of saliva, the chemical and
physical properties of enameJ.8
Intrinsic sources of acid'
Dental erosion due to intrinsic fac­
tors is caused by gastric acid
reaching the oral cavity and the
teeth as a result of vomiting, per­
sistent gastroesophageal reflux,
regurgitation or rumination. Since
the clinical manifestation of den­
tal erosion does not occur until
gastric acid has acted on the den­
tal hard tissues regularly over a
period of several years, dental ero­
sion caused by intrinsic factors
has been observed only in those
conditions which are associated
with chronic vomiting or persis­
tent gastroesophageal reflux.
Examples of such conditions are
listed in Tables 2 and 3.
sion. 16 ather possible causes of long
term regular vomiting resulting in
dental erosion are disorders of the
alimentary tract, metabolic and
endocrine disorders or medication
side effects (Table 2).
Another possible etiologic in­
trinsic factor of dental erosion is
persistent gastroesophageal reflux
Table 2
Potential causes of vomiting"'"
Disorders of the alimentary tract:
• chronic gastrit is
• peptic ulcer
• intestinal obstruction
Neurologic disorders:
• migraine headaches
• benign recurrent vertigo
• diabetic or alcoholic
polyneuropathia
Metabolic or Endocrine disorders:
•
•
•
•
•
uremia
hyperparathyroidism
diabetic ketoacidosis
adrenal insufficiency
hypo-hyperparathyroidism
Psychosomatic disorders:
• eating disorders
(bulimia, anorexia)
• stress induced psychogenic
vomiting
Tahle 3
Causes of oastroesophaaeal reflux and reaurclitation"o "-""
Incompetence of the gastroesophageal sphincter.
• Idiopathic
• impairment of sphincter
• neurohumoral induced decrease of gastroesophageal sphincter pressure
• destruction of sphincter by surgical resection
Increased intraabdominal pressure: • obesity • pre9 nancy Increased Intragastric volume: Bulimic eating disorder is the
underlying cause in most cases of
dental erosion due to chronic vomit­
ing. Recent studies suggest that
approximately 90% of bulimic
patients are affected by dental ero-
II
ORAL HEALTH· OCTOBER 1999
(GaR). GaR is the movement of
stomach acids through the lower
esophageal sphincter. In healthy
individuals, small amounts of gas­
tric acids reflux into the esopha­
gus. This physiological GaR usu­
ally occurs after eating and may be
associated with eructation. In
healthy people, most of the reflux­
ate is returned to the stomach by
• after meals • pyloric spasm • obstruction due to peptic ulcer • gastric stasis syndrome PRO ST H O DO NTICS
the peristalsis stimulated by swal­
lowing. 17 It is estimated that 60%
of the population suffer from this
phenomenon at some stage of their
lives. If the clearance mechanisms
cannot return the refluxate to the
stomach and the symptoms
become chronic, the condition is
known as pathological GOR or
GOR disease (GORD). In some
patients, the refluxate breaks
through the lower and upper
esophageal sphincter and oral
regurgitation occurs. Oral regurgi­
tation may cause severe damage to
the dentition lB (Figures 4A, B).
Causes of gastroesophageal reflux
and regurgitation are listed in
Table 3. Often the erosion is most
severe on palatal tooth surfaces,
but other surfaces may also be
affected when the gastric contents
are chewed or kept in the buccal
sulci before reswallowing.
FlGURE4 Forty six-year-old male with Gastroesophageal reflux; A&B Dental erosion of maxil-
lary and mandibular anteriors; FlGURE 4 C Occlusal view of palatal erosion.
