3

PART II
CONTENT
1.1 HIV
The human immunodeficiency virus (HIV) epidemic is not abating. By the
end of 1998 an estimated !" mi##ion individua#s $or#d$ide $ere infected. %#even
men $omen and chi#dren ha#f of these aged 1& to '" years ac(uire a ne$
infection every minute. )ppro*imate#y four peop#e succumb to this disease every
minute. )#though the death rate from HIV infection has s#o$ed do$n in the
+nited ,tates and -estern %urope due to ne$ and improved therapies .&///
ne$ infections is sti## recorded annua##y. This changing face of the epidemic
suggests an increasing number of peop#e #iving $ith HIV disease re(uiring hea#th
services. )s $ith a## chronic diseases a mu#tidiscip#inary approach to care resu#ts
in improved (ua#ity of #ife and decreased morbidity and morta#ity. This chapter
focuses on ora# #esions and conditions affecting the periodontium that are found in
individua#s $ith HIV infection and a#so e*p#ores the possib#e connection bet$een
the propagation of periodonta# infection and the propagation of HIV infection.
)s periodonta# manifestations have sho$n to be mar0ers for immune
deterioration and HIV disease progression ear#y recognition of these #esions and
an understanding of their significance in the course of HIV disease $i## impact on
the overa## systemic care for infected individua#s. 1e$ insights into the
pathogenesis of HIV infection have revea#ed much about the fate of as $e## as the
immune response to the virus. +nti# recent#y it $as genera##y be#ieved that HIV
$as constant#y rep#icating not $ith standing c#inica# asymptomatic periods.
Therapeutic interventions focused on s#o$ing do$n the rep#ication rate as $e## as
the transcription of vira# proteins. Ho$ever ne$ research has discovered the
e*istence of #atent#y infected 23" 4 T ce##. This phenomenon poses a significant
prob#em both for an effective immune response and for drug therapy.
4
The body5s natura# immune system cannot detect and e#iminate ce##s
#atent#y infected $ith HIV as these ce##s #ac0 the e*pression of vira# antigens on
the ce## surface. 6urthermore as the provira# 31) is a#ready integrated into the
ce##u#ar genome it cannot be targeted by e*isting antiretrovira# medications $hich
inhibit the 71) reverse transcriptase of HIV. Therefore e#imination of HIV can
on#y be accomp#ished by activating #atent#y infected ce##s in combination $ith
potent antiretrovira# therapy. This $i## create a situation $here #atent#y infected
ce##s are induced into a state of productive infection and die $hi#e the
antiretrovira# therapy prevents infectious viruses re#eased from these ce##s from
infecting ne$ ce##s.
)nother concern for infected individua#s is the state of their debi#itated
immune system. Thus in concert $ith targeting infected ce##s immune
reconstitution a#so needs to be addressed. The ha##mar0 of HIV disease is the
infection and subse(uent dep#etion of 23"4 Tce##s. )fter successfu# institution of
antiretrovira# therapy a sharp rise of 23"4 T ce##s can be noticed. Ho$ever this
increase apparent#y occurs as a resu#t of the redistribution of memory ce##s. These
T ce##s are severe#y #imited in their abi#ity to recogni8e different antigens. The
appearance of na#ve 23"4 T ce##s $ith specificities that had previous#y been #ost
may occur on#y after severa# months. Thus the immuno#ogic repertoire during the
course of HIV disease predisposes to increased susceptibi#ity to opportunistic
infections. The #eve# of immune deterioration or reconstitution determines the
individua#5s susceptibi#ity to specific infections. The inf#uence of periodonta#
infection on the pathogenesis of HIV disease has not been e#ucidated. Ho$ever
the immune system $ea0ened by HIV may have a direct inf#uence on the
pathogenesis of periodonta# disease.
Individua#s infected $ith HIV e*hibit ora# conditions and #esions often
associated $ith immune suppression. These ora# manifestations may ref#ect
systemic conditions or cou#d comp#icate systemic disease. )mong HIV9infected
individua#s no ora# #esions are found that are direct#y caused by HIV. Instead
#esions are most#y associated $ith immune suppression and opportunistic
pathogens and can therefore be found among other immunosuppressed individua#s
5
as $e##. 6or a #esion to be c#assified as :HIV9associated; the #esion needs to be
more common or e*hibit a different c#inica# course and appearance than those in
individua#s not infected $ith HIV.
) mu#titude of #esions that affect the periodontium have been described.
<oreover aggressive periodonta# #esions may be the first c#inica# e*pression of
the HIV Bacteria# vira# funga# or parasitic infections can a## affect the course of
HIV disease as $e## as ta0e on different c#inica# manifestations and severity or
re(uire different treatment moda#ities than in non9HIV infected individua#s. 3ue
to the impaired immune system characteristic of HIV disease infections often
present a more serious course compared $ith immunocompetent individua#s. This
is a#so found $ith infections of the periodonta# tissues. 2omparative studies
attempting to assess the association of periodonta# disease entities $ith HIV
infection are often #imited by severa# factors. They inc#ude the #ac0 of specific
diagnostic criteria the use of various HIV treatment regimens and #ac0 of
information on the immune status of the HIV9infected individua#. )n additiona#
prob#em is biased study popu#ations fre(uent#y se#ected on the basis of
institutiona# affi#iation. This means that usua##y the groups of HIV9infected
sub=ects under investigation are more serious#y affected by HIV disease than the
entire group of HIV9infected individua#s.
