Jan Lindhe. Clinical Periodontology

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PERIODONTAL SURGERY: ACCESS THERAPY • 555

Fig. 25-65. Diagram illustrating

the gain and loss of clinical attach

ment (Y-axis) in relation to initial

probing depth (X-axis) at

incisors,

premolars and molars, calculated

from measurements made at the

baseline examination and after 6

months. RPL = non-surgical scal-

ing and root planing. MWF =

modified Widman flap surgery.

The non-surgical approach (RPL)

consistently yielded lower critical

probing depth (CPD) values than

the surgical approach. (Data from

Lindhe et al. 1982b.)

With regard to post-treatment plaque accumula-

tion, there is no evidence to suggest that differences

exist between non-surgical or surgical treatment or

between various surgical procedures. In addition,

most studies have shown that the magnitude of gin-

givitis resolution is not influenced by the treatment

modality.

Probing pocket depth reduction

All surgical procedures result in a decrease in probing

pocket depths with greater reduction occurring at

initially deeper sites (Knowles et al. 1979, Lindhe et

al.

1984, Ramfjord et al. 1987, Kaldahl et al. 1996,

Becker

et al. 2001). Furthermore, surgical therapy

generally

creates greater short-term reduction of

probing depth than non-surgically performed scaling

and root plan-

ing. Flap surgery with bone

recontouring (pocket

elimination surgery) usually

results in the most pro-

nounced short-term pocket

reduction. Long-term (5-8

years) results show

various outcomes. Some studies

reported greater

probing depth reduction following

surgery while

others reported no differences in rela- tion to non-

surgical therapy. Also, the magnitude of

the initial probing depth reduction shows a tendency

to decrease with time, independent of treatment mo-

dality.

Clinical attachment level change

In sites with initially shallow probing depth, both

short-term and long-term data demonstrate that sur-

gery creates a greater loss of clinical attachment than

non-surgical treatment, whereas in sites with initially

deep pockets (>_ 7 mm), a greater gain of clinical attach

ment is generally obtained (Knowles et al. 1979,

Lindhe et al. 1984, Ramfjord et al. 1987, Kaldahl et al.

1996, Becker et al. 2001) (Fig. 25-64). When clinical

attachment levels following surgery with and without

osseous resection were compared, either no difference

was found between therapies or flap surgery without

osseous resection produced a greater gain. In addi-

tion, there was no difference in the longitudinal main

tenance of clinical attachment levels between sites

treated non-surgically and those treated surgically,

with or without osseous resection.

Based on data generated from a clinical trial com-

paring non-surgical and surgical (modified Widman

556 • CHAPTER 25

Gingival recession

Fig. 25-66. Longitudinal changes

in recession (REC) and clinical at

tachment levels (CAL) at sites

with initial probing depth of 6

mm following three periodontal

treatment modalities. RPL = scal-

ing and root planing. MWF =

modified Widman flap procedure.

FO = flap and osseous surgery.

(

Data from Kaldahl et al. 1996.)

Clinical attachment level

P. !nit P. Treat 1 Yr 2 Yr 3 Yr

4 Yr 5 Yr

6 Yr 7 Yr

flap) approaches to root debridement, Lindhe et al.

(

1982b) developed the concept of

critical probing depth

relation to clinical attachment level change. For

each

treatment approach, the clinical attachment

change

was plotted against the initial pocket depth

and

regression lines were calculated (Fig. 26-65). The

point where the regression line crossed the horizontal

axis (initial probing depth) was defined as the

critical

probing depth

(CPD), i.e. the level of pocket depth

below

which clinical attachment loss would occur as

the

result of the treatment procedure performed. The

CPD was consistently found to be greater for the

surgical approach than for the non-surgical treatment.

Furthermore, at incisors and premolars the surgical

therapy showed superior outcome only when the in-

itial probing depth was greater than 6-7 mm, while at

molars the corresponding cut-off point was 4.5 mm.

The interpretation of the latter finding would be that,

in the molar tooth regions, the surgical approach to

root debridement offers advantages over the non-sur-

gical approach. This interpretation is supported by the

observation that inferior results are obtained by non-

surgical therapy in molars compared to single-rooted

teeth (Nordland et al. 1987, Loos et al. 1988). Also, data

generated from studies comparing closed and open

root debridement in furcation sites favor surgical ac-

cess therapy in the treatment of molar tooth regions

(

Matia et al. 1986).

The removal of the pocket epithelium and the soft

tissue lesion by curettage (Echeverria & Caffesse 1983,

Ramfjord et al. 1987) or surgical excision (Lindhe &

Nyman 1985) is not a prerequisite for proper healing

of the treated periodontal site. In the study by Lindhe

& Nyman (1985), three treatment modalities were

used, i.e. excision of the soft tissue lesion during flap

surgery (modified Widman flap procedure), surgery

without removal of the soft tissue lesion (Kirkland

flap) and non-surgical scaling and root planing. The

1-year follow-up examination revealed about 1 mm of

gain in clinical attachment level for all three proce-

dures. Thus, deliberate excision of the soft tissue le-

sion did not improve the healing result.