PATHOGENESIS
Since the critical pH of dental
enamel is approximately 5.5, any
solution with a lower pH value
may cause erosion, particularly if
the attack is of long duration and
repeated over time. Saliva and the
salivary pellicle counteract the
acid attacks, but if the challenge
is severe, a total destruction of the
tooth tissue follows. Erosive
lesions are seen as characteristic
demineralization patterns within
the enamel. In dentine, the first
area to be affected is the peritubu­
lar dentine. With progressing
lesions, the dentinal tubules
become enlarged but disruption is
also seen in the intertubular
areas . If the erosion process is
rapid, increased sensitivity of the
teeth is the presenting symptom.
However, in cases with slower pro­
gression, the patient may remain
asymptomatic even though the
whole dentition may become
severely damaged. 19
CONCLUSION
The interrelationship of the four
modes of tooth wear and individ­
ual susceptibility influence the
degree of tooth wear. Recognition
of the multifactorial nature of
tooth wear is the first step in manORAL HEALTH· OCTOBER 1999
Ell
Astracaine
e
{ot1icoine hydnxNoride and epinepl!ri". Injedion}
PROSTHODONTICS
THERAPEUTIC CLASSIACATION Local AnesIheIic lor Dental Use
INDICATIONS AND CUNICAl USE ASTRACAINE (articaire hyliochloridll)
isrolCalOOlaitolJDlnnslhesiamneMltl<Xi<MleS1hesiainclirOCaldentistry.
CONlRAJNDlCATlONS Ar1icaile hjdrochloride iscoo!ainOlcaJOO in patieols
with aknow!l hypersens~ivi1y 10 local areslhe/ics 01100 amide type. AI; wiIh all
agernentoftoothwear.lntJ Prosth., 7:506-515, 1994.
vasocoostricIoo. epir~lIire is rortraildicaIed in hypertension,lhyroloxicosis,
5. Grippo, J.O. Abfractions: A new classification of hard
orse.oereheartdisease.p;rtirularlywhentK:hjca((flaispresert LocalaneslhElics
tissue lesions of teeth. J Esthet Dent, 3:14-19, 1991.
should noI be used in se.oeresh<Xi<orheart block. TheyshouldaJsonoibeused
6. Smith. B.G, Some facets of tooth wear. Ann R Aust
v.ilen!here is inlmlmalion or5ellSis in Ihe region 0I1he proposed injection.
Coli Dent Surg., 11 :37-51, 1991.
WARNINGS RESUSCITATIVE EQUIPMENT AND DRUGS SHOULD BE
IMMEDIATElY AVAIlABLE WHEN ANY LOCAl ANESTHEnC IS USED. AI; wilh
7. Zipkin, I., McClure, F.J. Salivary citrate and dental ero­
oIher local aneslhellcs, articaire hydrochloride is capable 01 prodLCing rneIhe­
sion. J Dent Res., 28:613-626, 1949.
moglobinemia. This has been obser\Ed wilh epidural anesIhesia. txA no! when
8. Zero, D.T., Etiology, dental erosion-extrinsic factors.
used as dilllcled in denial procedures. Methemoglobinemia values 01 less lhan
EurJOraISci.104:162-177,1996.
20% usuaHydo noI produce any clinical S)111lIoms. The usual clinical signs 01
9. Petersen, P. E. and Gormsen, C. Oral conditions
meItEmlgIobinemia arecyanosis 0I1he nail beds m lips. Allhough Ihe possibilily
among German battery factory workers. Community
01 meIhemoglobinemia oa:ooing indlnal paIi&1s isextremelyr.lre RI3l be rapidly
Ie\Il!Sedbylheuseoll-2~bodyweiltlolrrShyleneblllladminisleredln1Ja­
agement, as failure to appreciate
this may lead to inappropriate
management and ultimate failure
of restorative therapy, The second
part of this publication will dis­
cuss the management of tooth
wear, Treatment planning strate­
gies, as well as case presentations
will be presented.