2.1 TERMINOLOGY
a $ide spectrum of terms have been used to describe soft and hard tissue
inf#ammatory and>or destructive conditions of the periodontium presumab#y
associated $ith HIV infection. an internationa##y accepted c#assification of the
ora# manifestations of HIV infection and their diagnostic criteria has been
estab#ished by the %22 #earning house on ?ra# @rob#ems 7e#ated to HIV Infection
and the -H? 2o##aborating 2entre on ?ra# <anifestations of the
Immunodeficiency Virus (%29-H?) at a meeting in 199!.1&
The c#assification inc#udes three groups of #esions (Tab#e 1191)A (1) #esions
strong#y associated $ith HIV infection (2) #esions #ess common#y associated $ith
HIV infection and (!) #esions seen in HIV infection. <ost characteristic among
6
the #esions #isted in the #atter category are the types of infection $hich are
e*treme#y rare in noninfected individua#s. These inc#ude Histoplasma Capsulatum
and funga# infections other than candidiasis. )#though a number of these diseases
may affect the periodonta# tissues they are outside the scope of the present
chapter. Ho$ever conventiona# forms of periodonta# diseases affect HIV9infected
individua#s but may differ in their c#inica# course. This aspect $i## be discussed
be#o$ in the section :#esions seen in HIV infection.;
3.1 LESIONS STRONGLY ASSOCIATED WITH HIV INFECTION
Three periodonta# disease entities can be considered to be strong#y
associated $ith HIV infection. These are #inear gingiva# erythema (BC%)
necroti8ing gingivitis (1C) or necroti8ing u#cerative gingivitis (1+C) and
necroti8ing periodontitis (1@) or necroti8ing u#cerative periodontitis (1+@). It is
important to note that simi#ar #esions may occur in non9HIV9infected individua#s
even $ith simi#ar preva#ence. 2onse(uent#y a#though the initia# descriptions of
these #esions referred to them as HIV9associated gingivitis and HIV9associated
periodontitis the more descriptive termino#ogy of the #esions is used today. In the
#ist of #esions strong#y associated $ith HIV (Tab#e 119#) a fe$ supp#ementary
disease entities that may a#so affect the periodontium are inc#uded. These entities
are candidiasis DaposiEs sarcoma and non9Hodg0inEs #ymphoma.
3.1.1 Linear Gingiva Er!"#e$a
3.1.1.1 Diagn%&i& an' Cini(a Pre&en"a"i%n
Binear gingiva# erythema presents as a fiery red band of the margina#
gingiva characteri8ed by a disproportiona# inf#ammatory intensity in re#ation to
the amount of p#a(ue present. There are no u#cerations and no evidence of
poc0eting or attachment #oss. ) further characteristic of this type of #esion is its
#ac0 of response to improved ora# hygiene and to sca#ing. The first description of
BC% inc#uded a distinctive erythema of the free gingiva attached gingiva and
a#veo#ar mucosa in individua#s $ith HIV disease. 6ree gingiva# erythema
7
appearing as an intense #inear band e*tending ' to ! mm apica##y from the free
gingiva# margin $as seen in more than &/F of cases. @unctate or difhse erythema
of the attached gingiva $as another prominent feature. The #esions $ere
associated $ith pain in some instances and most fre(uent#y invo#ved the entire
mouth $ith an e(ua# distribution to a## (uadrants. ,ometimes they $ere #imited to
one or t$o teeth and the changes $ere present even $ith #itt#e or no p#a(ue
accumu#ations. The e*tent of gingiva# banding measured by the number of
affected sites $as #ater suggested to depend on tobacco -hi#e 1&F of affected
sites $ere origina##y reported to b#eed on probing and I IF e*hibited spontaneous
b#eeding a 0ey feature of #inear gingiva# erythema is no$ considered to be #ac0 of
b#eeding on probing.
3.1.1.2 Prevaen(e
) fe$ studies of unbiased groups of patients have indicated that gingivitis
$ith ban09shaped or punctate margina# erythema may be re#ative#y rare in HIV9
infected patients and probab#y represents a c#inica# finding $hich is not more
fre(uent than in the genera# popu#ation. ?ther studies of various groups of HIV9
infected patients have revea#ed the preva#ence of gingivitis $ith band9shaped
patterns in /.& to "9F. These preva#ence va#ues ref#ect some of the prob#ems $ith
non9standardi8ed diagnosis and se#ection of study groups as mentioned above.