Gingival recession

Gingival recession is an inevitable consequence of

periodontal therapy. Since it occurs primarily as a

result of resolution of the inflammation in the peri-

odontal tissues, it is seen following both non-surgical

and surgical therapy. Irrespective of treatment modal

ity used, initially deeper pocket sites will experience

more pronounced signs of recession of the gingival

margin than sites with initial shallow probing depths

Fig. 25-67. Schematic drawing illustrating alterations in the level of the marginal bone crest and the level of the bot-

tom of the bone defects in the test and control groups. Distance A denotes the depth of the bone defects at the initial

examination; test group 3.1 mm, control group 2.5 mm. Distance B denotes resorption of the marginal alveolar crest (

b,c), which anounted to 0.4 mm in the test patients (a) and 1.4 mm in the controls (c). Distance C denotes gain or

loss of bone in the apical portion of the defect. There was a refill of bone in test patients amounting to 2.8 mm (b),

whereas a further 0.7 mm loss of bone occurred in the control patients (c). (Data from Rosling et al. 1976a.)

(Badersten et al. 1984, Lindhe et al. 1987, Becker et al.

2001).

A general finding in short-term follow-up studies

periodontal therapy is that non-surgically per-

formed

scaling and root planing cause less gingival

recession

than surgical therapy, and that surgical treat

ment

involving osseous resection results in the most

pronounced recession. However, data obtained from

long-term studies reveal that the initial differences

seen in amount of recession between various treat-

ment modalities diminish over time due to a coronal

rebound of the soft tissue margin following surgical

treatment (Kaldahl et al. 1996, Becker et al. 2001) (Fig.

25-66). Lindhe & Nyman (1980) found that after api-

cally repositioned flap procedure the buccal gingival

margin shifted to a more coronal position (about 1

mm) during 10-11 years of maintenance. In interdental

areas denuded following surgery, Van der Velden

(

1982) found an upgrowth of around 4 mm of gingival

tissue 3 years after surgery, while no significant

change in attachment levels was observed. A similar

finding was reported by Pontoriero & Carnevale

(

2001) 1 year after apical positioned flap procedure for

crown lengthening.

Bone

fill

in angular bone defects

The potential for bone formation in angular defects

following surgical access therapy has been demon-

strated in a number of studies. Rosling et al. (1976a)

studied the healing of two-wall and three-wall angu-

lar bone defects following a modified Widman flap

procedure, including careful curettage of the bone

defect and proper root debridement, in 24 patients

with multiple osseous defects. Following active treat-

ment, patients assigned to the test group received

supportive periodontal care once every 2 weeks for a

2-year period, while the patients in the control group

were only recalled once a year for prophylaxis. Re-ex-

amination carried out 2 years after therapy demon-

strated that the patients who had been subjected to the

intensive professional tooth-cleaning regimen had ex-

perienced a mean gain of clinical attachment in the

angular bone defects amounting to 3.5 mm. Measure

ments performed on radiographs revealed a marginal

bone loss of 0.4 mm, but that the remaining portion of

the original bone defect (2.8 mm) was refilled with

bone (Fig. 25-67). All the 124 bone defects treated were

completely resolved. In the control group most of the

sites treated showed signs of recurrent periodontitis,

including further loss of clinical attachment and al-

veolar bone. Similar healing results were reported by

Polson & Heijl (1978). They treated 15 defects (two-

wall and three-wall) in 9 patients using a modified

Widman flap procedure. Following curettage of the

bone defect and root planing, the flaps were closed to

achieve complete soft tissue coverage of the defect

area. All patients were enrolled in a professional tooth

cleaning program. The healing was evaluated at a

re-

entry operation 6-8 months after the initial surgery.

Eleven of the 15 defects had resolved completely. The

healing was characterized by a combination of coronal

bone regeneration (77% of the initial depth of the

defects) and marginal bone resorption (18%). The

authors concluded that intrabony defects may pre-

dictably remodel after surgical debridement and es-

tablishment of optimal plaque control.

The results from the studies referred to demonstrate

that a significant bone fill may be obtained in two-wall

and three-wall intrabony defects at single-rooted

teeth, provided the postoperative supportive care is of

very high quality. Two recent reviews (Laurell et al.

1998, Lang 2000), focusing on the outcome of surgical

PERIODONTAL SURGERY: ACCESS THERAPY • 557

558 • CHAPTER 25

access therapy in angular bone defects, give addi-

tional information regarding expected bone regenera-

tion in angular defects following open flap debride-

ment (modified Widman flap). In the review by

Laurell et al. (1998), 13 studies were included repre-

senting a total of 278 treated defects with a mean depth

of 4.1 mm. The weighted mean bone fill in the angular

defects amounted to 1.1 mm. Lang (2000) reported an

analysis of 15 studies providing data generated from

radiographic assessments of the healing of 523 angu-

lar bone defects. Their analysis yielded a weighted

mean of 1.5 mm of bone gain. Since the included

studies in these reviews showed great variability in

bone fill, one may assume that the standard of post-

surgical plaque control varied between the studies. As

shown in the study by Rosling et al. (1976a), a

meticulous postsurgical plaque control and the close

profes

sional supervision of the patients are critical

for opti

mal healing conditions. One also has to

consider that

the potential for bone fill may differ

depending on the

morphology of the angular bone

defect. Most angular

defects appear as combinations

of one-wall, two-wall

and three-wall defects and

whereas the two-wall and three-wall component of an

angular bone defect may

show great potential for

bone fill during healing, the one-wall component will

rarely demonstrate this type

of healing.