W
wnously OYer a5-miou1e period. Because ASTRACAINE cOOains avasocoo­
S1ricIor. nshouldbe usedwilhexlrerrecautlon in palienis re::eMng drugs known
10 prtxlJce blOOd pressurealieraUons (lor ~Ie MAO inhibilolS.lrtyclicanU­
depressanlS, phenOlhiazires). as eiIhei seYere m SUSlaired hypotension oril;\ler­
ifflSioomayoa:ur. PRECAUTIONS General Thesafelyande/lectivenessol
kxaliIlflSItfIicsdepend~IlWlI~W18d~~~
Dr. Effrat Habsha,
andrtl!dinessloremerlJnies THE LOWESTOOSETHATRESUlTS IN EffiCTIVE
I>l-lSTHESIASHOULDBE USEDTOAVOIDHIGHPlASMALEVElSAAIlSElllOUS
DDS,
completed her
UNOESIRABLEAOVERSEEFFECTS. INJECTIONSSHOULOBEMAOESlOWlY.
DDS and Prosthodontic
WITH FREQUENT ASPlRAnONSBEFOREANDOURINGTHEINJECTION. nblOOd
isaspiraled.lhereedleshouldbe relocated. TolerancevarieswilhlhesIaIUs 0I1he
training at the Univer­
palient Oebililaledorelderly paUenlS, acutely ill palienIs. mchildren should be
giwn red<ud doses COfT'I'rerISUrale with lheir age and physical slalus. Use In
sity of Toronto_ She is
Pregnancy Sale use 01 articaine hylioch Ioride in preo-ool warren has nol been
currently researching the
eslablished. hOwever. animal sludies have nol demonstraled leralogenic or
embryoloxic eHecis. Nursing Mothers Articaine hydrocllioride is rapidly
effects of smoking on
fT'EtIboIi2ed and eliminaled and is 1hereI0re unlil<lllylo be lransferredlo the rOOher's
osseointegration. She staffprosthodon­
mil:. Patientswlth Spectal Dlseasesand Coodlllons ASTRACAINECOOIains
avasocoostricIa and should Iherefore be used wiIh caution in Ihe presence 01
tist at Mount Sinai Hospital, an Associ­
diseasesv.ilichmaya<M!lSe!yalfecllhepatien!·scardiovascularsy.;tem. Thedrug
ate in Dentistry, University of Toronto.
shoold be usedwih caJioo in persoos wiIh known drug sensRi~1ies. ASTRACAINE
corDnssOOlITlrn;lal)isumle. Sullalesmaycausealiefyicreactionsinsusceplib~
Her practice is limited to prosthodontics
~ The prevalence 01 sulfilesenslUvily in Ihe ~ populatioo is unknown
m Plotmiy kPw.1xlt i is seen morefreQuen!ly in~ts with broochial asthma.
and implant dentistry in Toronto.
Rea:tions 131 ircl~ ~adic S)111lIorns and lile-threatening or less ~
as!hmalic episodes. Many drugs used during !he conducl of anesthesia are
consideIed poIeniiai triggering agents lor lamilial malljlnanl hyperlhenm~. II has
Oral Health welcomes this original
00en shown IhaltOO use 01 amide local anesthe!ics in malignant h)perthenmia
article.
patients is safe. HC7>WW!.lhere is no guaooIee Ihat reural blocllade will prewol
Ihe ~opmenl 01 malignant hyperthemlia during surgery. HIs also diffK:u1t 10
(Jf:(fictlhereedlorSl.\lfllen'6llagereral<reilhesia ThereIore.aslandardtxttocol
Part II will appear in our November
lor Ihe managemenl 01 malignant hyperthermia should be available. Drug
Interadlons Serious cardiac anl1~mias may oo:urn preparalionscootaining
1999
issue of Oral Health.
avasocoostridor are errj)loyed in palients duringorlollawing tOOadministralioo
01 chlaoform. halothane. Cldoproprn,lrichloro-ehytere orother reialedageots.