There is no doubt that severa# studies comprise cohorts of patients $ith poor ora#
hygiene and the degree to $hich the reported inf#ammatory processes respond to
conventiona# therapy is current#y un0no$n. ) preponderance of HIV9associated
red banding $as not noted in a recent British study $hi#e diffuse and punctate
erythema $as significant#y more preva#ent in HIV9infected than in non9HIV9
infected individua#. 7ed gingiva# banding as a c#inica# feature a#one is therefore
not strong#y associated $ith HIV infection.
-hi#e severa# studies are avai#ab#e on HIV infected adu#ts fe$ reports
describe HIV9re#ated diseases among chi#dren. In t$o studies ho$ever as many as
!/F and !.F respective#y $ere diagnosed $ith so9ca##ed HIV9gingivitis $hich
is synonymous $ith BC%.
8
3.1.1.3 E"i%%g! an' Pa"#%gene&i&
There are suggestions that candida# infection is the etio#ogic agent in some
cases of gingiva# inf#ammation inc#uding BC%. Ho$ever some studies have
revea#ed microf#ora comprising both Candida albicans and a number of
periodontopathic bacteria consistent $ith those seen in conventiona# periodontitis
that is Porphyromonas gingivalis, Prevotella intermedia, Actinobacillus
actinomycetemcomitans, Fasobacterium nucleatum, and Campylobacter rectus.
,tudies using 31) probes have suggested the percentage of A.
actinomycetemcomitans-positive sites in HIV9associated gingivitis and matched
gingivitis sites of HIV seronegative patients to be '!F and .F respective#y.
6urthermore positive sites $ere &'F and 1.F for P. gingivalis, G!F and '9F for
P. intermedia, and &/F and 1"F for C. rectus, respective#y. C. albicans has been
iso#ated by cu#ture in about &/F of HIV9associated gingivitis sites in 'GF of
unaffected sites of HIV9seropositive patients and in !F of hea#thy sites of HIV
seronegative patients. The fre(uent iso#ation and the pathogenic ro#e of C.
albicans may be re#ated to the high #eve#s of the yeast in the sa#iva and ora#
mucosa of HIV9infected patients.
The significance of 23"4 T ce## dep#etion in the pathogenesis of BC% is
uncertain. ) study of patients $ith so9ca##ed HIV9associated gingivitis sho$ed
23">238 ratios $ithin the #o$ norma# range.'" In another study of the red
banding of the gingiva it $as conc#uded that the condition $as not re#ated to
immunosuppression as e(ua# number of cases had 23"4 T ce## counts above and
be#o$ "//>mrn!.#9 ) simi#ar resu#t has been obtained by others.'& Ho$ever a
more recent study comprising !9G HIV9seropositive individua#s c#assified
according to their periphera# 23"4 #ymphocyte counts revea#ed #inear gingiva#
erythema in ' patients $ith #ess than '// 23" ce##s>mm! as opposed to none
among patients $ith '// 23" ce##s>mm! or more
)n interesting histopatho#ogic finding in biopsy specimens from the
banding 8one has revea#ed no inf#ammatory infi#trate but an increased number of
b#ood vesse#s $hich e*p#ains the red co#or of the #esion. The incomp#ete
9
inf#ammatory reaction of the host tissue may be the cause of the #ac0 of response
to conventiona# treatment.
3.1.1.) Di**eren"ia Diagn%&i&
) number of diseases present c#inica# features resemb#ing those described
above and $hich according#y do not reso#ve after improved ora# hygiene and
debridement. ?ra# #ichen p#anus is fre(uent#y associated $ith a simi#ar
inf#ammatory red band of the attached gingiva and mucous membrane
pemphigoid may a#so have this appearance. Geotricum candidum infection and
hypersensitivity reactions manifesting as p#asma ce## gingivitis are other rare
differentia# diagnoses. In rare instances gingivitis9#i0e changes may a#so be the
resu#t of thrombocytopenia.
3.1.1.+ Trea"$en"
Important characteristics of the origina##y described entity of BC%
inc#uded a tempora# #ac0 of response to p#a(ue remova# and an erythematous
appearance disproportiona# to the amount of p#a(ue. 7eports of different
therapeutic resu#ts may be due to the varied definition of BC%. 2onventiona#
therapy $ith /.1'F ch#orhe*idine g#uconate mouth rinses t$ice dai#y has been
reported to sho$ significant improvement after ! months."' Ho$ever HIV9
associated free gingiva# erythema did not respond to remova# of p#a(ue by intense
sca#ing and root p#aning and improved p#a(ue contro# measures a#one or
supp#emented $ith povidoneiodine irrigation ! to & times dai#y. There $as no
significant improvement in c#inica# features or indices after 1 and ! months of
treatment. Ho$ever the povidone9iodine irrigation substantia##y reduced pain
reported to be associated $ith the #esions e*amined.
)s mentioned above BC% may in some cases be re#ated to the presence of
C. albicans. In accordance $ith this finding c#inica# observations indicate that
improvement is fre(uent#y dependent on successfu# eradication of intraora# C.
albicans $hich resu#ts in the disappearance of the characteristic features.
