Focus on furcation defects: guided tissue regeneration

21
Periodontology 2000, Vol. 22, 2000, 169–189 Copyright C Munksgaard 2000 Printed in Denmark ¡ All rights reserved PERIODONTOLOGY 2000 ISSN 0906-6713 Focus on furcation defects: guided tissue regeneration M ARIANO S ANZ &J EAN L OUIS G IOVANNOLI The main goal of periodontal therapy is to provide patients with a dentition that functions in health and comfort for the remainder of their lives. Historically, the procedures used to treat patients with advanced periodontitis were aimed at the elimination of sub- gingival plaque and calculus from the affected root surfaces. This therapy included scaling and root planing and periodontal flap surgery. These treat- ment methods usually healed through repair char- acterized by the formation of a long junctional epi- thelium adjacent to the previously diseased root surface. Several long-term clinical trials have dem- onstrated that this standard mode of therapy, if fol- lowed by an adequate postoperative supportive peri- odontal care, results in successful management of progressive periodontal disease (32, 36, 44, 63, 69). However, when molar teeth with furcation involve- ment were evaluated specifically, the long-term re- sponse to this conventional therapy differed from non-molar teeth. Hirschfeld & Wassermann (32), studying 600 periodontal patients after a mean ob- servation period of 22 years, reported that well- maintained patients having a good prognosis at the beginning of therapy, hardly lost teeth due to peri- odontitis (0.6%). However, when patients were de- fined as guarded prognosis, the teeth lost were 11.6% if furcation lesions were excluded and 19.5% when molars with furcation involvement at the beginning of the study were specifically considered. Pihlstrom et al. (63) investigated the response of molar and non-molar teeth to either scaling and root planing alone or scaling and root planing followed by a modified Widman flap. They reported less reduction in probing depth and loss of attachment in molars compared to non-molars for either mode of therapy. Kalkdahl et al. (36) also noted that following either non-surgical or surgical therapy there was a ten- dency for attachment loss in furcation regions dur- ing the second year of supportive care, irrespective from the type of therapy rendered. McGuire & Nunn (52) reported that the risk of periodontitis pro- 169 gression in the furcation lesions increases with the severity of the furcation involvement, and thus class I furcation lesions have better prognosis than class II and class III lesions. All these studies clearly show that the presence and severity of a furcation lesion reduces the success rate of conventional periodontal therapy in these specific areas and therefore worsens the long-term prognosis of that particular tooth. This different behavior has been explained, among other factors, by the complexity of the furcation mor- phology and hence, the limitation for accessibility to debride properly during periodontal therapy and to develop appropriate patient compliance in plaque control (13). In the course of periodontal history, several tech- niques have been proposed and promoted to treat these furcated molars and thus improve their prog- nosis. Grade I furcations have generally been well managed with routine periodontal surgical pro- cedures aimed to thoroughly debride the lesion, re- duce pockets and expose the furcation entrance for adequate plaque control. Grade III furcations have re- quired more extensive resective therapy such as tun- neling, root amputation or hemisection with the aim of eliminating the lesion and thus also allowing for proper infection control. Grade II furcations have pre- sented, however, a clinical problem that has troubled clinicians for many years. Various regenerative pro- cedures have been tried with the aim of closing grade II furcations, such as open flap debridement, bone re- placement grafts, coronally repositioned flaps and guided tissue regeneration barriers (13) (some of these therapeutic approaches have been extensively reviewed elsewhere in this journal). While some of these procedures have excited the dental profession based on reports of significant attachment gains and bone fill at the furcation defects, a systematic evalu- ation of the available scientific information does not clearly indicate the real impact of these therapeutic procedures on the final outcome and prognosis of the affected tooth and patient (26, 37).

Transcript of Focus on furcation defects: guided tissue regeneration

Page 1: Focus on furcation defects: guided tissue regeneration

Periodontology 2000, Vol. 22, 2000, 169–189 Copyright C Munksgaard 2000Printed in Denmark ¡ All rights reserved

PERIODONTOLOGY 2000ISSN 0906-6713

Focus on furcation defects:guided tissue regenerationMARIANO SANZ & JEAN LOUIS GIOVANNOLI

The main goal of periodontal therapy is to providepatients with a dentition that functions in health andcomfort for the remainder of their lives. Historically,the procedures used to treat patients with advancedperiodontitis were aimed at the elimination of sub-gingival plaque and calculus from the affected rootsurfaces. This therapy included scaling and rootplaning and periodontal flap surgery. These treat-ment methods usually healed through repair char-acterized by the formation of a long junctional epi-thelium adjacent to the previously diseased rootsurface. Several long-term clinical trials have dem-onstrated that this standard mode of therapy, if fol-lowed by an adequate postoperative supportive peri-odontal care, results in successful management ofprogressive periodontal disease (32, 36, 44, 63, 69).However, when molar teeth with furcation involve-ment were evaluated specifically, the long-term re-sponse to this conventional therapy differed fromnon-molar teeth. Hirschfeld & Wassermann (32),studying 600 periodontal patients after a mean ob-servation period of 22 years, reported that well-maintained patients having a good prognosis at thebeginning of therapy, hardly lost teeth due to peri-odontitis (0.6%). However, when patients were de-fined as guarded prognosis, the teeth lost were 11.6%if furcation lesions were excluded and 19.5% whenmolars with furcation involvement at the beginningof the study were specifically considered. Pihlstromet al. (63) investigated the response of molar andnon-molar teeth to either scaling and root planingalone or scaling and root planing followed by amodified Widman flap. They reported less reductionin probing depth and loss of attachment in molarscompared to non-molars for either mode of therapy.Kalkdahl et al. (36) also noted that following eithernon-surgical or surgical therapy there was a ten-dency for attachment loss in furcation regions dur-ing the second year of supportive care, irrespectivefrom the type of therapy rendered. McGuire & Nunn(52) reported that the risk of periodontitis pro-

169

gression in the furcation lesions increases with theseverity of the furcation involvement, and thus classI furcation lesions have better prognosis than classII and class III lesions. All these studies clearly showthat the presence and severity of a furcation lesionreduces the success rate of conventional periodontaltherapy in these specific areas and therefore worsensthe long-term prognosis of that particular tooth. Thisdifferent behavior has been explained, among otherfactors, by the complexity of the furcation mor-phology and hence, the limitation for accessibility todebride properly during periodontal therapy and todevelop appropriate patient compliance in plaquecontrol (13).

In the course of periodontal history, several tech-niques have been proposed and promoted to treatthese furcated molars and thus improve their prog-nosis. Grade I furcations have generally been wellmanaged with routine periodontal surgical pro-cedures aimed to thoroughly debride the lesion, re-duce pockets and expose the furcation entrance foradequate plaque control. Grade III furcations have re-quired more extensive resective therapy such as tun-neling, root amputation or hemisection with the aimof eliminating the lesion and thus also allowing forproper infection control. Grade II furcations have pre-sented, however, a clinical problem that has troubledclinicians for many years. Various regenerative pro-cedures have been tried with the aim of closing gradeII furcations, such as open flap debridement, bone re-placement grafts, coronally repositioned flaps andguided tissue regeneration barriers (13) (some ofthese therapeutic approaches have been extensivelyreviewed elsewhere in this journal). While some ofthese procedures have excited the dental professionbased on reports of significant attachment gains andbone fill at the furcation defects, a systematic evalu-ation of the available scientific information does notclearly indicate the real impact of these therapeuticprocedures on the final outcome and prognosis of theaffected tooth and patient (26, 37).

Page 2: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

The purpose of this chapter is to evaluate theavailable evidence on the efficacy of guided tissueregeneration therapy in the treatment of molars withfurcation lesions.

Evidence-based approach

Traditionally, most clinical decisions in dentistryhave been based upon the experience of gifted clini-cians. Therapies tested in this fashion are often un-predictable, since the clinician may not know whichfactors are important for success and which factorscontribute to failure. The evidence-based approachis based on the systematic evaluation of all availableinformation on a given therapeutic procedure. How-ever, not all evidence is given the same weight. Thestronger the evidence, the stronger the recommen-dation it will support. This approach puts the mostweight on randomized controlled clinical studieswith clearly defined goals that objectively measurethe risks and benefits of the procedure, that ac-knowledge potential sources of bias in the study de-sign and that use analytic methods to determineboth statistical and clinical significance (35).

Following this approach, we shall evaluate theavailable information on the efficacy of guided tissueregeneration in the treatment of molars with fur-cation lesions. We shall rank this evidence using therandomized controlled clinical study as the standardstudy for evidence, and in this way we shall be ableto test the real efficacy of this therapeutic procedureand help the clinician to make the appropriate de-cisions.

Therapeutic end-points of success

One of the most important factors in determiningthe outcome of regenerative therapy is the ability todetermine and analyze the types of healing out-comes that result. These outcomes can be relevantto the patient, to the defect treated or to the tissuehealing response.

McGuire & Nunn (52) clearly showed that thepresence of furcation lesions worsens both theaffected tooth and the overall patient prognosis. Thisworsening is also dependent on the severity of thefurcation lesion. Therefore, the main clinical end-point of any given therapy to treat these lesionswould be the full closure of the furcation. If this ob-jective could not be attained completely, then thesecondary objective would be the conversion of a

170

deep furcation lesion into a shallower one, thus con-verting a class II or III lesion into a class I. Otherpossible surrogate endpoints will be gains in clinicalattachment, mainly horizontal, together with gainsin bone height.

To assess these outcomes, most of the studieshave used clinical or radiological methods. Thesemethods have generally included assessments ofgingival inflammation expressed as bleeding onprobing, periodontal probing for the evaluation ofsoft tissue changes and re-entry bone fill or radio-graphic bone changes for hard tissue evaluation.When related specifically to furcation lesions, thesemeasurements have usually been expressed as gainsin vertical and horizontal attachment, reductions inprobing depth, bone fill or degree of furcation clo-sure. Furcation closure is usually reported either inpercentages or as total or partial closure (clinicalchange from class II to class I). Results have beendetermined by comparing pre and post-treatmentmeasurements.

When these clinical and radiographic outcomesare used in the evaluation of the treatment efficacyof regenerative procedures, it is important to takeinto account their inherent limitations. Changes ingingival inflammation, normally expressed asbleeding on probing measurements, do not reflectany outcome specific to periodontitis. Periodontalprobing is used to measure changes in probingdepth, changes in the position of the gingival mar-gin and changes in clinical attachment levels.Changes in probing depth are also not specific toperiodontitis since they may just reflect changes inthe inflammatory status of the periodontal tissues,and therefore may not represent the best clinicaloutcome measurement to evaluate success after re-generative surgery. Clinical attachment levels usinga fixed reference point (such as the cemento-enamel junction) reflect more clearly the histologi-cal status of the tooth’s attachment apparatus andare widely accepted as one of the primary clinicaloutcomes to evaluate success after regenerativesurgery. However, clinical attachment levels maynot measure accurately the coronal level of theconnective tissue attachment to the tooth surfaceand, therefore, they do not indicate the type oftissue healing obtained after the regenerative pro-cedure.