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Caution should be exercised when administering articaine hydrochloride coo­
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links. Eur J Oral Sci., 104:151-155, 1996.
bin (e.g. sulphooamkles). ADVERSE REACTIONS ReaciionstoASTRACAINE
(articaine hyliochloride) are characteristic 0I11lose associated wilh ami~
2. Smtth, B.G.N and Knight J,K. M index for measuring
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excessiw dcsage. rapid absorpIion a ina<M!rten1 inlr3vascular injectioo. or rriJy
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result from ah)persenslUviIy. idiosyrcasy or diminished lolerance oolhepart 01
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systeman!VorlhecardiOVolSClJlarsystem. Cenlnl NervousSystem CNS rmni­
is
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dizzi'ess. blimdvisionandlrermrs, loIIu.o.edbydrlr<lsiness.COfMJlsions. uncoo­
sciousnessand possibly respiratory arrest. The excilalory reaclions may be wry
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10. Centerwall, B.S., Armstrong, C.w., Funkhouser, G.S.,
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18. Bartlett, D and Smtth. B. Clinical investigations of gas­
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briel or may not oa:ur at all,inv.ilich case.1he first rmnifeslallons oItoxicily may
be~rrsgingnollUJl!dousressilllrespirmy_
CanfiovasaJIar
System CanflOvaSCUlar reaclions are depresm. and may be characterized by
~ion. myocardial depressjoo,ixa!t,t:aroJaand possibly cardiac arrest.
Allergic Aliefyic reaclonsarechiYac!llri2ad bya.taneous lesions. urticar'a, edenIa
oranaphylactoid reaclions.Thedeteclion 01 sensitivilyby sI<in tesling isoldoubtful
value. Sweiling m pelSistenl paresthesia 01100 lips and oral lissues haw been
reported after blocking !he interior alveolar rerve. fOIl SYMPTOMS AND
TREATMENT OF OVERDOSAGE PlEASE REFEII TO THE PRODUCT MON­
GRAPH DOSAGE AND ADMINISTlIA110N AI; with all local aneslhetics, Ihe
dcsage varies and 00perds L\lOOIhe area to beareslhe/i2ed,1he vascularily 0I1he
Iissues,Ihe nurrbel 01 ne.xonaI segments 10 be blocl<ed, indiviWaitoleranceand
lhe~dnstEsia TheIa..estdosagereededIOpu.;reellectiwnslhes~
'nisIe
A
Pr
ure
lion
AIN. F AT
Vlu
m
net
TM AINE 4%
T lOose
.5-3.
oral sur
1.D-S.4
Adults lis
dosageshouldnolexceed7
1\,111
in adulls and in generallhe rmximllTllotat dose should nOI exceed 500 mg
(125 ml or7 cartridges). Chlld!en Dosages in children shouldbereOO::edcorn­
mensuralewilh IheirageandlWlghL Experience in childrenyomgerlhan 4year.;
01 ~ has noI been doaJmenied. The dosage shoold no! exceed S~ body
weight in Children betwee!1IOO ages 014 and 12. Stability and Storage
RecommendaUons Store aI coriroIled room IemperabJre (15-3O"C). Protecl
trom li~ Do nol use tl soIWon is jjrl<ish or darI<er lhall slighUy yellow or ~ ~
cootalnsaprecipitale. ASlRACAINEsolulionsarewilhoulpreseMiwandareior
sing~ useooly. Oilc<¥dtruSedportioo. AVAIlABlUTY OF DOSAGE FORMS
ASTRACAINE 4% FORTE (art/caine hydrochloride 40 mwmL and epinephrine
inj8:!ion 1:100.!XXJ) and ASTRACAINE4% (articaire hjdrochloride 40 ~
and epineltlrire injeclion l:200.!XXJ)areavailable in denial cartridges 0I1.8ni
in boxes 0150. Prodl.d Mooograph avallab~ upon request
Watch for these articles coming soon in the November issue of Oral Health: • Prosthodontics • Continuing Education ASTRA
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ORAL HEALTH· OCTOBER 1999