2onse(uent#y attempts to identify the presence of hnga# infection either by
10
cu#ture or smear are recommended fo##o$ed by antimycotic therapy in C.
albicans 9positive cases.
3.1.2 Ne(r%"i,ing -.(era"ive/ Gingivi"i& an' Peri%'%n"i"i&
3.1.2.1 Diagn%&i& an' Cini(a Pre&en"a"i%n
The necroti8ing (u#cerative) diseases 1C 1@ and necroti8ing stomatis
(1,) are the most severe periodonta# disorders presumab#y caused by bacteria.
These entities may represent various stages of simi#ar disease process. The
distinction bet$een 1C and periodontitis is para##e# to the distinction bet$een
gingivitis and periodontitis. Thus 1C shou#d be #imited to #esions on#y invo#ving
gingiva# tissue $ith no #oss of periodonta# attach9 In most patients ho$ever the
disease process rapid#y resu#ts in #oss of attachment in $hich case 1@ is the
correct termino#ogy. @revious#y progression of the disease process across the
mucogingiva# =unction $ou#d have (ua#ified for the diagnosis of 1, but the
description of 1@ as proposed by %29-H? incorporates tissue destruction
e*tending across the mucogingiva# border. 2onse(uent#y the differentia#
diagnosis bet$een 1@ and 1, is not a#$ays c#ear as 1, is sometimes described
as e*tending from areas of 1@. 1ecroti8ing stomatitis is mentioned be#o$ in the
section on :#esions #ess common#y associated $ith HIV infection.;
There is considerab#e variation in the c#inica# manifestations ranging from
initia# #esions $ith necrosis #imited to the top of the interdenta# papi##ae to
moderate manifestations $ith invo#vement of the entire attached gingiva $ith
tooth mobi#ity and se(uestration of parts of the cresta# bone to severe cases $ith
e*tensive bone #oss and necrosis of supporting tissues. 6etor oris evo#ves in most
cases as a characteristic feature.
The initia# #esion typica##y presents $ith changes in gingiva# contour such
as interpro*ima# necrosis u#ceration and cratering. The most distinguishing
feature is soft tissue necrosis and the rapid destruction of periodonta# attachment
and bone. ,evere cases can affect a## teeth but more fre(uent#y severa# #oca#i8ed
areas are affected independent#y and a## regions appear to have simi#ar chances of
11
being affected. The #esions are not a#$ays associated $ith deep poc0et formation
as e*tensive gingiva# necrosis often coincides $ith #oss of cresta# a#veo#ar bone.
?n the other hand the rapid progression of the soft tissue necrosis sometimes
#eads to the e*posure of the a#veo#ar bone $hich becomes se(uestrated and #eaves
deep interdenta#. 6re(uent#y such defects are #ocated in the mo#ar>premo#ar
region.
,evere pain has been mentioned as a distinguishing feature of HIV9
associated periodontitis and the chief reasons for patient see0ing treatment.
B#eeding on probing is a prominent feature and about &/F of invo#ved sites b#eed
spontaneous#y. The number of sites affected by papi##ary destruction have been
sho$n to be significant#y determined by tobacco )bout 8&F of individua#s $ith
HIV9associated periodontitis #esions have been described to be a$are of their
serostatus at their initia# visit.'!
3.1.2.2 Prevaen(e
<eaningfu# comparisons of preva#ence data among the avai#ab#e studies
remain unavai#ab#e because of the diversity in the study methods and diagnostic
criteria and the variance in groups under investigation. ?ne ma=or prob#em is the
#ac0 of a c#ear distinction bet$een 1C and 1@ in the ma=ority of the #iterature.
Ho$ever even ta0ing these #imitations into account studies sho$ that 1C is more
common among HIV9seropositive individua#s than in the genera# popu#ation. The
preva#ence in these studies ranges from & to 11F. In contrast other more recent
studies have either found #o$ preva#ence (/ to 0.7%) no significant difference
bet$een cohorts of HIV9seropositive and HIV9negative patients.'' The anterior
gingiva is most common#y $hich agrees $ith 1C in HIVseronegative patients."9
Cingiva# u#ceration may affect individua# teeth or e*tend to severa# areas of the
=a$s.8 1ecroti8ing periodontitis has been described in 88F among 1!G HIV9
infected patients.'8 Ho$ever most studies have sho$n considerab#y #o$er
preva#ence va#ues of 1@ among HIV9infected individua#s such as G.!F of .//
HIV9seropositive patients and in 1F of '// HIV9seropositive patients.'9 Het
other studies have suggested that HIV9associated periodontitis $ith u#ceration and
12
tissue necrosis may be re#ative#y rare and that the preva#ence may in fact not
differ significant#y from that of simi#ar #esions of the genera# popu#ation.