REFERENCES

Ah, M.K.B., Johnson, G.K., Kaldahl, W.B., Patil, K.D. & Kalkwarf,

K.L. (1994). The effect of smoking on the response to peri-

odontal therapy.

Journal of Clinical Periodontology

21, 91-97.

American Dental Association and American Academy of Ortho-

paedic Surgeons (1997). Advisory statement. Antibiotic pro-

phylaxis for dental patients with total joint replacements.

Journal

the American Dental Association

128, 1004-1008.

Ariaudo, A.A. & Tyrell, H.A. (1957). Repositioning and increas-

ing the zone of attached gingiva.

Journal of Periodontology 28,

106-110.

Axelsson, P. & Lindhe, J. (1981). The significance of maintenance

care in the treatment of periodontal disease.

Journal of Clinical

Periodontology 8,

281-294.

Badersten, A., Nilveus, R. & Egelberg, J. (1981). Effect of nonsur

gical periodontal therapy. I. Moderately advanced periodon-

titis.

Journal of Clinical Periodontology 8,

57-72.

Badersten, A., Nilveus, R. & Egelberg, J. (1984). Effect of nonsur

gical periodontal therapy. II. Severely advanced periodonti

tis.

Journal of Clinical Periodontology

11, 63-76.

Becker, W., Becker, B.E., Caffesse, R., Kerry, G., Ochsenbein, C.,

Morrison, E. & Prichard, J. (2001). A longitudinal study com

paring scaling, osseous surgery and modified Widman pro-

cedures: Results after 5 years.

Journal of Peridontology 72,

1675-1684.

Blomlof, J. & Lindskog, S. (1995a). Root surface texture and early

cell and tissue colonization after different etching modalities.

European Journal Oral Sciences

103, 17-24.

Blomlof, J. & Lindskog, S. (1995b). Periodontal tissue-vitality

after different etching modalities.

Journal of Clinical Peridon-

tology 22,

464-468.

Blomlof, L., Jonsson, B., Blomlof, J. & Lindskog, S. (2000). A

clinical study of root surface conditioning with an EDTA gel.

II. Surgical periodontal treatment.

International Journal

Pe-

riodontics and Restorative Dentistry 20,

566-573.

Bowers, G.M., Chadroff, B., Carnevale, R., Mellonig, J.T., Corio,

R., Emerson, J., Stevens, M. & Romberg, E. (1989). Histologic

evaluation of new human attachment apparatus formation in

humans, Part III.

Journal of Periodontology 60,

683-693.

Bragger, U., Lauchenauer, D. & Lang, N.P. (1992). Surgical

lengthening of the clinical crown.

Journal of Clinical Periodon-

tology

19, 58-63.

Caffesse, R.G., Sweeney P.L. & Smith, B.A. (1986). Scaling and

root planing with and without periodontal flap surgery

Jour-

nal

Clinical Periodontology

13, 205-210.

Caton, J., Nyman, S. & Zander, H. (1980). Histometric evaluation

of periodontal surgery II. Connective tissue attachment levels

after four regenerative procedures.

Journal of Clinical Periodon-

tology 7,

224-231.

Caton, J.G. & Zander, H.A. (1976). Osseous repair of an infrabony

pocket without new attachment of connective tissue.

Journal

Clinical Periodontology 3,

54-58.

Cortellini, P., Pini Prato, G. & Tonetti, M.S. (1993). Periodontal

regeneration of human infrabony defects. 1. Clinical meas-

ures.

Journal of Periodontology 64,

254-260.

Cortellini, P., Pini Prato, G. & Tonetti, M.S. (1995a). Periodontal

regeneration of human intrabony defects with titanium rein-

forced membranes. A controlled clinical trial.

Journal

Perio-

don tology

66,

797-803.

Cortellini, P., Pini Prato, G. & Tonetti, M. (1995b). The modified

papilla preservation technique. A new surgical approach for

interproximal regenerative procedures.

Journal of Periodontol-

ogy 66,

261-266.

Cortellini, P., Pini Prato, G. & Tonetti, M. (1999). The simplified

papilla preservation flap. A novel surgical approach for the

management of soft tissues in regenerative procedures.

Inter-

national Journal of Periodontics and Restorative Dentistry

19,

589-599.

Dajani, AS., Taubert, K.A., Wilson, W., Bolger, A.F., Bayer, A.,

Ferrieri, P., Gewitz, M.H., Shulman, S.T., Nouri, S., Newbur-

ger, J.W., Hutto, C., Pallasch, T.J., Gage, T.W., Levison, M.E.,

Peter, G. & Zuccaro, G. Jr. (1997). Prevention of bacterial

endocarditis: recommendations by the American Heart Asso-

ciation.