Bone fill at a re-entry procedure is the only com-ponent of a regenerated periodontium that can beaccurately assessed clinically. However, this involvesa second surgical procedure. This measurement pro-vides a very accurate assessment of any bone re-

Page 3: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

modeling at the treated site but does not allow anassessment of whether new cementum and a newperiodontal ligament are also present.

Changes in bone height and density are usuallyevaluated by comparing pre- and post-treatmentradiographs. Although recent significant progresshas been made in the assessment of the alveolarbone status (15), post-treatment gains in height,density and volume of alveolar bone provide evi-dence of regeneration of just one component of theperiodontium.

Histological evaluation remains the only reliablemethod of determining the nature of the attachmentapparatus resulting from regenerative periodontaltherapy. Histological evaluation provides an accurateassessment of all the components of the new attach-ment apparatus and allows an accurate determi-nation of whether clinical results represent regenera-tion or some form of repair. Due to evident diffi-culties in obtaining human biopsy material, thisevaluation method has only been used in studies onanimal models, mostly beagle dogs and non-humanprimates (26, 33).

Relevant patient-related outcome measurementshave seldom been used in regenerative therapystudies and therefore efficacy issues related to long-term stability of the patient’s dentition, patient’scomfort and patient’s absence of pain or sensitivityare seldom measured. Therefore the real impact ofthese regenerative techniques on the patient and thepatient’s perception of these types of therapy is un-known.

In the course of the last 15 years since the firstanimal studies demonstrating the biological prin-ciples of guided tissue regeneration, different barriermembrane materials have been used with differentdegrees of reported clinical success. The first gener-ation of guided tissue regeneration studies were car-ried out using nonresorbable expanded polyte-trafluoroethylene membranes, which created thebasis for the clinical use of this technique. In the last5 years a second generation of resorbable barriermembrane materials has been proposed, and severalclinical studies have been carried out to test theirefficacy. This chapter then evaluates independentlythe efficacy of this therapeutic approach with eitherresorbable and nonresorbable membrane materials.

It has also become clear that the main clinical in-dication for this therapeutic approach in the treat-ment of furcation lesions is the first mandibular mo-lar with a class II furcation lesion. Other furcationlesions in other areas of the mouth have also beenapproached with this therapeutic principle, although

171

rendering different outcomes. We therefore reviewthese lesions independently.

Using this evidence-based approach, we haveevaluated the available information on the efficacyof guided tissue regeneration in the treatment of mo-lars with furcation lesions. We have used these de-fined main and secondary end-points of success ofthis mode of therapy and we have taken into con-sideration the previously mentioned limitations ofthe outcome variables most widely used. Based onthis information, we have aimed to provide answersthat allow the clinician to determine the most appro-priate mode of therapy in the treatment of molarswith furcation involvement.

Efficacy of nonresorbable barriermembranes in the treatment ofmandibular class II furcation

Since the publication of the first case reports at thebeginning of the 1980s (27, 60) using the guidedtissue regeneration principle by placing nonre-sorbable expanded polytetrafluoroethylene mem-branes, several authors have attempted to demon-strate the efficacy of this procedure in the treatmentof class II furcation defects in mandibular molars.

Table 1 summarizes the randomized controlledstudies carried out to test this regenerative surgicalprocedure. These studies have selected subjects withsimilar furcation lesions and have compared the out-come of placement of expanded polytetrafluoro-ethylene membranes versus the standard mode oftherapy (surgical debridement of the furcation de-fects). Among these studies, Pontoriero et al. (65)clearly demonstrated significant clinical attachmentwhen this regenerative therapy was used (3.8 mm ofhorizontal attachment gain in the guided tissue re-generation group versus 2.0 mm in the controlgroup). In this study Pontoriero et al. (65) reported a67% closure of the furcation lesions in the guidedtissue regeneration group versus a 9% in the controlgroup. However, others have not substantiated themagnitude of the results from this study. Lekovic etal. (40) also reported significant clinical attachmentlevel gains in the guided tissue regeneration group(2.9 mm) versus attachment loss in the controlgroup. However, the bone gain assessed at re-entrywas minimal (0.2 mm) and they could not attain anyfurcation closure in either the membrane or the con-trol groups. The rest of the controlled studies (1, 11,53) comparing the placement of expanded polyte-

Page 4: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

Tab

le1.

Cli

nic

alo

utc

om

eo

fcl

ass

IIm

and

ibu

lar

furc

atio

nd

efec

tstr

eate

dw

ith

guid

edti

ssu

ere

gen

erat

ion

(no

nab

sorb

able

mem

bra

nes

)co

mp

ared

wit

hsu

rgic

ald

ebri

dem

ent

Cli

nic

alat

tach

-P

ock

etp

rob

ing

dep

thm

ent

leve

lch

ange

Def

ect

fill

(mm

)

Def

ect

Red

uc-

Ho

r-H

or-

Au

tho

rsTr

eatm

ent

nty

pe

Init

ial

Fin

alti

on

Rec

Vert

ical

izo

nta

lVe

rtic

aliz

on

tal

%St

ud

y

Pon

tori

ero

Exp

and

edp

oly

tetr

aflu

oro

-21

F-I

I6.

01.

54.

5–

4.1

4.1

––

–R

and

om

ized

con

tro

l14

/21

clo

sed

etal

.(6

5)et

hyl

ene

mem

bra

ne

clin

ical

tria

lSu

rgic

ald

ebri

dem

ent

21F

-II

6.0

3.2

2.8

–1.

51.

9–

––

Cli

nic

alre

-eva

luat

ion

2/21

clo

sed

6m

on

ths

Leko

vic

Exp

and

edp

oly

tetr

aflu

oro

-12

F-I

I6.

72.

64.

11.

32.

9–

0.2

0.2

–R

and

om

ized

con

tro

lN

ocl

inic

alcl

osu

res

etal

.(4

0)et

hyl

ene

mem

bra

ne

clin

ical

tria

lre

po

rted

Surg

ical

deb

rid

emen

t12

F-I

I6.

04.

81.

21.

0.1

–ª

0.2

ª0.

1–

Re-

entr

y6

mo

nth

s

Mel

lon

igE

xpan

ded

11F

-II

6.2

3.6

2.8

0.9

1.6

–2.

44.

5–

Ran

do

miz

edco

ntr

ol

1/11

clin

ical

lyet

al.

(53)

po

lyte

trafl

uo

roet

hyl

ene

clin

ical

tria

lcl

ose

dSu

rgic

ald

ebri

dem

ent

11F

-II

6.1

4.8

1.3

0.2

1.1

–0.

91.

3–

Re-

entr

y6

mo

nth

sN

ocl

osu

res

An

der

sso

nE

xpan

ded

po

lyte

trafl

uo

ro-

8F

-II

5.1

3.5

1.6

0.9

0.7

––

––

Ran

do

miz

edco

ntr

ol

Rx

bo

ne

gain

in2/

8et

al.

(1)

eth

ylen

em

emb

ran

ecl

inic

altr

ial

Co

ron

ally

po

siti

on

edfl

aps

8F

-II

3.9

2.6

1.3

0.8

0.4

Cli

nic

alre

-eva

luat

ion

No

Rx

bo

ne

gain

1ye

ar

Caf

fess

eE

xpan

ded

po

lyte

trafl

uo

ro-

9F

-II

5.7

2.9

2.8

–1.

80.

8–

––

Cli

nic

alca

sese

ries

No

clin

ical

clo

sure

set

al.

(11)

eth

ylen

em

emb

ran

eSu

rgic

ald

ebri

dem

ent

4F

-II

4.5

2.9

1.6

–0.

60.

3–

––

Cli

nic

alre

-eva

luat

ion

6m

on

ths

Pon

tori

ero

Exp

and

edp

oly

tetr

aflu

oro

-21

F-I

II–

––

––

3.1

Ran

do

miz

edco

ntr

ol

8cl

ose

d;

10p

artl

yet

al.

(66)

eth

ylen

em

emb

ran

ecl

inic

altr

ial

clo

sed

;3

op

enSu

rgic

ald

ebri

dem

ent

21F

-III

––

––

–1.

2C

lin

ical

re-e

valu

atio

n10

par

tly

clo

sed

;6

mo

nth

s11

op

en

172

Page 5: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

trafluoroethylene membranes versus open flap de-bridement report very limited horizontal attachmentgains in the guided tissue regeneration group (lessthan 2 mm) and the differences between guidedtissue regeneration and open flap debridement areminimal and not clinically relevant (around 1 mm).

Therefore, it is clear from the evaluation of thesestudies that placement of expanded polytetrafluor-oethylene barrier membranes in the treatment ofmandibular molars with class II furcation lesionsdoes not render predictable results. While one study(65) reported significant clinical improvements and asignificant number of furcations closed, these resultswere not corroborated by the rest of the studies (1,11, 40, 53) which have only reported minimal gainsof doubtful clinical significance. Most of the studiesfailed to reach the main end-point of this therapy,closure of the furcation.

Efficacy of resorbable barriermembranes in the treatment ofmandibular class II furcation

Since the publication of the first series of case re-ports using bovine derived collagen membranes (62)and polylactic acid–based membranes (39) in thetreatment of furcation defects, different randomizedcontrolled clinical trials have been carried out. Theirmain objective has been to test the efficacy of guidedtissue regeneration with the use of these bioresorb-able barrier membrane materials when compared toopen flap debridement in the treatment of class IIfurcation defects. Table 2 summarizes the resultsfrom these studies. When collagen membranes wereused as guided tissue regeneration barrier (42, 62, 77,79) the results obtained demonstrate rather modestclinical attachment gains (horizontal attachmentgains around 2 mm) and bone fill measurements as-sessed during re-entry ranging between 0.9 and 2.0mm. In no case were differences between the experi-mental (guided tissue regeneration with a collagenmembrane) and control (open flap debridement)groups clinically significant (differences greater than1.5 mm). This cut-off point of 1.5 mm is consideredrelevant since 1 mm it is the expected average errorin manual periodontal probing, and therefore differ-ences close to this figure do not rule out an instru-mentation error versus real clinical difference. Fur-thermore, in very few defects (4 out of 12 in a study(79) and 5 out of 28 in another (77)) was more than50% bone fill obtained. No furcation closure is re-ported in any of these studies.