3.1.2.3 E"i%%g! an' Pa"#%gene&i&
%stab#ished 0no$#edge of the pathogenic bac0ground of tissue necrosis in
1C and 1@ is #imited. ?ne of the most interesting (uestions is $hether #ess
pathogenic organisms can cause tissue necrosis in HIV9infected as compared $ith
non9HIV9infected individua#s. 3ata on the microf#ora associated $ith necrotic
periodonta# #esions are unfortunate#y compromised by fre(uent #ac0 of precise
description of the sites from $hich the microbio#ogic samp#es $ere obtained.
There is no doubt that many samp#es are obtained from deep poc0ets and
conse(uent#y the findings may not be direct#y re#ated to tissue necrosis. 1o c#ear
distinction can therefore be dra$n bet$een 1@ and other forms of HIV9associated
periodontitis in the description of the microbio#ogic profi#e. ) further
comp#ication is that the avai#ab#e information on the microbio#ogy of HIV9
associated 1C is very #imited. The iso#ated organisms inc#ude Borrelia, gram9
positive cocci @9hemo#ytic streptococci and C. albicans. The occurrence of P.
gingivalis, spirochetes and moti#e eubacteria in periodonitis has been found to be
the same in HIV9infected patients and in systemica##y hea#thy adu#t. )#so the
microf#ora iso#ated from HIV9associated periodontitis $as simi#ar to that of
c#assic adu#t periodontitis e*cept that P. gingivulis $as more preva#ent in
conventiona# periodontitis. Creater numbers of P. gingivalis have been revea#ed in
samp#es from non9HIV9infected sub=ects $ith hea#thy periodontium than in
samp#es from HIV9associated periodontitis. ?ther findings have indicated that
subgingiva# p#a(ue in ac(uired immunodeficiency syndrome ()I3,) patients $ith
periodontitis can harbor high proportions of the same periodonta# pathogens as are
associated $ith periodontitis in non9HIV9infected individua#s but additiona# high
proportions of other opportunistic pathogens #i0e Clostridium, Enterococcus, and
C. albicans. The suggestion that the predominant subgingiva# microf#ora in HIV9
associated periodontitis is in many $ays simi#ar to that of progressing
periodontitis #esions in systemica##y hea#thy adu#ts has been supported by
13
others.&! ?n the other hand this investigation of HIV9associated periodontitis
#esions a#so revea#ed organisms rare#y associated $ith common types of
periodontitis. Higher proportions of C. albicans and C. rectus $ere characteristic
of HIV9associated periodontitis the (ua#itative profi#es of HIV9associated
gingivitis and HIV9associated periodontitis being simi#ar and on#y C. rectus
sho$ing ma=or (uantitative differences. 1one of the avai#ab#e studies ans$er the
important (uestion $hether other pathogens cause tissue brea0do$n in HIV9
associated disease un#i0e in non9HIV associated disease. 1ecroti8ing gingivitis
has been associated $ith periphera# 23"4 #ymphocyte dep#etion in a fe$ studies.
Ho$ever the disease has a#so been found to be unre#ated to immunosuppression
$ith e(ua# numbers of patients having 23"4 T ce## counts above and be#o$
"//>mm!.
The severity of periodonta# destruction has been associated $ith the
progression of HIV disease in severa# studies. The causes mentioned in these
studies is that the progressive dep#etion of immune effector and regu#atory ce##s in
HIV9seropositive patients compromises the #oca# host defense to such an e*tent
that the susceptibi#ity to periodonta# disease increases. ?ne study even suggested
that 1@ $as a stronger predicator of HIV disease progression and immune
suppression than estab#ished )I3, defining i##neses. ) tempora# re#ationship
bet$een 1@ and poor surviva# $as a#so suggested $here a#most G/F of patients
$ith 1@ died $ithin 18 months of the periodonta# diagnosis. Ho$ever other
studies have indicated that the association bet$een HIV9re#ated immune dep#etion
and periodonta# destruction is #ess strong.
3.1.2.) Di**eren"ia Diagn%&i&
) number of ora# mucosa# diseases can be confused $ith 1C and 1@.
These inc#ude bu##ous #esions of benign mucous membrane pemphigoid and
erythema mu#tiforme e*udativum but the progressive nature and the #oca#i8ed
occurrence of 1C and 1@ usua##y distinguish these diseases from bu##ous mucosa#
diseases. )cute forms of #eu0emia may be associated $ith necroti8ing gingiva#
u#cers of the ora# mucosa $hich sometimes manifest in the margina# gingiva. The
14
gingiva# #esions are often b#uish red and edematous. <edica# e*amination $i##
revea# the cause in suspect cases. ,ince sero#ogic>hemato#ogic e*amination
usua##y is necessary for patients una$are of a possib#e HIV infection or another
cause of the necroti8ing periodonta# disease a possib#e supp#ementary b#ood
e*amination to #oo0 for #eu0emia is =ustifiab#e.