Journal of the American Dental Association

128, 1142-

1151.

Echeverria, J.J. & Caffesse, R.G. (1983). Effects of gingival curet

tage when performed 1 month after root instrumentation. A

biometric evaluation.

Journal of Clinical Periodontology

10, 277

286.

Egelberg, J. (1995).

Periodontics the scientific way. Synopsis of hu-

nian clinical studies,

2nd edn. Malmo: Odonto Science, p. 113.

Engler, W.O., Ramfjord, S.P. & Hiniker, J.J. (1966). Healing fol-

lowing simple gingivectomy. A tritiated thymidine ra-

dioautographic study. I. Epithelialization.

Journal

Periodon-

tology 37,

298-308.

Fay, J.T. & O'Neal, R.B. (1984). Dental responsibility for the

medically compromised patient.

Journal of Oral Medicine 39,

218-255.

Friedman, N. (1955). Periodontal osseous surgery: Osteoplasty

and ostectomy

Journal of Periodontology 26,

257-269.

Friedman, N. (1962). Mucogingival surgery The apically reposi-

tioned flap.

Journal

Periodontology 33,

328-340.

Goldman, H.M. (1950). Development of physiologic gingival

contours by gingivoplasty

Oral Surgery, Oral Medicine and

Oral

Pathology 3,

879-888.

Goldman, H.M. (1951). Gingivectomy.

Oral Surgery, Oral Medi-

cine and Oral Pathology

4, 1136-1157.

Gottlow, J., Nyman, S., Lindhe, J., Karring, T. & Wennstrom, J.

(1986). New attachment formation in the human periodon-

PERIODONTAL SURGERY: ACCESS THERAPY • 559

tium by guided tissue regeneration.

Journal of Clinical Perio-

dontology

13, 604-616.

Grant, D.A., Stern, I.B. & Everett, F.G. (1979).

Periodontics in the

tradition of Orban and Gottlieb.

5th edn. St. Louis: C.V. Mosby

Co.

Hammarstrom, L. (1997). Enamel matrix, cementum develop-

ment and regeneration.

Journal

of Clinical Periodontology

24,

658-668.

Hamp, S.E., Rosling, B. & Lindhe, J. (1975). Effect of chlor-

hexidine on gingival wound healing in the dog. Ahistometric

study.

Journal of Clinical Periodontology

2, 143-152.

Haugen, E., Gjermo, P. & Orstavik, D. (1977). Some antibacterial

properties of periodontal dressings.

Journal of Clinical Perio-

dontology

4, 62-68.

Heijl, L., Heden, G., Svardstrom, G. & Ostgren, A. (1997). Enamel

matrix derivative (Emdogain®) in the treatment of intrabony

periodontal defects.

Journal of Clinical Periodontology

24, 705-

714.

Herrero, F., Scott, J.B., Maropis, P.S. & Yukna, R.A. (1995). Clinical

comparison of desired versus actual amount of surgical

crown lengthening.

Journal of Periodontology

66,

568-571.

Isidor, F. & Karring, T. (1986). Long-term effect of surgical and

non-surgical periodontal treatment. A 5-year clinical study.

Journal of Periodontal Research

21, 462-472.

Kaldahl, W.B., Kalkwarf, K.L. & Patil, K.D. (1993). A review of

longitudinal studies that compared periodontal therapies.

Journal of Periodontology

64, 243-253.

Kaldahl, W.B., Kalkwarf, K.L., Patil, K.D., Molvar, M.P. & Dyer,

J.K. (1996). Long-term evaluation of periodontal therapy: I.

Response to 4 therapeutic modalities.

Journal of Periodontology

67, 93-102.

Karring, T., Cumming, B.R., Oliver, R.C. & Loe, H. (1975). The

origin of granulation tissue and its impact on postoperative

results of mucogingival surgery

Journal of Periodontology

46,

577-585.

Kirkland, O. (1931). The suppurative periodontal pus pocket; its

treatment by the modified flap operation.

Journal of the Ameri-

can Dental Association

18, 1462-1470.

Knowles, J.W., Burgett, F.G., Nissle, R.R., Schick, R.A., Morrison,

E.C. & Ramfjord, S.P. (1979). Results of periodontal treatment

related to pocket depth and attachment level. Eight years.

Journal of Periodontology

50, 225-233.

Lang, N.P. (2000). Focus on intrabony defects – conservative

therapy.

Periodontology 2000

22, 51-58.

Laurell, L., Gottlow, J., Zybutz, M. & Persson, R. (1998). Treat-

ment of intrabony defects by different surgical procedures. A

literature review.

Journal of Periodontology

69,

303-313.

Lindhe, J. & Nyman, S. (1980). Alterations of the position of the

marginal soft tissue following periodontal surgery.

Journal of

Clinical Periodontology

7, 525-530.

Lindhe, J. & Nyman, S. (1985). Scaling and granulation tissue

removal in periodontal therapy.

Journal of Clinical Periodontol-

ogy

12, 374-388.

Lindhe, J., Nyman, S., Socransky, S.S., Haffajee, A.D. & Westfelt,

E. (1982b). "Critical probing depth" in periodontal therapy.

Journal of Clinical Periodontology

323-336.