173

The magnitude of these gains was improved whenpolylactic acid–based barrier membranes were usedfor guided tissue regeneration procedures. Clinicallysignificant horizontal attachment gains are reportedin several studies (5, 14, 39, 64, 71) (ranging between2.5 and 3.3 mm). These gains, nevertheless, have notbeen confirmed by direct assessment of bone fill atre-entry, and furcation closure is seldom attained inthese studies. Only Laurell et al. (39) in a case seriesstudy showed that about 50% of their class II fur-cations closed (9 of 19) and the rest (10 of 19)changed into class I. In the controlled studies (14,64), no furcation closure was obtained and between50% and 75% of the lesions changed from class II toclass I.

When comparing these outcomes with similarcontrolled clinical studies using nonresorbable ex-panded polytetrafluoroethylene membranes, theyshow similar attachment gains and similar bone fillmeasurements as well as lack of furcation closure(Table 1). One exception is the study by Pontorieroet al. (65) in which the clinical attachment gains andrate of furcation closure are clearly of a higher mag-nitude.

Are there differences in thetreatment of mandibular class IIfurcation when barriermembranes of different materialsare compared?

The introduction of resorbable membrane materialsbrings clear advantages in clinical management inguided tissue regeneration procedures (36): mainly,the avoidance of a second surgical intervention andthus the prevention from exposure of the newlyformed tissue underneath the membrane.

In order to fully recommend the use of this newgeneration of barrier membranes, these advantagesin clinical handling must be coupled with the attain-ment of at least similar outcomes when used inguided tissue regeneration procedures in the treat-ment of furcation defects. To test this hypothesis,several controlled clinical studies have been carriedout comparing guided tissue regeneration with bi-oresorbable barrier membranes versus the standardguided tissue regeneration technique using nonre-sorbable expanded polytetrafluoroethylene mem-branes. Table 3 summarizes the data from thesestudies (6–9, 12, 15, 25, 34, 81).

In studies where the resorbable barrier membrane

Page 6: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

Tab

le2.

Cli

nic

alo

utc

om

eo

fcl

ass

IIm

and

ibu

lar

furc

atio

nd

efec

tstr

eate

dw

ith

guid

edti

ssu

ere

gen

erat

ion

(bio

abso

rbab

lem

emb

ran

es)

com

par

edw

ith

surg

ical

deb

rid

emen

t

Cli

nic

alat

tach

-P

ock

etp

rob

ing

dep

thm

ent

leve

lch

ange

Def

ect

fill

(mm

)

Def

ect

Red

uc-

Ho

r-H

or-

Au

tho

rsTr

eatm

ent

nty

pe

Init

ial

Fin

alti

on

Rec

Vert

ical

izo

nta

lVe

rtic

aliz

on

tal

%St

ud

y

Cat

on

Poly

glac

tin

20F

-II

7.3

3.2

3.9

0.8

3.1

2.0

––

–R

and

om

ized

con

tro

lled

15/2

0cl

ass

Iet

al.

(14)

clin

ical

tria

lSu

rgic

ald

ebri

dem

ent

20F

-II

6.5

4.9

1.6

1.0

0.6

0.1

––

–C

lin

ical

re-e

valu

atio

n1/

20cl

ass

I6

mo

nth

s

Leko

vic

Co

nn

ecti

veti

ssu

em

atri

x15

F-I

I6.

52.

34.

20.

72.

4–

2.0

1.6

–R

and

om

ized

con

tro

lled

etal

.(4

)cl

inic

altr

ial

Surg

ical

deb

rid

emen

t15

F-I

I6.

34.

71.

61.

10.

5–

ª1.

0.2

–R

e-en

try

6m

on

ths

Wan

get

al.

X-b

ovin

eco

llage

n12

F-I

I6.

94.

12.

80.

81.

7–

2.5

2.0

50(1

0)R

and

om

ized

con

tro

lled

4/12

±50

%(7

9)cl

inic

altr

ial

ho

rizo

nta

lb

on

efi

llSu

rgic

ald

ebri

dem

ent

12F

-II

6.9

5.0

1.9

1.1

1.1

–1.

51.

150

(5)

Re-

entr

y6

mo

nth

s2/

12±

50%

ho

rizo

nta

lb

on

efi

ll

Van

Swo

lX

-bov

ine

colla

gen

28F

-II

5.4

3.3

1.9

–1.

4–

1.7

2.3

–R

and

om

ized

con

tro

lled

5/28

±50

%fi

llet

al.

(77)

clin

ical

tria

lC

oro

nal

lyp

osi

tio

ned

flap

10F

-II

3.9

2.6

1.3

0.8

0.4

Re-

entr

y3

mo

nth

s0/

10±

50%

fill

Pau

lB

ovin

eco

llage

n7

F-I

I5.

03.

51.

50.

11.

6–

0.7

0.9

–R

and

om

ized

con

tro

lled

No

def

ect

etal

.(6

2)cl

inic

altr

ial

clo

sure

sSu

rgic

ald

ebri

dem

ent

7F

-II

4.3

3.4

0.9

0.1

1.0

–0.

40.

0–

Re-

entr

y6

mo

nth

s

Pols

on

Poly

lact

icac

id29

F-I

I6.

03.

82.

20.

41.

72.

5–

––

No

nco

ntr

olle

d14

/29

clas

sI

etal

.(6

4)ca

sese

ries

Cli

nic

alre

-eva

luat

ion

12m

on

ths

Lau

rell

Poly

lact

icac

id19

F-I

I6.

62.

93.

70.

23.

43.

3–

––

No

nco

ntr

olle

d9/

19cl

ose

d;

etal

.(3

9)ca

sese

ries

10/1

9cl

ass

IC

lin

ical

re-e

valu

atio

n12

mo

nth

s

Bec

ker

Poly

lact

icac

id–

31F

-II

6.1

3.6

2.5

ª0.

42.

11.

8–

––

No

nco

ntr

olle

det

al.

(5)

po

lygl

yco

lic

acid

case

seri

esC

lin

ical

re-e

valu

atio

n12

mo

nth

s

San

zPo

lyla

ctic

acid

–10

F-I

I6.

52.

93.

61.

51.

83.

2–

––

No

nco

ntr

olle

det

al.

(71)

po

lygl

yco

lic

acid

case

seri

esC

lin

ical

re-e

valu

atio

n12

mo

nth

s

174

Page 7: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

Tab

le3.

Co

mp

aris

on

of

clin

ical

ou

tco

mes

of

clas

sII

man

dib

ula

rfu

rcat

ion

def

ects

trea

ted

wit

hgu

ided

tiss

ue

rege

ner

atio

n(n

on

abso

rbab

leve

rsu

sb

ioab

sorb

able

mem

bra

nes

)

Cli

nic

alat

tach

-P

ock

etp

rob

ing

dep

thm

ent

leve

lch

ange

Def

ect

fill

(mm

)

Def

ect

Red

uc-

Ho

r-H

or-

Au

tho

rsTr

eatm

ent

nty

pe

Init

ial

Fin

alti

on

Rec

Vert

ical

izo

nta

lVe

rtic

aliz

on

tal

%St

ud

y

Hu

goso

nPo

lyla

ctic

acid

38F

-II

5.3

3.3

2.0

0.3

0.8

2.2

––

–R

and

om

ized

con

tro

lled

34%

clo

sed

etal

.(3

4)cl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-38

F-I

I5.

63.

42.

20.

90.

41.

4–

––

Cli

nic

alre

-eva

luat

ion

11%

clo

sed

eth

ylen

em

emb

ran

e12

mo

nth

s

Blu

men

thal

X-b

ovin

eco

llage

n12

F-I

I5.

82.

73.

11.

71.

82.

51.

62.

547

Ran

do

miz

edco

ntr

olle

dN

ocl

osu

res

eith

eret

al.

(7)

clin

ical

tria

lm

emb

ran

eE

xpan

ded

po

lyte

trafl

uo

ro-

12F

-II

5.2

2.5

2.7

1.8

1.1

1.8

1.0

1.7

34R

e-en

try

12m

on

ths

eth

ylen

em

emb

ran

e

Bla

ckX

-bov

ine

colla

gen

13F

-II

4.6

3.2

1.5

0.6

0.9

1.5

–2.

0–

Ran

do

miz

edco

ntr

olle

d5/

13cl

osu

res

etal

.(6

)cl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-13

F-I

I6.

95.

01.

91.

11.

1–

1.5

1.1

50(5

)C

lin

ical

re-e

valu

atio

n3/

13cl

osu

res

eth

ylen

em

emb

ran

e6

mo

nth

s

Bo

uch

ard

Co

nn

ecti

veti

ssu

em

atri

xπ12

F-I

I5.

23.

31.

9–

1.2

1.5

0.8

1.5

19R

and

om

ized

con

tro

lled

2/11

clo

sed

etal

.(8

)cl

inic

alat

tach

men

tcl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-12

F-I

I5.

12.

92.

3–

1.3

2.8

0.4

2.2

30R

e-en

try

12m

on

ths

4/11

clo

sed

eth

ylen

em

emb

ran

eπcl

inic

alat

tach

men

t

Yukn

aFr

eeze

-dri

edd

ura

mat

er11

F-I

I4.

03.

31.

01.

00.

0–

1.0

2.0

40R

and

om

ized

con

tro

lled

No

clo

sure

sei

ther

etal

.(8

1)cl

inic

altr

ial

mem

bra

ne

Exp

and

edp

oly

tetr

aflu

oro

-11

F-I

I4.

03.

31.

01.

00.

0–

1.0

1.0

20R

e-en

try

12m

on

ths

eth

ylen

em

emb

ran

e

Ch

rist

gau

Poly

lact

icac

id5

F-I

I–

––

1.0

–2.

0–

–66

.7R

and

om

ized

con

tro

lled

2/5

clo

sed

etal

.(1

5)cl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-5

F-I

I–

––

ª1.

0–

2.0

––

66.7

Cli

nic

alre

-eva

luat

ion

No

clo

sed

eth

ylen

em

emb

ran

e5

mo

nth

s

Bo

uch

ard

Poly

lact

icac

id–

15F

-II

4.8

2.7

2.1

0.8

1.5

2.5

––

–R

and

om

ized

con

tro

lled

etal

.(9

)p

oly

glyc

oli

cac

idcl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-15

F-I

I4.

72.

91.

80.

61.

22.

7–

––

Cli

nic

alre

-eva

luat

ion

eth

ylen

em

emb

ran

e12

mo

nth

s

Caf

fess

ePo

lyla

ctic

acid

–6

F-I

I6.

43.

92.

50.

12.

41.

8–

––

Ran

do

miz

edco

ntr

olle

det

al.

(12)

po

lygl

yco

lic

acid

clin

ical

tria

lE

xpan

ded

po

lyte

trafl

uo

ro-

6F

-II

5.8

3.2

2.6

1.1

1.5

2.3

––

–C

lin

ical

re-e

valu

atio

net

hyl

ene

mem

bra

ne

12m

on

ths

Gar

rett

Poly

lact

icac

id82

F-I

I(*

)5.