3.1.2.+ Trea"$en"
The treatment aspects of 1C and 1@ are simi#ar. In HIV9infected patients
the diseases do not routine#y respond to conventiona# treatment $ith sea#ing and
improved ora# hygiene.'" Ho$ever the ad=unctive use of metronida8o#e in these
patients is reported to be e*treme#y effective in reducing acute pain and promoting
rapid hea#ing. due to the susceptibi#ity of HIV9infected patients to candida#
infectionsI simu#taneous treatment $ith appropriate antimycotic agents may be
necessary. )#though it has been postu#ated that hea#ing is de#ayed in HIV9infected
patients and pain may be pro#onged. ?ther studies did not revea# increased
incidence of de#ayed hea#ing after e*traction or other comp#ications even in
severe#y immunocompromised individua#s. Therefore prophy#actic antimicrobia#s
$ere not recommended. 6re(uent use of antibiotics may give rise to prob#ems due
to microbia# resistanceJ hence a restrictive attitude is important.
6o##o$9up care for HIV9associated necroti8ing periodonta# diseases is
essentia# to ensure success in treatment. Inade(uate p#a(ue contro# in sites affected
by 1@ is often associated $ith de#ayed hea#ing and continued rapid destruction. In
many cases e*tensive tissue destruction resu#ts in residua# defects $hich may
ma0e it very difficu#t for the patient to maintain ora# hygiene. ?ra# hygiene in
these areas often re(uires the use of interpro*ima# devices and soft sma##er
brushes. )ntibiotic prophy#a*is may not be necessary in re#ation to sca#ing since
bacteria $ere recovered from venipuncture 1& minutes after sca#ing but $ere not
detectab#e in samp#es obtained at !/ minute. remova# of se(uestra does not a#$ays
appear to re(uire antibiotic coverage.
15
).1 LESIONS LESS COMMONLY ASSOCIATED WITH HIV
INFECTION
) number of #esions #ess common#y associated $ith HIV infection may
affect the periodonta# tissues. 1ecroti8ing stomatitis is among the most serious
but other important diseases are #esions caused by herpes simp#e* virus human
papi##oma virus and varice##a98oster virus. These #esions ho$ever are not
inc#uded in this chapter.
).1.1 Ne(r%"i,ing S"%$a"i"i&
1ecroti8ing stomatitis (1,) is defined as a #oca#i8ed acute#y painfu#
u#ceronecrotic #esion of the ora# mucosa e*posing under#ying bone or penetrating
or e*tending into contiguous tissues. The #esions may e*tend from areas of 1@.
).1.1.1 Diagn%&i& an' Cini(a Pre&en"a"i%n
The c#inica# aspects of 1, resemb#e those of 1C and 1@ 1ecroti8ing
stomatitis is the most severe and is not as common as 1C and 1@. The e*tensive#y
destructive #esions are rapid#y progressive u#cerative and necroti8ing. In most
cases the #esions e*tend from the gingiva into the ad=acent mucosa and bone
causing destruction of both ora# soft tissues and under#ying bone. The disease
appears to be re#ated to the immune dep#etion caused by HIV infection.I
Important#y it may be #ife threatening and the c#inica# features of 1, resemb#e
noma as described by Tempest.G8 @rogression of 1@ to 1, may resu#t in
progressive osseous destructions $ith se(uestration and>or the deve#opment of
oroantra# fistu#a and osteitis. The differentia# diagnostic and treatment aspects for
1, are simi#ar of those of 1C and 1@.
+.1 LESIONS SEEN IN HIV INFECTION
Individua#s infected by HIV may suffer from common forms of
periodonta# diseases $ithout tissue necrosis or other characteristic features of HIV
infection as described above. These diseases $ith #ess dramatic c#inica# features
16
inc#ude adu#t periodontitis and rapid#y progressive periodontitis. The most
interesting aspect of these diseases in HIV9infected popu#ations is $hether their
preva#ence figures and progression of attachment #oss are simi#ar to those
encountered in non9HIV9infected individua#s.
+.2 C%nven"i%na A'0" Peri%'%n"i"i&1 Ra2i'! Pr%gre&&ive Peri%'%n"i"i&
+.2.1 Prevaen(e
) number of studies among HIV9seropositive individua#s have reported
high preva#ence figures of severe attachment #oss but others have fai#ed to sho$
differences bet$een HIV9seropositive and HIV9seronegative individua#. The
reported preva#ence figures of periodontitis among HIVseropositive patients sho$
considerab#e variation (& to G9F) the variation being due to differences in study
groups. 6or instance severa# studies comprise groups of patients $ho are se#ected
on the basis of admission to hospita#s or to the denta# setting but it is not possib#e
to identify mechanisms of se#ection in a## referred studies.