Lindhe, J., Socransky, S.S., Nyman, S. & Westfelt, E. (1987).

Dimensional alteration of the periodontal tissues following

therapy.

International Journal

Periodontics & Restorative Den-

tistry 7(2),

9-22.

Lindhe, J., Westfelt, E., Nyman, S., Socransky, S.S. & Haffajee,

A.D. (1984). Long-term effect of surgical/non-surgical treat-

ment of periodontal disease.

Journal of Clinical Periodontology

11, 448-458.

Lindhe, J., Westfelt, E., Nyman, S., Socransky, S.S., Heijl, L. &

Bratthall, G. (1982a). Healing following surgical/non-surgi-

cal treatment of periodontal disease. Journal

Clinical Perio-

dontology

115-128.

Loos, B., Claffey, N. & Egelberg, J. (1988). Clinical and microbio-

logical effects of root debridement in periodontal furcation

pockets.

Journal of Clinical Periodontology

15, 453-463.

Matia, J.I., Bissada, N.P., Maybury, J.E. & Ricchetti, P. (1986).

Efficiency of scaling of the molar furcation area with and

without surgical access.

International Journal of Periodontics

and Restorative Dentistry

24-35.

Nabers, C.L. (1954). Repositioning the attached gingiva.

Journal

of Periodontology

25,

38-39.

Neuman, R. (1920).

Die Alveolar-Pyorrhoe and ihre Behandlung.

3rd

edn. Berlin: Herman Meusser.

Nordland, P. Garrett, S., Kiger, R., Vanooteghem, R., Hutchens,

L.H. & Egelberg, J. (1987). The effect of plaque control and

root debridement in molar teeth.

Journal of Clinical Periodon-

tology

14, 231-236.

Nyman, S., Lindhe, J., Karring, T. & Rylander, H. (1982). New

attachment following surgical treatment of human periodon-

tal disease.

Journal

Clinical Periodontology

290-296.

Nyman, S., Lindhe, J. & Rosling, B. (1977). Periodontal surgery

in plaque-infected dentitions.

Journal of Clinical Periodontology

4, 240-249.

O'Neil, T.C.A. (1975). Antibacterial properties of periodontal

dressings.

Journal of Periodontology

46, 469-474.

Palcanis, K.G. (1996). Surgical pocket therapy.

Annals of Periodon-

tology

1, 589-617.

Pliiss, E.M., Engelberger, PR. & Rateitschak, K.H. (1975). Effect

of chlorhexidine on dental plaque formation under periodon-

tal pack.

Journal of Clinical Periodontology

136-142.

Poison, A.M. & Heijl, L. (1978). Osseous repair in infrabony

periodontal defects.

Journal of Clinical Periodontology

5, 13-23.

Pontoriero , R. & Carnevale, G. (2001). Surgical crown lengthen-

ing: A 12-month clinical wound healing study

Journal of

Periodontology

72, 841-848.

Preber, H. & Bergstrom, J. (1990). Effect of cigarette smoking on

periodontal healing following surgical therapy

Journal of

Clinical Periodontology

17, 324-328.

Ramfjord, S.P., Caffesse, R.G., Morrison, E.C., Hill, R.W., Kerry,

G.J., Appleberry, E.A., Nissle, R.R. & Stults, D.L. (1987). Four

modalities of periodontal treatment compared over 5 years.

Journal of Periodontology

14, 445-452.

Ramfjord, S.P. & Costich, E.R. (1968). Healing after exposure of

periosteum on the alveolar process.

Journal of Periodontology

38, 199-207.

Ramfjord, S.E, Engler, W.O. & Hiniker, J.J. (1966). A ra-

dioautographic study of healing following simple gingivec

tomy

II. The connective tissue.

Journal of Periodontology

37,

179-189.

Ramfjord, S.P., Morrison, E.C., Burgett, F.G., Nissle, R.R., Schick,

R.A., Zann, G.J. & Knowles, J.W. (1982). Oral hygiene and

maintenance of periodontal support.

Journal of Periodontology

53, 26-30.

Ramfjord, S.P. & Nissle, R.R. (1974). The modified Widman flap.

Journal of Periodontology

45,

601-607.

Robicsek, S. (1884). Ueber das Wesen and Entstehen der Alveo-

lar-Pyorrhoe and deren Behandlung. The 3rd Annual Report

of the Austrian Dental Association (Reviewed in

Journal of

Periodontology

36, 265, 1965).

Robinson, R.E. (1966). The distal wedge operation.

Periodontics

4, 256-264.

Rosling, B., Nyman, S. & Lindhe, J. (1976a). The effect of systemic

plaque control on bone regeneration in infrabony pockets.

Journal of Clinical Periodontology

38-53.

Rosling, B., Nyman, S., Lindhe, J. & Jern, B. (1976b). The healing

potential of the periodontal tissue following different tech-

niques of periodontal surgery in plaque-free dentitions. A

year clinical study.

Journal of Clinical Peridontology

233-

255.