63.

32.

30.

32.

02.

1–

––

Co

ntr

olle

dca

seet

al.

(25)

seri

es–

mu

ltic

entr

icE

xpan

ded

po

lyte

trafl

uo

ro-

80F

-II

(*)

5.5

3.4

2.1

0.5

1.6

2.1

––

–C

lin

ical

re-e

valu

atio

net

hyl

ene

mem

bra

ne

12m

on

ths

*B

oth

man

dib

ula

ran

dm

axil

ar.

175

Page 8: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

material was bovine collagen the clinical outcomesreached were very similar compared with standardexpanded polytetrafluoroethylene membranes (6–8,81). No significant differences were found in any ofthe parameters measured. However, the improvedclinical outcomes obtained with both procedureswere very modest (vertical attachment gain rangingbetween 1.0 and 2.0 mm, horizontal attachment gainbetween 1.5 and 2.5 mm and bone fill around 2.0mm). Closure of the furcation hardly ever occurredwith both modalities of guided tissue regenerationtherapy.

In studies where the resorbable barrier membranematerial was polylactic acid based (9, 12, 15, 25, 34),again differences in clinical outcomes comparedwith standard expanded polytetrafluoroethylenenever reached statistical significance. All studies re-port vertical attachment gain ranging between 1.0and 2.0 mm and horizontal attachment gain be-tween 1.5 and 2.5 mm. Most of these studies do notreport bone fill re-entry measurements, and in onestudy where closure of the furcation was assessed, ithappened very seldom with both modalities of treat-ment (34).

In summary, the results obtained from most ofthe studies when guided tissue regeneration wasused as the treatment of class II furcation defects,regardless of the barrier membrane material used,clearly show the limitations of this therapeutic pro-cedure in this clinical indication. If we considerfurcation closure as the main end-point of thistherapy, then the results obtained with guidedtissue regeneration procedures are very limited,since in no study was this outcome reached evenin 50% of the cases. If our secondary objective isconversion from class II to class I, this procedure isthen very unpredictable. In some studies, this eventoccurs in the majority of cases, while in others, theincidence does not reach 50% of the cases. If thecriteria of success is clinical attachment gain, thenthe expected gains would be around 2.0 mm in ver-tical attachment gain and around 2.5 mm in hori-zontal attachment gain. Considering that the stan-dard mode of therapy (open flap debridement) ob-tains around 1.0 mm both vertically andhorizontally, this 1.0–1.5 mm of benefit is onlymodest and of doubtful clinical significance.

Guided tissue regeneration procedures in thetreatment of furcation defects demonstrate similaroutcomes when different membrane barrier ma-terials were compared. Advantages in patient man-agement would therefore recommend the use ofpolylactic acid based resorbable materials.

176

Efficacy of root-conditioningagents or systemic antibiotics inconjunction with guided tissueregeneration in class IImandibular furcations

Table 4 summarizes the studies aimed to testwhether root conditioning in conjunction withplacement of a nonresorbable barrier membraneswould improve the clinical results of this regenera-tive procedure (8, 22, 48, 49, 61). From these studies,it is clear that the conditioning of the root, either bymeans of citric acid, tetracycline or thorough rootplaning, did not improve the clinical results com-pared with placing the membrane alone. Clinicalattachment gains both vertically and horizontally areof similar magnitude to the controlled studiesshowed in Table 1 (ranging from 1.0 to 2.5 mm). Thisdemonstrates again the limited clinical significanceof this therapeutic procedure irrespective of the con-ditioning of the affected roots.

Efficacy of bone replacement graftin combination with barriermembranes in class II mandibularfurcations

Table 5 shows the summary data from studies de-signed to test this hypothesis. Some studies (24, 41,51, 72) show that the placement of a bone graftunder the membrane (either decalcified freeze-driedbone allograft or porous hydroxyapatite) significant-ly improves the vertical clinical attachment andbone gains obtained (differences of around 2 mmcompared with membrane alone). However, wheneither horizontal clinical attachment gains or bonefill is assessed, the differences are reduced (around 1mm) and controlled studies do not show significantdifferences in the amount of furcation closure, whichis very limited for both regenerative procedures (2,41). Moreover, there are two studies, one (78) usingexpanded polytetrafluoroethylene membranes andother (46) using polyactic acid membranes wherethe combination of decalcified freeze-dried boneallograft with guided tissue regeneration did notshow any advantage over using the membrane alone.

This possibly improved clinical effect of placing ofa bone graft under the membrane showed in somestudies does not provide information on the nature ofthe tissue healing under the membrane. Since similar

Page 9: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

Tab

le4.

Cli

nic

alo

utc

om

eo

fcl

ass

IIm

and

ibu

lar

furc

atio

nd

efec

tstr

eate

dw

ith

guid

edti

ssu

ere

gen

erat

ion

wit

han

dw

ith

ou

tco

nd

itio

nin

go

fth

ero

ot

surf

ace

or

adm

inis

trat

ion

of

syst

emic

anti

bio

tics

Cli

nic

alat

tach

-P

ock

etp

rob

ing

dep

thm

ent

leve

lch

ange

Def

ect

fill

(mm

)

Def

ect

Red

uc-

Ho

r-H

or-

Au

tho

rsTr

eatm

ent

nty

pe

Init

ial

Fin

alti

on

Rec

Vert

ical

izo

nta

lVe

rtic

aliz

on

tal

%St

ud

y

Mac

hte

iE

xpan

ded

po

lyte

trafl

uo

ro-

18F

-II

5.7

2.5

3.2

–2.

31.

4–

––

Ran

do

miz

edco

ntr

olle

det

al.

(48)

eth

ylen

em

emb

ran

ecl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-18

F-I

I5.

32.

23.

1–

2.3

1.0

––

–C

lin

ical

re-e

valu

atio

net

hyl

ene

mem

bra

neπ

6m

on

ths

tetr

acyc

lin

e

Para

shis

&E

xpan

ded

po

lyte

trafl

uo

ro-

9F

-II

5.1

2.7

2.4

–1.

64.

8–

––

Ran

do

miz

edco

ntr

olle

dM

itis

(61)

eth

ylen

em

emb

ran

eπcl

inic

altr

ial

tetr

acyc

lin

eE

xpan

ded

po

lyte

trafl

uo

ro-

9F

-II

5.4

2.9

2.6

–1.

74.

7C

lin

ical

re-e

valu

atio

net

hyl

ene

mem

bra

ne

6m

on

ths

Bo

uch

ard

Exp

and

edp

oly

tetr

aflu

oro

-12

F-I

I5.

12.

92.

60.

81.

32.

8–

––

Ran

do

miz

edco

ntr

olle

det

al.

(8)

eth

ylen

em

emb

ran

eπcl

inic

altr

ial

tetr

acyc

lin

eC

on

nec

tive

tiss

ue

graf

t12

F-I

I5.

23.

31.

90.

61.

21.

5–

––

Re-

entr

y12

mo

nth

s

Mac

hte

iE

xpan

ded

po

lyte

trafl

uo

ro-

15F

-II

––

––

1.1

2.7

2.2

1.9

50R

and

om

ized

con

tro

lled

etal

.(4

9)et

hyl

ene

mem

bra

ne

clin

ical

tria

lE

xpan

ded

po

lyte

trafl

uo

ro-

15F

-II

––

––

2.3

1.0

1.7

1.8

50R

e-en

try

12m

on

ths

eth

ylen

em

emb

ran

eπro

ot

pla

nin

g

Dem

olo

nE

xpan

ded

po

lyte

trafl

uo

ro-

12F

-II

5.1

3.1

21.

21.

4–

––

32R

and

om

ized

con

tro

lled

No

clin

ical

clo

sure

set

al.

(22)

eth

ylen

em

emb

ran

ecl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-12

F-I

I5.

13.

31.

80.

81.

5–

––

32R

e-en

try

12m

on

ths

eth

ylen

em

emb

ran

eπA

ugm

enti

nA

177

Page 10: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

Tab

le5.

Cli

nic

alo

utc

om

eo

fcl

ass

IIm

and

ibu

lar

furc

atio

nd

efec

tstr

eate

dw

ith

guid

edti

ssu

ere

gen

erat

ion

wit

han

dw

ith

ou

tth

ep

lace

men

to

fa

bo

ne

graf

t

Cli

nic

alat

tach

-P

ock

etp

rob

ing

dep

thm

ent

leve

lch

ange

Def

ect

fill

(mm

)

Def

ect

Red

uc-

Ho

r-H

or-

Au

tho

rsTr

eatm

ent

nty

pe

Init

ial

Fin

alti

on

Rec

Vert

ical

izo

nta

lVe

rtic

aliz

on

tal

%St

ud

y

Sch

allh

orn

&E

xpan

ded

po

lyte

trafl

uo

ro-

16F

-II

––

4.0

0.8

3.1

–3.

63.

1–

Cli

nic

alca

sese

ries

2/16

com

ple

tefi

llM

cCla

in(7

2)et

hyl

ene

mem

bra

ne

and

III

Exp

and

edp

oly

tetr

aflu

oro

-38

F-I

I–

–4.

80.

54.

3–

5.1

4.2

–R

e-en

try

6m

on

ths

25/3

8co

mp

lete

fill

eth

ylen

em

emb

ran

eπan

dII

Id

ecal

cifi

edfr

eeze

-dri

edb

on

eal

logr

aft

An

der

egg

Exp

and

edp

oly

tetr

aflu

oro

-15

F-I

I5.

33.

12.

20.

81.

4–

1.7

1.0

50R

and

om

ized

con

tro

lled

4/27

clo

sed

etal

.(2

)et

hyl

ene

mem

bra

ne

clin

ical

tria

lE

xpan

ded

po

lyte

trafl

uo

ro-

15F

-II

6.1

3.0

3.1

0.0

3.1

–3.

52.

485

Re-

entr

y6

mo

nth

s1/

3cl

ass

III

or

eth

ylen

em

emb

ran

eπcl

ass

IId

ecal

cifi

edfr

eeze

-dri

edb

on

eal

logr

aft

Leko

vic

Exp

and

edp

oly

tetr

aflu

oro

-15

F-I

I6.

82.

93.

90.

62.

4–

0.1

0.1

Ran

do

miz

edco

ntr

olle

det

al.

(42)

eth

ylen

em

emb

ran

ecl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-15

F-I

I6.

92.

54.

40.

92.

9–

2.3

1.6

85R

e-en

try

6m

on

ths

eth

ylen

em

emb

ran

eπp

oro

us

hyd

roxy

apat

ite

Wal

lace

Exp

and

edp

oly

tetr

aflu

oro

-7

F-I

I5.

03.

61.

41.

30.

1–

3.7

2.1

Ran

do

miz

edco

ntr

olle

d2/

7cl

ose

det

al.