,evere periodonta# destruction $as revea#ed in 11F of "" HIV9
seropositive patients and progressive periodontitis comparab#e $ith rapid#y
progressive peridontitis $as diagnosed $ith simi#ar fre(uency among 11/ HIV9
seropositive patients.8 T$enty9seven percent of '// HIV9seropositive patients had
moderate or advanced adu#t periodontitis In a study of 181 heterose*ua# men and
$omen $ith )I3, 9'F of the patients being intravenous drug users the
preva#ence $as much higher than in other studies. The c#inica# features $ere not
reported in detai# and figures for patients $ithout tissue necrosis cou#d not be
identified. %ar#y periodontitis $as found in '"F moderate in '!F and advanced
in ''F. ,ignificant#y increased severity of periodontitis $as seen in $omen as
compared $ith men.'G
) number of studies have sho$n #imited preva#ence figures. )mong 1" 1
HIV9seropositive homose*ua# ma#es 5% had severe periodontitis as compared
$ith /.'F among G/G seronegative homose*ua# ma#es. The reported preva#ence
$as mar0ed#y #o$er than that reported for severe periodontitis in adu#t ma#es in
17
the +nited ,tates. 1o radiographic e*amination $as avai#ab#e. 22 ,tudies based
on the registration of periodonta# indices have sho$n that #oss of attachment
associated $ith HIV infection is a re#ative#y rare condition at #east in some
cohorts of patients. ?ne of the most recent studies revea#ed no significant
differences in b#eeding on probing poc0et formation or attachment #oss among
HIV9seronegative and HIVseropositive individua#s and )I3, patients in Tan8ania
Ho$ever $hen using c#inica# attachment #oss and radiographic assessment of
a#veo#ar bone #oss definite trends are evident pointing to HIV infection being a
ris0 indicator for progression of periodontitis.
+.2.2 E"i%%g! an' Pa"#%gene&i&
7eports of the microbio#ogy of HIV9associated periodontitis do not a#$ays
state $hether microbia# samp#es have been obtained from #esions $ith or $ithout
necrosis. The avai#ab#e microbio#ogic data are described above in re#ation to 1C
and 1I. The reports on the significance of HIV9re#ated immune deterioration and
#oss of attachment are conf#icting. Ho$ever most studies have revea#ed an
association bet$een progression of periodontitis and decreased number of
periphera# T9he#per ce##s. ?ne study has sho$n that periodontitis in patients $ith
more advanced stages of HIV infection $as re#ated to severity of systemic disease
and to decreasing numbers of 23"4 #ymphocytes but not to visib#e p#a(ue inde*
or occurrence of periodonta# pathogenic microorganism. ) '/9month fo##o$9 up
study of I 1" homose*ua# and bise*ua# men sho$ed re#ative attachment #oss of !
mm or more occurring G.1G times more fre(uent#y among sub=ects $ith 23"4
counts K '// compared $ith sub=ects $ith counts of '// or more. )mong
individua#s aged !& years and over the incidence (!!F) of re#ative attachment
#oss of ! mm or more $as significant#y higher in more immunosuppressed
individua#s compared $ith the incidence (5%) in #ess immunosuppressed sub=ects.
In .8 individua#s seen at fo##o$9up visits mean gingiva# indices increased and
$ere significant#y higher in the seropositive sub=ects compared $ith the
seronegative ones but gingiva# indices $ere not re#ated to 23"4 T ce## counts
$ithin the seropositive group. The study suggested a greater sensitivity to p#a(ue
18
in the seropositive group. The authors conc#uded that immunosuppression
especia##y in combination $ith o#der age may be a ris0 for attachment #oss and
HIV seropositivity independent of 23"4 T ce## counts maybe a ris0 factor for
gingiva# inf#ammation. In a study of HIVseropositive patients and '. contro#
patients the HIV9seropositive patients had a higher mean percent of sites
e*hibiting suppuration than the contro# group. )mong !91' men $ith HIV
infection decreased 23" #ymphocyte counts predicted the e*tent and severity of
periodonta# attachment #oss but not poc0eting $hich $as on#y re#ated to HIV
infection $hen compared $ith 'G/ men $ithout HIV. In contrast a recent report
from Tan8ania did not revea# any significant associations bet$een periodonta#
indicies $ith regard to #ymphocyte and 23"4 T ce## counts among the HIV9
infected individua#s inc#uding )I3, patients.&8
+.2.3 Trea"$en"
,ince deterioration of the immune deficiency may be a ris0 factor for
attachment #oss and HIVseropositivity may be a ris0 factor for gingiva#
inf#ammation it is particu#ar#y important that HIV9infected individua#s practice
intensive ora# hygiene and receive fre(uent professiona# preventive denta#
treatment.19 This supports the idea of providing intensive ora# care programs to
be initiated as soon as the diagnosis of HIV infection is estab#ished.
TA3LE I I4 I. Revi&e' Ca&&i*i(a"i%n %* Ora Le&i%n& A&&%(ia"e' 5i"# HIV
In*e("i%n.