Sanz, M., Newman, M.G., Anderson, L., Matoska, W., Otomo-

Corgel, J. & Saltini, C. (1989). Clinical enhancement of post-

periodontal surgical therapy by a 0.12% chlorhexidine glu-

conate mouthrinse.

Journal of Periodontology

60,

570-576.

Scabbia, A., Cho, K.S., Sigurdsson, T.J., Kim, C.K. & Trombelli, L.

(2001). Cigarette smoking negatively affects healing response

following flap debridement surgery.

Journal of Periodontology

72, 43-49.

Schluger, S. (1949). Osseous resection – a basic principle in

560 • CHAPTER 25

periodontal surgery?

Oral Surgery, Oral Medicine and Oral

Pathology 2,

316-325.

Siana, J. E., Rex, S. & Gottrup, F. (1989). The effect of cigarette

smoking on wound healing.

Scandinavian Journal of Plastic and

Reconstructive Surgery and Hand Surgery 23,

207-209.

Stahl, S.S., Witkin, G.J., Cantor, M. & Brown, R. (1968). Gingival

healing. IT. Clinical and histologic repair sequences following

gingivectomy.

Journal of Periodontology 39,

109-118.

Takei, H.H., Han, TJ., Carranza, F.A., Kennedy, E.B. & Lekovic,

(1985). Flap technique for periodontal bone implants. Pa

pilla

preservation technique.

Journal of Periodontology

56,

204

210.

Townsend-Olsen, C., Ammons, W.F. & Van Belle, C.A.

(1985).

longitudinal study comparing apically repositioned flaps

with and without osseous surgery.

International Journal of

Periodontics & Restorative Dentistry 5(4),

11-33.

Van der Velden, U. (1982). Regeneration of the interdental soft

tissues following denudation procedures.

Journal of Clinical

Periodontology

455-459.

Vaughan, M.E. & Garnick, J.J. (1989). The effect of a

0.125%

chlorhexidine rinse on inflammation after periodontal sur-

gery

journal of Periodontology

60,

704-708.

Wachtel, H.C. (1994). Surgical periodontal therapy. In: Lang, N.P.

& Karring, T., eds.

Proceedings of the 1st European Workshop on

Periodontology.

London: Quintessence, pp. 159-171.

Waerhaug, J. (1955). Microscopic demonstration of tissue reac-

tion incident to removal of subgingival calculus.

Journal of

Periodontology

26,

26-29.

Waerhaug, J. (1978). Healing of the dentoepithelial junction fol-

lowing subgingival plaque control. II. As observed on ex-

tracted teeth.

Journal of Periodontology

49,

119-134.

Widman, L. (1918). The operative treatment of pyorrhea alveo-

laris. A new surgical method.

Svensk Tandldkaretidskrift

(re-

viewed in

British Dental Journal

293,

1920).

Wood, D.L., Hoag, P.M., Donnenfeld, O.W. & Rosenfeld, L.D.

(

1972). Alveolar crest reduction following full and partial

thickness flaps.

Journal of Periodontology

42, 141-144.

Zentler, A. (1918). Suppurative gingivitis with alveolar involve-

ment. A new surgical procedure.

Journal of the American Medi-

cal Association

71, 1530-1534.

CHAPTER

The Effect of Therapy on the

Microbiota in the

Dentogingival Region

ANNE D. HAFFAJEE, SIGMUND S. SOCRANSKY AND JAN LINDHE

Introduction

The goals of periodontal infection control

Measurement of microbiological endpoints

Treatment of periodontal biofilms

The physical removal of microorganisms –

mechanical debridement

Antibiotics in the treatment of periodontal

infections

Therapies that affect the microbial environment –

supragingival plaque removal

Combined antimicrobial therapies

Long-term effects of antimicrobial therapy

Concluding remarks

INTRODUCTION

The information in Chapter 4 indicated that the

biofilms that colonize tooth surfaces and oral soft

tissues are complex and the resident bacteria have

intriguing interactions with each other and with the

surfaces that they colonize. The data indicated that

organisms in biofilms are "worthy" adversaries for

control and /or eradication. Of concern to the therapist

in treating such dental infections is the fact that the

pathogenic species exist in very large numbers, are

widely distributed within the oral cavity and exist in

community structures (biofilms) that provide protec-

tion against host defense mechanisms and antimicro

bial agents. Further, the organisms can rapidly multi

ply and have a talent for attaching to new surfaces of

the host or to other organisms that are already at-

tached to the host; thus, spread and recolonization are

a persistent threat. Given this formidable opponent, it

is worth remembering that periodontal therapies, by

and large, have a beneficial effect in terms of arresting

progression of periodontal disease and maintaining

the periodontium. The "by and large" is a phrase that

certainly indicates that conventional, i.e mechanical

therapies, are not always successful and that alterna

tive or adjunctive methods are sometimes essential.

The purpose of this chapter is to examine the micro-

biological changes that are brought about by therapies

of different types, alone and in combination, and the

effect that these changes have on clinical outcomes in

both the short and longer-term.

The goals of periodontal infection control

The desired clinical outcomes of periodontal therapy

have been clearly defined. These include reduction in

(1) probing pocket depth, (2) the percentage of sites

that exhibit bleeding on probing, (3) suppuration, (4)

overt gingivitis, and (5) visible plaque accumulation.