(78)

eth

ylen

em

emb

ran

ecl

inic

altr

ial

Exp

and

edp

oly

tetr

aflu

oro

-10

F-I

I5.

43.

32.

11.

30.

8–

5.2

2.1

Re-

entr

y6

mo

nth

s3/

10cl

ose

det

hyl

ene

mem

bra

neπ

dec

alci

fied

free

ze-d

ried

bo

ne

allo

graf

t

Luep

kePo

lyla

ctic

acid

mem

bra

ne

14F

-II

5.0

3.7

1.3

0.0

1.8

1.7

–1.

8R

and

om

ized

con

tro

lled

etal

.(4

6)cl

inic

altr

ial

Poly

lact

icac

idm

emb

ran

e14

F-I

I5.

43.

32.

11.

31.

31.

1–

2.1

Re-

entr

y6

mo

nth

dec

alci

fied

free

ze-d

ried

bo

ne

allo

graf

t

178

Page 11: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

clinical results are obtained irrespective of the graftused (autografts, allografts and alloplastic materials),these grafts may well just behave as defect spacefillers, thus avoiding the collapse of the membraneinto the defect and allowing more tissue to be gained.

The results obtained in controlled studies demon-strate that the use of bone replacement grafts to-gether with barrier membranes is of limited signifi-cant additional benefit, if any, to the use of mem-branes alone. Although a significant clinical benefithas been reported in some studies, this is unpredict-able and does not demonstrate an improved tissuehealing response. Therefore, the use of replacementgrafts to improve the results of guided tissue regene-rative therapy is not clearly justified.

Efficacy of guided tissueregeneration in the treatment ofmaxillary class II furcations

Table 6 summarizes studies aimed to test this hypo-thesis (53, 54, 67, 68). It is clear from these studiesthat the placement of a barrier membrane in thisclinical situation does not add any benefit whencompared with the standard treatment (open flapdebridement). Both vertical and horizontal attach-ment gains are of a magnitude of within 1 mm, andin no case is there any furcation closed or any sig-nificant difference between the guided tissue re-generation and open flap debridement. Pontorieroet al. (67, 68) clearly demonstrate that the locationof the maxillary furcation (buccal, mesial or lingual)does not change this clinical outcome. Therefore,placement of a barrier membrane should not be in-dicated in the treatment of maxillary molars withfurcation involvement.

Efficacy of guided tissueregeneration in the treatment ofmandibular class III furcations

Pontoriero et al. (66) also designed a randomizedcontrolled clinical study to test this hypothesis. Inthis clinical situation, the use of expanded polyte-trafluoroethylene membranes was less effectivesince the majority of treated defects still harboredthe lesion at re-evaluation (8 cases were totallyclosed and 10 cases partly closed of 21 cases treatedin the guided tissue regeneration group versus no

179

single case closed in the control group). Althoughsome degree of closure could be attained occasion-ally, this event was highly unpredictable and notsubstantiated in other studies. Gain of horizontalattachment was also more modest in these class IIIfurcation lesions (3.1 mm versus 1.2 mm in the con-trol group at 6 months). Similar results have beenreported by Becker et al. (4). In studies where guidedtissue regeneration was supplemented with theplacement of bone replacement grafts under themembranes, these poor results could not be signifi-cantly improved (24, 51).

Factors affecting the outcomesachieved with guided tissueregeneration in the treatment offurcation lesions

It has been shown (see Tables 1–4) that the use ofthis therapeutic approach in the treatment of fur-cation defects results in a great variability of clinicaloutcomes. Although significant clinical improve-ments can be expected in the treatment of mandibu-lar class II furcations, this therapeutic procedure isclearly not indicated in the treatment of maxillaryclass II furcations and class III furcations in eithermandible or maxilla. In the treatment of mandibularclass II furcations the results are not always consist-ent demonstrating in some reports significant clin-ical attachment and bone gains, while in othersthese results are either not significant or very limitedwhen compared with open flap debridement. Thevariability in these clinical results has been ex-plained in the literature through a variety of factorswhich may be related either to the case selection orto the therapeutic procedure, or both (75). Some ofthese factors are similar to those reported in thetreatment of infrabony defects by guided tissue re-generation, others however, are specific of the treat-ment of molar furcations (37).

Factors related to the case selection

Two types of factors can be considered in the diag-nosis and selection of a case for guided tissue re-generation therapy: general factors related to the pa-tient and local factors related to the defect (50).

General factors. In patients whose systemic statusdoes not contraindicate periodontal surgical therapy,the factors influencing guided tissue regeneration

Page 12: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

Tab

le6.

Cli

nic

alo

utc

om

eo

fcl

ass

IIm

axil

lary

furc

atio

nd

efec

tstr

eate

dw

ith

guid

edti

ssu

ere

gen

erat

ion

(no

nab

sorb

able

mem

bra

nes

)co

mp

ared

wit

hsu

rgic

ald

ebri

dem

ent

Cli

nic

alat

tach

-P

ock

etp

rob

ing

dep

thm

ent

leve

lch

ange

Def

ect

fill

(mm

)

Def

ect

Red

uc-

Ho

r-H

or-

Au

tho

rsTr

eatm

ent

nty

pe

Init

ial

Fin

alti

on

Rec

Vert

ical

izo

nta

lVe

rtic

aliz

on

tal

%St

ud

y

Met

zler

Exp

and

edp

oly

tetr

aflu

oro

-17

F-I

I5.

03.

31.

70.

71.

0–

1.5

0.9

–R

and

om

ized

con

tro

lled

No

clin

ical

clo

sure

set

al.

(54)

eth

ylen

em

emb

ran

em

axil

lary

clin

ical

tria

lSu

rgic

ald

ebri

dem

ent

17F

-II

4.6

3.7

0.9

0.7

0.2

–0.

60.

3–

Re-

entr

y6

mo

nth

sm

axil

lary

Mel

lon

igE

xpan

ded

po

lyte

trafl

uo

ro-

8F

-II

5.3

3.5

1.8

0.7

1.3

–1.

81.

0–

Ran

do

miz

edco

ntr

olle

det

al.

(53)

eth

ylen

em

emb

ran

em

axil

lary

clin

ical

tria

lSu

rgic

ald

ebri

dem

ent

8F

-II

4.9

3.8

1.1

0.8

0.4

–0.

90.

3–

Re-

entr

y6

mo

nth

sm

axil

lary

Pon

tori

ero

Exp

and

edp

oly

tetr

aflu

oro

-11

F-I

I–

––

–1.

5–

1.1

1.1

–R

and

om

ized

con

tro

lled

etal

.et

hyl

ene

mem

bra

ne

max

illa

ryb

ucc

alcl

inic

altr

ial

(67,

68)

Surg

ical

deb

rid

emen

t11

F-I

I–

––

–0.

0–

0.8

0.3

–R

e-en

try

6m

on

ths

Pon

tori

ero

Exp

and

edp

oly

tetr

aflu

oro

-10

F-I

I–

––

–0.

7–

0.2

0.4

–R

and

om

ized

con

tro

lled

etal

.et

hyl

ene

mem

bra

ne

max

illa

rym

esia

lcl

inic

altr

ial

(67,

68)

Surg

ical

deb

rid

emen

t10

F-I

I–

––

–0.

1–

0.1

0.2

–R

e-en

try

6m

on

ths

Pon

tori

ero

Exp

and

edp

oly

tetr

aflu

oro

-8

F-I

I–

––

–0.

6–

0.2

0.2

–R

and

om

ized

con

tro

lled

etal

.et

hyl

ene

mem

bra

ne

max

illa

ryd

ista

lcl

inic

altr

ial

(67,

68)

Surg

ical

deb

rid

emen

t8

F-I

I–

––

–0.

1–

0.2

0.2

–R

e-en

try

6m

on

ths

180

Page 13: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

Fig. 1. A class II furcation on the buccal aspect of the first left mandibular molar

outcomes are related to patient compliance in self-performed plaque control. Studies on the treatmentof infrabony defects by guided tissue regenerationdemonstrated significant better clinical attachmentlevel gains in patients with optimal levels of plaquecontrol compared with patients with poor oral hy-giene (18). The evaluation of plaque control is there-fore very important in patient selection, and a goodlevel of oral hygiene must be ensured and main-tained during the whole healing period.

Another important patient factor is the level of re-sidual periodontal infection in the remaining den-tition. In patients with high levels of residual infec-tion, the obtained attachment gains are significantlylower (49, 75).

Other behavioral factors such as stress and ciga-rette smoking have also been studied.

In a 1-year clinical retrospective study oninfrabony defects, Tonetti et al. (76) demonstratedthat the attachment gains obtained in subjectstreated by guided tissue regeneration changed sig-nificantly in patients smoking more than 10 ciga-rettes per day, when compared with nonsmoking pa-tients. Rosenberg & Cutler (70) evaluated the clinicaloutcomes of guided tissue regeneration in 38 class IIfurcations in patients smoking more than 10 ciga-rettes per day for over 5 years. They indicated thatthe success rate was significantly lower in smokersand the outcome for 80% of these cases was con-sidered as failure. Therefore, smoking is clearly detri-mental in guided tissue regeneration therapy in fur-cation defects.

It can be then concluded that smoking, compli-ance in oral hygiene and the presence of residual in-

181

fection significantly influence the clinical outcomesobtained with guided tissue regeneration.

Local factors. The referred variability in the resultscan also be explained in part by the complexity ofthe furcation morphology. Current furcation classi-fication systems are not ideal since they do not con-sider all local conditions affecting the furcation de-fect. They are mostly based in the horizontal andvertical probing depths at the defect. Some authorshave also included the number and location of thebony walls within the lesion (31); however, no onetakes into consideration the relationship betweenthe furcation and the root trunk length. The residualosseous morphology, the radicular anatomy of theaffected tooth or the root trunk length may have im-portant prognostic influence and therefore shouldbe properly evaluated by the clinician before decid-ing upon the therapeutic procedure.

Most of the studies using guided tissue regenera-tion have shown that the depth and width of theinfrabony component of the defect influence theamount of clinical attachment and bone gain. Whenguided tissue regeneration was applied to deepthree-, two- and one-wall infrabony defects resultedin respectively 95%, 82% and 39% bone fill (17).Similar studies, also in infrabony defects, have dem-onstrated that the deeper is the defect the greater isthe amount of attachment gain and bone repair. Onthe contrary, the wider the defect, the lesser the clin-ical improvement (17, 75). This significant lower gainin one-wall defects or very wide defects could be ex-plained by the reduced number of progenitor cellsavailable for the repopulation of the wound area or

Page 14: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

Fig. 2. Horizontal (left) and vertical (right) probing after flap elevation and debridement

Fig. 3. A nonresorbable expanded polytetrafluoroethylene membrane positioned to cover the furcation entrance

by the difficulty of placing the barrier membrane ina proper position, thus allowing the maintenance ofthe required space between the membrane and theremaining bone.