Gr%02 1A Besions strong#y associated $ith HIV infection
2andidiasis
%rythematous
@seudomembranous
Hairy #eu0op#a0ia
DaposiEs sarcoma
1on9Hodg0inEs #ymphoma
@eriodonta# disease
Binear gingiva# erythema
1ecroti8ing (u#cerative) gingivitis
1ecroti8ing (u#cerative) periodontitis
Gr%02 2A Besions #ess common#y associated $ith HIV infection
Bacteria# infections
19
Mycobacterium avium-intracelluhre
Mycobacterium tuberculosis
<e#anotic hyperpigmentation
1ecroti8ing (u#cerative) stomatitis
,a#ivary g#and disease
3ry mouth due to decreased sa#ivary f#o$ rate
+ni#atera# or bi#atera# s$e##ing of ma=or sa#ivary g#ands
Thrombocytopenic purpura
+#ceration 1?, (not other$ise specified)
Vira# infections
Herpes simp#e* virus
Human papi##omavirus ($arty9#i0e #esions)
Condyloma acuminatum
6oca# epithe#ia# hyperp#asia
Verruca vu#garis
Varice##a98oster virus
Herpes 8oster
Varice##a
Gr%02 3A Besions seen in HIV infection
Bacteria# infections
Actinomyces israelii
Escbericbia coli
Klebsielh pneumoniae
2at9scratch disease
3rug reactions (u#cerative erythema mu#tiforme #ichenoid to*ic epidermo#ysis)
%pithe#ioid (baci##ary) angiomatosis
6unga# infection other than candidiasis
Cyp tococcus neoo mans
!eotricbum candidum
"istophsma capsuhtum
<ucoraceae (<ucormycosis>8ygomycosis)
Asperigillus #vus
6acia# pa#sy
Trigemina# neura#gia
7ecurrent aphthous stomatitis
Vira# infections
1euro#ogic disturbances
2ytomega#ovirus
Molluscum contag
20
PART III
RES.ME
HIV Infection are have the re#ation $ith periodonta# disease because due
to the impaired immune system characteristic of HIV disease infections often
present a more serious course compared $ith immunocompetent individua#s. This
is a#so found $ith infections of the periodonta# tissues.

21
3I3LIOGRAPHY
1. -H? %nd of year annua# report on HIV and )I3,. CenevaA -H?J 1998.
'. 2hun T$ ,tuyer B <i8e## ,B et a#. @resence of inducib#e HIV9 1 #atent
reservoir during high#y active antiretrovira# therapy. @roc 1at#
)cad ,ci
!. 6in8i 3 Herman0ova < @eirson T et a#. Identification of a reservoir for HIV9
1 in patients on high#y active antiretrovira# therapy. ,cience
". Beandersson )2 Bratt C 6redri0son < et a#. ,pecific T9ce## responses in
HIV9infected patients after high#y active anti re t r ovi ra# therapy
(H))7T). )bstract !191"'. CenevaA 1'
th
-or#d )I3,
2onferenceJ 1998.
&. C#ic0 < <uy0a B2 Burie 3 ,a#0in B<. ?ra# manifestations associated $ith
HIV disease as mar0ers for immune suppression and )I3,. ?ra#
,urg ?ra# <ed ?ra# @atho# 199"J..A!""99.
G. 2eba##os9,a#obrena ) )guirre9+ri8ar L< Bagan9,ebastian LV. ?ra#
manifestations associated $ith human immunodeficiency virus
infection in a ,panish popu#ation. L ?ra# @atho# <ed 199GJ'& A
&'!9G.
.. 6icarra C Berson )< ,i#verman , et a#. DaposiEs sarcoma of the ora# cavityA
a study of 1!" patients $ith a revie$ of the pathogenesis
22
epidemio#ogy c#inica# aspects and treatment. ?ra# ,urg ?ra# <ed
?ra# @atho# 1988JGGA&"!9&/.
8. 7eichart @) Ce#derb#om H7 Bec0er L Dunt8 ). )I3, and the ora# cavity.
The HIV9infectionA viro#ogy etio#ogy origin immuno#ogy
precautions and c#inica# observations in 11/ patients. Int L ?ra#
<a*i##ofac ,urg 198.J1GA1'99&!. 199.J9"A1!19!9.. 199.J'.8A
1'9&9!//.
9. ,chicat < @indborg LL. )I3, and the ora# cavity. %pidemio#ogy and c#inica#
ora# manifestations of human immune deficiency virus infectionA a
7evie$. Int L ?ra# <a*i##ofac ,urg 198.J1GA191".
1/. ,cu##y 2 Bas0aris C @indborg LL et a#. ?ra# manifestations of HIV infection
and their management. I. <ore common #esions. ?ra# ,urg ?ra#
<ed ?ra# @atho# 199 1 J. 1 A 1 5 89GG.
11. -in0#er L7 7obertson @B. @eriodonta# disease associated $ith HIV9infection.
?ra# ,urg ?ra# <ed ?ra# @atho# 199'J.!A1"&9&/.
1'. -estergaard L. @eriodonta# diseases in HIV9infected patients. L 2#in
@eriodonta# 199"J
1!. -estergaard L. HIV infection and periodonta# diseases. @eriodonta1 '///
1998J 18A !.9"G.
1". 7obinson @C -in0#er L7 @a#mer C et a#. The diagnosis of periodonta#
conditions associated $ith HIV infection. L @eriodonto# 199"JG&A
'! G9"!.