Even more critical is maintaining the stability of the

periodontal attachment level as measured by probing

attachment and alveolar bone level assessments.

Given the complexity of the periodontal microbiota,

microbial therapeutic endpoints are less well defined.

Ideally, putative periodontal pathogens would be

eliminated from the oral cavity. However, this is rarely

achieved since many periodontal pathogens appear to

be indigenous species and can frequently be found in

periodontally healthy subjects albeit in lower num-

bers and proportions. Thus, the therapist is left with

the problem of lowering the numbers of pathogenic

species while maintaining or raising the level of host

compatible species. Further, these changes in the mi-

crobiota must be maintained for the life of the patient

if future disease episodes are to be prevented.

Fig. 26-1. Diagrammatic representation of methods of describing microbial changes in plaque samples. The left

panel depicts changes in counts, the middle panel changes in proportions and the right panel changes in the per-

centage of sites colonized (in this instance percentage of teeth colonized).

Measurement of microbiological endpoints

Changing the composition of the subgingival micro-

biota in a directed fashion is not easy and if the micro

biota is altered, how would the change be measured?

Fig. 26-1 presents three microbiological parameters

that have been used to describe changes in the com-

position of the subgingival microbiota after periodon-

tal therapy. The first is a measure of the change in

counts (numbers) of one or more pathogenic species.

In this method, the plaque samples are taken at one or

more sites before and after therapy, using, for instance,

scalers or paper points. The test species in the sam-

ple(s) are enumerated by cultural, microscopic, DNA

probe or immunologic techniques. In some studies,

the counts at multiple sites in a subject are averaged

prior to and after therapy and reductions identified.

In the second example, the proportion of each species

in the total sample is computed. From these data,

changes in the proportions of each species resulting

from therapy can then be determined. The third

method requires sample taking from multiple sites

within each subject. The percentage of sites colonized

by each of the pathogens is computed and the differ-

ence in prevalence determined before and after ther-

apy. Each of these measures provides different infor-

mation. Counts indicate pathogen load at the sampled

site(s) and usually are the most easily changed by

therapy. The change in proportions at a site indicates

the shifts in the composition of the sampled micro-

biota. If such shifts occur, one or more species would

be reduced in proportion, while other species increase.

The prevalence (percentage of sites colonized) is usu-

ally the most difficult parameter to change as a result

of therapy. This parameter indicates the extent of the

distribution of a species in the oral cavity and reduc-

tion in this parameter requires "elimination" of the

species from one or more sites. It must be understood

that "elimination" is dependent on the sensitivity of

the microbiological method used. Thus, cultural or

DNA probe techniques that indicate elimination of a

species really mean reduction of the species to below

detection limits of the method.

The first two techniques of microbial assessment,

e. change in counts and change in proportions of test

species, are commonly employed in therapeutic stud-

ies. The change in prevalence (percentage of sites

colonized) is less frequently employed because multi-

ple sites in the same subject must be individually

sampled and analyzed.

TREATMENT OF PERIODONTAL

BIOFILMS

At the present time, periodontal therapies designed to

affect the composition of the subgingival microbiota

can be grouped in three broad categories:

•

Physically removing microorganisms, often called

mechanical debridement

•

Attempting to kill or affect the metabolism of the

organism, such as antiseptics and antibiotics

562 • CHAPTER 26

THE EFFECT OF THERAPY ON THE MICROBIOTA IN THE DENTOGINGIVAL REGION • 563

Fig. 26-2. Bar charts of the mean counts (x 1

SEM) (left panel), mean proportions (± SEM) (middle panel) and

mean percentage of sites colonized (± SEM) (right panel) pre and 3 months post SRP for red complex species in 71

subjects (N samples = 3546). The red bar of each pair summarizes pretherapy values and the yellow bar post-ther

apy values. The significance of differences in mean counts, prevalence and percentage of sites colonized between

pre and post-therapy was determined using the Wilcoxon signed ranks test after adjusting for multiple compari

sons (Socransky et al. 1991).

• Affecting the environment (habitat) of the organ-

isms.

Other types of therapy are on the horizon, such as

possible vaccines against oral pathogens or replace-

ment therapy in which a species is introduced to the

biofilm in order to control potentially pathogenic mi-

croorganisms. These two approaches will not be dis-

cussed further, although their addition to the thera-

pist's armamentarium may eventually become real.

The physical removal of microorganisms -

mechanical debridement

Given the remarkable resistance of organisms in

biofilms to host defense mechanisms and antimicro-

bial agents, the logical first step in the control of these

organisms would be their removal by physical means.

Fortunately, biofilms in the oral cavity, unlike many

other biofilms, are readily accessible, allowing their

physical removal. Indeed, the most common form of

periodontal therapy is the removal of supragingival

and subgingival plaque by procedures such as self-

performed oral hygiene, scaling and root planing

(

SRP), sometimes combined with periodontal surgery.

Although many studies have documented the clinical

effects of SRP, few have evaluated comprehensively

the microbiological changes associated with SRP.