In the treatment of furcation defects, the predict-ability of the regenerative procedure also improves ifthe defect present a deep vertical component in thedefect (Fig. 2) while maintaining the level of inter-proximal bone level close to the cementoenameljunction. This facilitates the retention of the mem-brane in a proper position and allows for the co-ronally replacement of the flap and full coverage ofthe membrane (Fig. 3, 4).

The horizontal depth of the furcation involvementalso influences the clinical outcomes, and in mostof the studies in class II furcations, the preoperative

182

horizontal probing depth, correlated with the magni-tude of attachment gain and bone repair obtainedafter 1 year (Tables 1, 2).

The predictability of treatment outcomes also im-proves if thorough debridement of the exposed rootsurfaces in the furcation area is achieved. Factors af-fecting the ability of the operator to debride this areaproperly, such as root proximity or root deformities,could therefore influence the results of guided tissueregeneration therapy. The mandibular molar fur-cation entrance is in many cases smaller than thediameter of a standard Gracey curette (1.0 mm) (10).Moreover, the roots in mandibular molars frequentlypresent deep concavities, presence of ridges at thedome of the furcation or enamel pearls, which maymake difficult appropriate debridement. The ana-

Page 15: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

Fig. 4. From left to right: membrane coverage with the of removalflap; the area after 1 week; membrane still covered at time

tomy of maxillary molars is even less favorable (10),and this may account for the poorer results obtainedin this lesion.

The dimension of the root trunk of a molar andthe presence of a furcation involvement have beenshown to be correlated (33). This dimension may in-fluence the selection of the most adequate thera-peutic approach once the furcation has been in-volved. In resective therapeutic procedures such astunnelization, hemisection or root resection, thepresence of a short root trunk may be considered apositive factor in prognosis (13). Conversely, inguided tissue regeneration therapy, the presence ofa long root trunk facilitates the placement of the bar-rier membrane under the cementoenamel junction,thus achieving full coverage of the furcation defectand the placement of the replacement flap fullycovering the membrane (Fig. 4).

Gingival thickness has also been correlated withthe amount of recession obtained after the use ofguided tissue regeneration therapy in furcation de-fects (3). Anderegg et al. (3) demonstrated that siteswith gingival thickness of more than 1 mm exhibitedless gingival recession than sites with narrower gin-gival thickness. A thicker mucoperiosteal flap hasmore resistance to ischemia when placed over anonvascularized membrane. Besides, the coronalrepositioning of the flap aiming at full membranecoverage may apply excessive tension and may alsoinduce ischemia. These factors, in the presence ofa thin gingiva, lead to increased recession and thusreduced clinical attachment gains.

Factors related to the procedural technique

A successful guided tissue regeneration technique inthe treatment of furcation defects requires the sameprinciples and careful respect of the surgical pro-cedure as described for the treatment of intrabony

183

defects (28). These include: careful flap design,proper root surface preparation, correct placementof the membrane barrier, good wound closure andoptimal postoperative care (4, 11, 40, 66).

Flap design. Surgery is usually initiated by intracrev-icular incisions on the buccal and lingual aspects ofthe mandible followed by vertical releasing incisionson the buccal aspect extending into the alveolar mu-cosa with the aim of achieving proper access to thedefect, as well as for obtaining coronal displacementof the flap, once the membrane has been placed fullyclosing the furcation defect (Fig. 2, 4). These releasingincisions should be placed at least more than onetooth mesial and/or distal to the furcation involvedtooth. During the procedure, care must be taken topreserve as much as gingival connective tissue in theflap as possible. A horizontal releasing incisionthrough the periosteum on the inner aspect of the flapcan be performed in order to facilitate the coronalrepositioning of the flap. Such incision should notcompromise the flap blood supply. The inner surfaceof the flap should be curetted or excised in order toremove remnants of pocket epithelium.

After elevation of the flap, all granulation tissueshould be removed. In some cases a minor osseousrecontouring can be performed at the interproximalareas with the aim of eliminating exostosis and thusfacilitating the adaptation of the membrane barrierto the defect and the flap over of the membrane.

Root surface preparation. All subgingival soft andhard deposits at the furcation area should be re-moved through mechanical root instrumentation.

Since the width of the furcation entrance and theinternal morphology of the interradicular area maylimit the access of the curettes for proper debride-ment, it must frequently be complemented withultrasonic and rotary instruments.

Page 16: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

Fig. 5. From left to right: membrane uncovered after flap replacement of the flap to protect the regenerated tissueelevation; the regenerated tissue after membrane removal;

Fig. 6. One-year control of the treated area

Besides mechanical root preparation, someauthors have also included chemical root condition-ing of the roots with the aim of improving the re-generative outcomes. This root conditioning hasbeen carried out either with citric acid or topical te-tracycline. However, as demonstrated earlier in thischapter, these attempts have not provided any clin-ical benefit and therefore its use should not be rec-ommended (Table 4).

Selection and placement of the membrane barrier.Various types of both nonresorbable and bioresorb-able barrier membranes are available in a variety ofconfigurations designed for the treatment of fur-cation defects. Earlier in this chapter, it was shownthat the resorbability of the material does not sig-nificantly influence the clinical outcomes (Table 3).The nonresorbable membranes are made of ex-panded polytetrafluoroethylene material. This ma-terial has shown good cell barrier properties, to-gether with appropriate tissue integration and clin-

184

ical management. However, since they arenonresorbable, they must be removed once the heal-ing has occurred, in a second surgical procedure(Fig. 5). This second surgery not only adds moremorbidity but also exposes the newly formed tissuesbelow the membrane, which could jeopardize the re-sults obtained.

In recent years, bioresorbable barrier materialshave been introduced with the aim of avoiding thissecond operation for membrane removal. Bioresorb-able membranes made of collagen are mostly frombovine origin, and their resorption pattern is con-trolled through the collagen cross-linking. Resultswith the use of these membranes are described else-where in this chapter (Table 2) and demonstrate avery high variability, probably because of differencesin the properties of the different collagen materialsused and the difficulties in clinical handling inherentto these membranes. Besides, several complicationssuch as early degradation and epithelial downgrowthhave been described and, together with the possi-

Page 17: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

bility of crossed transmission of infectious agents in-herent to bovine materials, these factors limit the useof this material for barrier membranes.

Barrier membrane materials made of polylacticacid or co-polymers of polylactic acid and poly-glycolic acid are also available and have been evalu-ated in clinical human studies (Tables 2, 3). The clin-ical outcomes obtained with this material are similarto nonresorbable materials, but at the same time,their use has shown less clinical complications (34).This fact, together with the avoidance of a secondsurgical procedure, has made barrier membranesmade of polylactic acid or their co-polymers the ma-terial of choice for the guided tissue regenerationtreatment of class II furcations in mandibular mo-lars.

Placement of the membrane. Once the barrier ma-terial has been selected, this membrane must betrimmed and tailored to the defect morphology inorder to adapt it closely to the tooth and completelycover the entrance of the furcation area, extendingapproximately 3 mm of alveolar bone apical to thefurcation (Fig. 3). When the membrane is placed, itis essential to ensure that it is well adapted to thealveolar bone adjacent to the furcation defect, avoid-ing overlaps or folds of the material. Ideally, its co-ronal border should be placed 2 mm below thecementoenamel junction without exposing the en-trance of the furcation. This coronal portion of themembrane should be tightly adapted to the tooth bya sling suture. This assures good stability of the bar-rier and protects the underlying blood clot duringhealing. However, the presence of a concavity in 94%of the root trunk surfaces (45) may difficult theachievement of a complete seal and closure of thefurcation entrance.

Space maintenance under the membrane is oneof the basic principles of guided tissue regeneration.The achievement of an adequate space between theinner face of the membrane barrier and the root sur-faces appears to be dictated by the osseous mor-phology and the presence of a vertical component inthe furcation lesion with a retaining buccal osseousplate. It has been shown that the healing potentialand the amount of tissue regeneration are reducedin the event of a collapse of the membrane into thedefect (28, 75). The use of titanium-reinforced mem-branes (19) and the placement of bone graft substi-tute into the defect (51, 72) are both aimed to pre-vent the collapse of the membrane and thus increas-ing this space under the membrane and achievingan improved clinical result (Table 5).

185

Wound closure. In order to achieve good closure andcomplete coverage of the membrane barrier, a verti-cal mattress suturing technique has been advocated(Fig. 4).

To maximize the coronal displacement of the flap,a horizontal releasing incision in the periosteummay help when suturing the wound. However, careshould be taken not to perforate the flap and thuscompromise its blood supply.

Post-operative care. To reduce the risk of infectionand to ensure optimal healing, the patient should heinstructed not to brush or to brush the operated areagently with an ultra-soft toothbrush and to rinsewith chlorhexidine (0.2%) for a period of 4–6 weeks.During this period, frequent visits for monitoringand professional polishing are recommended. If anonresorbable barrier has been used, it should beremoved after 4–6 weeks. However, if complicationsdevelop, it may be necessary to remove it earlier.

Most of the complications are related to an inad-equate surgical procedure or to poor patient compli-ance in post-operative care. They may include flapperforation or sloughing and abscess formation.

Membrane exposure, however, is the most fre-quently reported complication. Its prevalence rangesfrom 50 to 80% (4, 17, 20, 21, 57, 74). When exposed,the membrane is immediately contaminated withbacteria (20, 21, 48, 56, 59, 73). Several clinicalstudies (20, 58, 74, 75) have demonstrated that con-tamination of exposed nonresorbable and bioresorb-able membranes are associated with reduced clinicalattachment level gains. Nowzari & Slots (58) demon-strated an inverse relationship between the numberof bacteria recovered from nonabsorbable barriermembranes and gain of probing attachment in treat-ment of furcation and interproximal periodontal de-fects. These authors (58, 59) have identified specificbacteria associated with failing periodontal re-generation, such as Porphyromonas gingivalis,Actinobacillus actinomycetemcomitans, Campylobac-tor rectus and total counts of Peptostreptococcusmicros and Capnocytophaga species. In sites exhibit-ing little or no gain in clinical attachment gain, thesebacteria were found colonizing both sides of the bar-rier membrane. Conversely, the sites demonstratingthe most gain in clinical attachment did not evi-dence bacteria on the tooth-facing surface of thebarrier membrane. Machtei et al. (49) also associatedA. actinomycetemcomitans colonization with failingregenerative therapy and Demolon et al. (22) alsofound an association between demonstration of P.gingivalis and Bacteroides forsythus on the surface of

Page 18: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

nonresorbable barrier membranes and clinical signsof inflammation.