Studies in the earlier years emphasized use of dark-

field or phase contrast microscopy and indicated that

the proportion of spirochetes and motile rods declined

after SRP, while cocci and non-motile rods increased

(

Listgarten et al. 1978, Mousques et al. 1980, Lindhe et

al. 1983a,b, Muller et al. 1986, Lavanchy et al. 1987).

Other studies employed cultural techniques generally

on small numbers of sites and subjects, largely be-

cause of the cost in terms of labor and time. Such

studies indicated a decrease in groups of microorgan-

isms such as "black pigmented

Bacteroides"

(Pedraz-

zoli et al. 1991) or specific species such as

Porphyro-

monas gingivalis

(Sbordone et al. 1990, Ali et al. 1992)

and

Actinobacillus actinomycetemcomitans

(Ali et al.

1992). However, other studies found minimal long-

term effects of SRP on the subgingival microbiota

(

Sbordone et al. 1990) particularly for species such as

A. actinomycetemcomitan

(Sato et al. 1993, Saxen &

Asikainen 1993, Gunsolley et al. 1994, Mombelli et al.

1994, Nieminen et al. 1995). Other long-term studies

reported a decrease in the levels and prevalence of

certain species including

Bacteroides forsythus, Tre-

ponema gingivalis, Prevotella intermedia

and T.

denticola

(

Simonson et al. 1992, Rawlinson et al. 1993, Shiloah

& Patters 1994, Lowenguth et al. 1995, Takamatsu et

al. 1999, Darby et al. 2001)

The use of DNA probe techniques has permitted

larger scale studies of the effect of therapies on the

composition of the subgingival microbiota. The fol-

lowing data demonstrate the effect of SRP on the

composition of the subgingival plaque. In this study,

an extension of the study described by Haffajee et al.

(1997), 71 subjects with chronic periodontitis were

monitored clinically at six sites per tooth. Subgingival

plaque samples were taken from the mesiobuccal sur

face of each tooth and individually analyzed for their

content of 40 bacterial species using a checkerboard

DNA-DNA hybridization technique. Clinical meas-

urements and microbial samples were taken at base-

564 •

CHAPTER

Fig. 26-3. Bar chart of the mean pocket depth and at-

tachment level (± SEM) at baseline and 3 months post

SRP (N subjects = 71). The significance of differences

between pre and post-therapy visits was determined

using the Wilcoxon signed ranks test. Note that the y-

axis does not start at O.

line and 3 months after treatment, which consisted of

full mouth SRP accompanied by oral hygiene instruc-

tion. The data indicated that 37 out of 40 species

monitored did not change significantly. However,

three species of the "red" complex (see Chapter 4), B.

forsythus, P. gingivalis

and

denticola

were signifi-

cantly decreased in counts, proportions and percent-

age

of sites colonized 3 months post SRP (Fig. 26-2).

These

microbial changes were accompanied by im

proved

clincial parameters such as a significant de-crease in

mean probing pocket depth and mean prob

ing

attachment level (Fig. 26-3).

The data of this and other investigations are of

interest in the light of the discussion in Chapter 4 on

biofilms. The mechanical procedures undoubtedly re-

moved major proportions (90%) of the organisms that

colonized the tooth surface. However, given the rapid

multiplication rates of bacteria, it is not surprising that

the majority of the species returned to almost baseline

levels at 3 months. Data in the literature suggest that

the return to baseline

total counts

of microorganisms

may occur within 4-8 days after treatment (Sharawy et

al. 1966, Furuichi et al. 1992). However, certain

species

were affected by SRP. These bacterial species

might

have been diminished by the mechanical pro

cedures

and returned more slowly, in part because of

their

fastidious nature, and in part because the envi

ronment

presented by the healing tissues may have

been

changed.

Few studies have evaluated the effect of periodon

tal

surgery on the composition of the subgingival

microbiota. Rosenberg et al. (1984) used dark field

microscopy to examine the composition of the sub-

gingival microbiota after a procedure that included

open

flap curettage with some osseous recontouring

and

apical repositioning of the flaps. After surgery, the

Fig. 26-4. Plots of the mean counts (x 10

± SEM) of red complex species,

forsythus, P. gingivalis

and

denticola

baseline (B), 3 months post SRP (0 on the x-axis) and at 3, 6, 9 and 12 months post apically repositioned flap sur-

gery. 18 patients with chronic periodontitis were monitored clinically and sampled microbiologically at baseline

(B).

They then received full mouth SRP and instruction in proper home care procedures. 3 months after SRP, the

subjects were clinically and microbiologically monitored again (at time 0) to determine the effect of SRP on clinical

and microbiological parameters and to determine which areas of the mouth required periodontal surgery. The time 0

monitoring also served as the starting values for the surgical phase of treatment. The subjects then received api-

cally repositioned flap surgery at sites with PPD > 5 mm. Subjects were remonitored clinically and microbiologi-

cally at 3, 6, 9 and 12 months after the surgical treatment phase. The vertical dotted lines indicate the time of peri-

odontal surgery. Significance of differences over time was tested using the Quade test and adjusted for multiple

comparisons (Socransky et al. 1991).