To prevent membranes from becoming infected,efforts should be directed towards the elimination ormarked suppression of pathogens both in the treatedsite and in the rest of the mouth prior to the regene-rative surgery. After the regenerative surgery, appli-cation of local antimicrobial therapy is rec-ommended for at least 6 weeks (chlorhexidine rins-ing 0.012%). Systemic administration of antibioticssuch as amoxicillin–clavulanic acid (59) and ornida-zole (55) has been recommended in order to im-prove the clinical benefits of the regenerative pro-cedures. However, since an antibiotic agent may bemore or less efficient or resistant, depending on thespecific microbiota present, the choice of the anti-biotic should not be made on mere clinical judg-ment but rather on microbial diagnosis.

Second-stage surgery. This minor surgical pro-cedure is only performed if a nonresorbable barrierhas been used. To gain access to the barrier material,a small incision is made, extending one tooth mesialand distal of the border of the barrier. The soft tissueflap is gently reflected and the barrier material dis-sected free from the flap using a sharp blade. Duringthis procedure, it is essential not to compromise thenewly regenerated tissue (Fig. 5). At membrane re-moval a small pseudo-pocket formation is frequentlypresent at the outer surface of the barrier material.It is important that this pocket epithelium be re-moved so that gingival connective tissue is in directcontact with the newly regenerated tissue. The newlyregenerated tissue should always be completely cov-ered by the flap when suturing. Incomplete coveragehas been associated with reduced attachment andbone gain (75).

Long-term supportive care. Supportive periodontaltherapy in essential in the long-term stability of theachieved clinical outcomes.

Gottlow et al. (29) demonstrated that guidedtissue regeneration results could be maintained forup to 5 years in a patient population with goodplaque control. Cortellini et al. (18) in a 4-year study,confirmed these results and showed that the stabilityof the gained clinical attachment is dependent uponpatient compliance and plaque control. Althoughthere are no specific studies available related to thelong-term results of guided tissue regeneration infurcation defects, we may assume that, similarly tothe treatment of infrabony defects, a stringentplaque control and compliance with a frequent recall

186

system are essential for the long-term maintenanceof the results achieved (80).

Conclusions

A thorough evaluation of the efficacy of guidedtissue regeneration techniques in the treatment ofmolars with furcation defects demonstrates highvariability and unpredictability.

Depending on the therapeutic end-point, the as-sessment of this therapeutic procedure may vary. Ifthe primary objective is the complete elimination ofthe furcation defect within the inter-radicular space,thus establishing anatomic conditions that facilitateoptimal plaque control, the evaluation of the resultsshows that this outcome is rarely achieved and,when achieved, is unpredictable.

If on the contrary, we consider the more realisticobjective of reducing the magnitude of the defect,thus facilitating the patient’s plaque control andlong-term maintenance of the affected tooth, thenthe therapeutic end-point will be conversion of aclass III into class II, conversion of a class II into aclass I and the attainment of significant reductionsin vertical and horizontal attachment levels. Even inthis situation, guided tissue regeneration in class IIIfurcation lesions and maxillary class II furcationsdoes not fulfill these outcomes. Therefore, guidedtissue regeneration should not be the treatment ofchoice in these clinical indications. However, inmandibular class II furcations, mostly when there isa deep vertical component with maintenance of theinterproximal bone levels, the guided tissue re-generation procedure has demonstrated significantgains in clinical attachment levels both horizontallyand vertically. These results have not been fully con-sistent across the different studies, which may reflectthe variability in the factors, described in this chap-ter, which are inherent to this specific lesion andmay thus affect the outcome.

The predictability of this therapeutic techniquehas not improved significantly with either placementof bone graft substitutes or with the advent of newmembrane materials, such as bioresorbable barriermaterials.

Therefore, guided tissue regeneration in the treat-ment of furcation lesions, specifically in class IImandibular furcations, represents a step forward,since clear clinical improvements can be expected.However, the significance of this limited achievedgains for the long-term prognosis of the affectedtooth is not yet known, nor is the impact of this

Page 19: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

mode of therapy in the overall guarded prognosis ofteeth affected by furcation involvement. Clearly,more clinical research on this indication is needed.This research should be conducted trying to controlor limit the factors that specifically affect this lesion.

References

1. Andersson B, Bratthall G, Kullendorf F, Grondahl K, RohlinM, Attstrom R. Treatment of furcation defects. Guidedtissue regeneration versus coronally positioned flap inmandibular molars: a pilot study. J Clin Periodontol 1994:21: 211–216.

2. Anderegg CR, Martin ST, Gray JL, Mellonig JT, Gher ME.Clinical evaluation of decalcified freeze-dried bone allo-graft with guided tissue regeneration in the treatment ofmolar furcation invasions. J Periodontol 1991: 60: 264–268.

3. Anderegg CR, Metzler DG, Nicoll BK. Gingival thickness inguided tissue regeneration and associated recession at fa-cial furcation defects. J Periodontol 1995: 66: 264–268.

4. Becker W, Becker BE, Berg L, Prichard J, Caffesse R, Rosen-berg E. New attachment after treatment with root isolationprocedures: report for treated class III and class II fur-cations and vertical osseous defects. Int J Periodontics Re-storative Dent 1988: 8: 8–23.

5. Becker W, Becker BE, Mellonig J, Caffesse RG, Warrer K,Caton JG, Reid T. A prospective multi-center study evalu-ating periodontal regeneration for class II furcation in-vasions and intrabony defects after treatment with bioab-sorbable barrier membrane: 1 year results. J Periodontol1996: 67: 641–649.

6. Black BS, Gher ME, Sandifer JB, Fucini SE. Comparativestudy of collagen and expanded polytetrafluoroethylenemembranes in the treatment of human class II furcationdefects. J Periodontol 1994: 65: 598–604.

7. Blumenthal NM. A clinical comparison of collagen mem-branes with ePTFE membranes in the treatment of humanmandibular buccal class II furcation defects. J Periodontol1993: 64: 925–933.

8. Bouchard P, Ouhayun JP, Nilveus RE. Expanded polyte-trafluoroethylene membrane and connective tissue graftssupport bone regeneration for closing mandibular class IIfurcation. J Periodontol 1993: 64: 1193–1198.

9. Bouchard P, Giovannoli J-L, Mattout C, Davarpanah M, Etti-enne D. Clinical evaluation of a bioabsorbable regenerativematerial in mandibular class II furcation therapy. J ClinPeriodontol 1997: 24: 511–518.

10. Bower R. Furcation morphology relative to periodontaltreatment. Furcation entrance architecture. J Periodontol1979: 50: 23–27.

11. Caffesse RG, Smith BA, Duff B, Morrisson EC, Merrill D,Becker W. Class II furcations treated by guided tissue re-generation: case reports. J Periodontol 1990: 61: 510–514.

12. Caffesse RG, Mota LF, Quinones CR, Morrison EC. Clinicalcomparison of resorbable and non-resorbable barriers forguided periodontal tissue regeneration. J Clin Periodontol1997: 24: 747–752.

13. Carnevale G, Pontoriero R, Lindhe J. Treatment of fur-cation-involved teeth. In: Lindhe J, ed. Clinical periodonto-logy and implant dentistry. Copenhagen: Munksgaard,1997: 683–710.

187

14. Caton J, Greensten G, Zappa U. Synthetic bioabsorbablebarrier for regeneration in human periodontal defects. JPeriodontol 1994: 65: 1037–1045.

15. Christgau M, Schmalz G, Reich E, Wenzel, A. Clinical andradiographical split mouth study on resorbable versus non-resorbable GTR-membranes. J Clin Periodontol 1995: 22:306–315.

16. Cortellini P, Pini-Prato GP, Tonetti MS. Periodontal re-generation of human infrabony defects. I. Clinical meas-urements. J Periodontol 1993a: 64: 254–260.

17. Cortellini P, Pini-Prato GP, Tonetti MS. Periodontal re-generation of human infrabony defects. Re-entry pro-cedures and bone measures. J Periodontol 1993: 64: 261–268.

18. Cortellini P, Pini-Prato GP, Tonetti MS. Periodontal re-generation of human infrabony defects. Effect of oral hy-giene on long term stability. J Clin Periodontol 1994: 21:606–610.

19. Cortellini P, Pini-Prato GP, Tonetti MS. Periodontal re-generation of human infrabony defects with titanium re-inforced membranes. A controlled clinical trial. J Peri-odontol 1995: 66: 797–803.

20. De Sanctis M, Clauser C, Zucchelli G. Bacterial colonizationof resorbable barrier materials and periodontal regenera-tion. J Periodontol 1996: 67: 1193–1200.

21. De Sanctis M, Clauser C, Zucchelli G. Bacterial colonizationof barrier material and periodontal regeneration. J ClinPeriodontol 1996: 23: 1039–1046.

22. Demolon IA, Persson R, Ammons WA, Johnson RH. Effectof antibiotic treatment on clinical conditions of guidedtissue regeneration. J Periodontol 1994: 65: 1029–1036.

23. Garrett S, Martin M, Egelberg JH. Treatment of periodontalfurcation defects. Coronally positioned flap versus dura-mater membranes in class II defects. J Clin Periodontol1990: 17: 179–185.

24. Garrett S, Gantes B, Zimmerman G, Egelberg JH. Treatmentof mandibular class III periodontal furcation defects. Co-ronally positioned flap with and without ePTFE mem-branes. J Periodontol 1994: 65: 592–597.

25. Garrett S. Periodontal regeneration around natural teeth.Ann Periodontol 1996: 1: 621–666.

26. Garrett S, Polson AM, Stoller NH, Drisko CL, Caton JG, Har-rold CQ, Bogle G, Greenwell H, Lowenguth RA, Duke SP,DeRouen TA. Comparison of a bioabsorbable GTR barrierto a nonabsorbable barrier in treating human class II fur-cation defects. A multicenter parallel design randomizedsingle-blind trial. J Periodontol 1997: 68: 667–675.

27. Gottlow J, Nyman S, Karring T, Lindhe J. New attachmentformation as the result of controlled tissue regeneration. JClin Periodontol 1984: 11: 494–503.

28. Gottlow J, Nyman S, Karring T, Lindhe J. New attachmentformation in the human periodontium by guided tissue re-generation. J Clin Periodontol 1986: 21: 604–616.

29. Gottlow J, Nyman S, Karring T. Maintenance of the newattachment gained through guided tissue regeneration. JClin Periodontol 1992: 19: 315–317.

30. Greenstein G, Caton J. Biodegradable barriers and guidedtissue regeneration. Periodontol 2000 1993: 1: 36–45.

31. Heins PJ, Canter SR. Furca involvement: a classification ofbony deformities. Periodontics 1968: 6: 84–87.

32. Hirschfeld L, Wasserman B. A long term survey of toothloss in 600 treated periodontal patients. J Periodontol 1978:49: 225–237.

Page 20: Focus on furcation defects: guided tissue regeneration

Sanz & Giovannoli

33. Hou HL, Tsai CC. Types and dimensions of root trunklength correlating with diagnosis of molar furcations. J ClinPeriodontol 1997: 24: 129–135.

34. Hugoson A, Ravald N, Fornell J, Johard G, Teiwik A, GottlowJ. Treatment of class II furcation involvements in humanswith bioresorbable guided tissue regeneration barriers. Arandomised multicenter study. J Periodontol 1995: 66: 624–634.

35. Jeffcoat MK, McGuire M, Newman MG. Evidence-basedperiodontal treatment. Highlights from the 1996 WorldWorkshop in Periodontics. J Am Dent Assoc 1997: 128: 713–724.

36. Kaldahl WB, Kalkwarf KL, Patil KD, Dyer JK, Bates RE.Evaluation of four modalities of periodontal therapy: meanprobing depth, probing attachment level and recessionchanges. J Periodontol 1988: 59: 783–793.

37. Karring T, Lindhe J, Cortellini P. Regenerative periodontaltherapy. In: Lindhe J, ed. Clinical periodontology and im-plant dentistry. Copenhagen: Munksgaard, 1997: 597–647.

38. Kenney EB, Lekovic V, Elbaz JJ, Kovacvic K, Carranza FA,Takei HH. The use of porous hydroxylapatite implant inperiodontal defects. II. Treatment of class II furcationlesions in lower molars. J Periodontol 1988: 59: 67–72.

39. Laurell L, Falk H, Fomell J, Johard G, Gottlow J. Clinical useof a bioresorbable matrix barrier in guided tissue regenera-tion therapy. Case series. J Periodontol 1994: 65: 967–975.

40. Lekovic V, Kenney EB, Kovacevic K, Carranza FA. Evaluationof guided tissue regeneration in class II furcation. A clinicalre-entry study. J Periodontol 1989: 60: 694–698.

41. Lekovic V, Kenney EB, Carranza FA, Martignoni M. The useof autogenous periosteal grafts as barriers for the treatmentof class II furcation involvements in lower molars. J Peri-odontol 1991: 62: 775–780.

42. Lekovic V, Kenney EB, Carranza FA, Danilovic V. Treatmentof class II furcation defects using porous hydroxylapatite inconjuction with polytetrafluoroethylene membrane. J Peri-odontol 1990: 61: 575–578.

43. Lekovic V, Kenney EB. Guided tissue regeneration using cal-cium phosphate implants together with 4 different mem-branes. A study on furcations in dogs. J Periodontol 1993:64: 1154–1156.

44. Lindhe J, Westfelt E, Nyman S, Socransky SS, Haffajee AD.Long term effect of surgical/non surgical treatment of peri-odontal disease. J Clin Periodontol 1984: 11: 448–458.

45. Lu HKJ. Topographical characteristics of root trunk lengthrelated to guided tissue regeneration. J Periodontol 1992:63: 215–219.

46. Luepke PG, Mellonig JT, Brunsvold MA. A clinical evalu-ation of a bioabsorbable barrier with and without decalci-fied freeze-dried bone allograft in the treatment of molarfurcations J Clin Periodontol 1997: 24: 440–446.

47. Martin M, Gantes B, Garret S, Egelberg J. Treatment of peri-odontal furcation defects. 1. Review of the literature anddescription of a regenerative surgical technique. J Clin Peri-odontol 1988: 15: 227–231.

48. Machtei EE, Dunford RG, Norderyd OM, Zambon JJ, GencoRJ. Guided tissue regeneration and anti-infective therapy inthe treatment of class II furcation defects. J Periodontol1993: 64: 968–973.

49. Machtei EE, Cho MI, Dunford RG, Norderyd OM, ZambonJJ, Genco RJ. Clinical, microbiological and histological fac-tors which influence the success of regenerative peri-odontal therapy. J Periodontol 1994: 65: 154–161.

188

50. Machtei EE, Schallhorn RG. Successful regeneration ofmandibular class II furcation defects. An evidence-basedtreatment approach. Int J Periodontics Restorative Dent1995: 15: 147–167.

51. McClain PK, Schallhorn RG. Long-term assessment of com-bined osseous composite grafting, root conditioning, andguided tissue regeneration. Int J Periodontics RestorativeDent 1993: 13: 9–27.

52. McGuire M, Nunn M. The effectiveness of clinical par-ameters in accurately predicting tooth survival. J Peri-odontol 1996: 67: 666–674.

53. Mellonig JT, Seamons BC, Gray JL, Towle HJ. Clinical evalu-ation of guided tissue regeneration in the treatment ofgrade II molar furcation invasions. Int J Periodontics Re-storative Dent 1994: 14: 255–271.

54. Metzler DG, Seamons BD, Mellonig JT, Gher ME, Gray JL.Clinical evaluation of guided tissue regeneration in thetreatment of maxillary class II molar furcation invasions. JPeriodontol 1991: 62: 353–360.

55. Mombelli A, Zappa U, Bragger U, Lang NP. Systemic anti-microbial treatment and guided tissue regeneration. J ClinPeriodontol 1996: 23: 386–396.

56. Mombelli A, Lang NP, Nyman S. Isolation of periodontalspecies after guided tissue regeneration. J Periodontol1993: 64: 1171–1175.

57. Murphy KG. Postoperative healing complications associ-ated with Gore-Tex Periodontal Material. I. Incidence andcharacterization. Int J Periodontics Restorative Dent 1995:15: 363–376.

58. Nowzari H, Slots J. Microorganisms in polytetrafluoroethy-lene barrier membranes for guided tissue regeneration. JClin Periodontol 1994: 21: 203–210.

59. Nowzari H, Matian F, Slots J. Periodontal pathogens on poly-tetrafluoroethylene membranes for guided tissue regenera-tion inhibit healing. J Clin Periodontol 1995: 22: 469–474.

60. Nyman S, Lindhe J, Karring T, Rylander H. New attachmentfollowing surgical treatment of human periodontal disease.J Clin Periodontol 1982: 9: 290–296.

61. Parashis AO, Mitis FJ. Clinical evaluation of the effect oftetracycline root preparation on guided tissue regenerationin the treatment of class II furcation defects. J Periodontol1993: 64: 133–136.

62. Paul BF, Mellonig JT, Towle HJ, Gray JL. Use of a collagenbarrier to enhance healing in human periodontal furcationdefects. Int J Periodontics Restorative Dent 1992: 12: 123–131.

63. Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C.Comparison of surgical and nonsurgical treatment of peri-odontal disease. A review of current studies and additionalresults after 61⁄2 years following two methods of periodontaltherapy. J Clin Periodontol 1983: 10: 524–541.

64. Polson AM, Southard GL, Dunn RL, Polson AP, Billen JR,Laster LL. Initial study of guided tissue regeneration inclass II furcation defects after use of a biodegradablebarrier. Int J Periodontics Restorative Dent 1995: 15: 42–55.

65. Pontoriero R, Lindhe J, Nyman S, Karring R, Rosenberg E,Sanavi F. Guided tissue regeneration in degree II furcationinvolved mandibular molars. A clinical study. J Clin Peri-odontol 1988: 15: 247–254.

66. Pontoriero R, Lindhe J, Nyman S, Karring T, Rosenberg E,Sanavi F. Guided tissue regeneration in the treatment offurcation defects in mandibular molars. A clinical study of

Page 21: Focus on furcation defects: guided tissue regeneration

Focus on furcation defects: guided tissue regeneration

degree III involvements. J Clin Periodontol 1989: 16: 170–174.

67. Pontoriero R, Lindhe J. Guided tissue regeneration in thetreatment of degree II furcation defects in maxillary molars.J Clin Periodontol 1995: 22: 756–763.

68. Pontoriero R, Lindhe J. Guided tissue regeneration in thetreatment of degree III furcation defects in maxillary mo-lars. J Clin Periodontol 1995: 22: 810–812.

69. Ramfjord SP, Caffesse RG, Morrison EC, Hill RW, Kerry GJ,Appleberry EA, Nissle RR, Stults DL. Four modalities ofperiodontal treatment compared over 5 years. J Clin Peri-odontol 1987: 14: 445–452.

70. Rosenberg ES, Cutler SA. The effect of cigarette smokingon the long term success of guided tissue regeneration. Apreliminary study. Ann R Aust Coll Dent Surg 1994: 12: 89–93.

71. Sanz M, Zabalegui I, Villa A, Sicilia A. Guided tissue re-generation in human class II furcations and interproximalintrabony defects after using a bioabsorbable membranebarrier. Int J Periodontics Restorative Dent 1997: 11: 563–573.

72. Schallhorn RG, McClain PK. Combined osseous compositegraft, root conditioning, and guided tissue regeneration. IntJ Periodontics Restorative Dent 1988: 8: 9–31.

73. Selvig KA, Nilveus RE, Fitzmorris L, Kersten B, KhorsandiSS. Scanning electron microscopic observations of cellpopulation and bacterial contamination of membranesused for guided tissue regeneration. J Periodontol 1990: 61:510–520.

74. Selvig KA, Kersten B, Chamberlain AD, Wikesjo UM, Nil-

189

veus RE. Regenerative surgery of intrabony periodontal de-fects using e-PTFE membranes: scanning electronmicrosopic evaluation of retrieved membranes versus clin-ical healing. J Periodontol 1992: 63: 974–978.

75. Tonetti M, Pini-Prato G, Williams RC, Cortellini P. Peri-odontal regeneration in human infrabony defects. IV. De-terminants of healing response. J Periodontol 1993: 64:934–940.

76. Tonetti M, Pini-Prato G, Cortellini P. Effect of cigarettesmoking on periodontal healing following GTR ininfrabony defects. J Clin Periodontol 1995: 22: 229–234.

77. Van Swol R, Ellinger R, Pfeifer J, Barton N, Blumenthal N.Collagen membrane barrier therapy to guide regenerationin class II furcations in humans. J Periodontol 1993: 64:622–629.

78. Wallace SC, Gellin RG, Miller MC, Mishkin DJ. Guidedtissue regeneration with and without decalcified freeze-dried bone in mandibular class II furcation invasions. JPeriodontol 1994: 65: 244–254.

79. Wang H, O’Neal R, Thomas C, Shyr Y, McNeil R. Evaluationof an absorbable collagen membrane in treating class IIfurcation defects. J Periodontol 1994: 65: 1029–1036.

80. Weigel C, Bragger U, Hammerle C, Mombelli A, Lang NP.Maintenance of new attachment 1 and 4 years followingguided tissue regeneration. J Clin Periodontol 1995: 22:661–669.

81. Yukna R. Clinical human comparison of expanded polyte-trafluoroethylene barrier membrane and freeze dried dura-mater allografts for guided tissue regeneration of lost peri-odontal support. J Periodontol 1992: 63: 431–442.