Jan Lindhe. Clinical Periodontology

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ENDODONTICS AND PERIODONTICS • 343

play a crucial role in the pathogenesis of root dentin

hypersensitivity, most procedures hitherto attempted

are logically aimed to induce a block of their periph-

eral ends by an astringent or coagulating effect. Exam-

ples of agents commonly employed for both self-ap-

plied and dentist-applied treatments are strontium

chloride, sodium monofluorophosphate, sodium

fluoride, calcium hypophosphate, calcium hydroxide,

potassium nitrate, potassium oxalates, glutaralde-

hyde, stannous fluoride, cavity varnishes, and dentin-

bonding agents (for reviews see Gangarosa 1994,

Zappa 1994, Ikola 2001). Why these methods fail to

provide an effective clinical treatment result may have

several explanations. One is likely to be technical in

nature in that it is often difficult to attain a completely

dry dentin surface during the application procedure

due to continuous release of gingival fluid from the

sulcus, which is not easily restrained by compressed

air or other methods. Consequently, upon application

of an astringent agent, protein from this exudate

might primarily be brought to coagulation rather than

the tubular content. The precipitate is then easily re-

moved upon subsequent tooth cleaning measures.

Most agents furthermore may only cause a superficial

block that may be dissolved over the course of time.

Also topical applications do not address the pain

mechanisms associated with either peripheral or cen-

tral sensitization of nociceptors. Agents able to de-

crease the excitability of intradental nerves have there-

fore been proposed based on the assumption that

potassium ions released from formulations containing

potassium salts (e.g. chlorides, nitrates, citrate and

oxalates) diffuse along the dentinal tubules to inacti-

vate intradental nerve activity (Markowitz & Kim

1992, Orchardson & Peacock 1994). Recent experi-

ments employing electrophysiological recordings in

dogs, however, have shown that the effect of topical

application is weak and becomes abolished after irri-

gation (Ikola 2001). A review of clinical trials employ-

ing potassium-containing preparations in gels,

mouthwashes and toothpastes revealed inconsistent

results (Orchardson & Gillam 2000). While several

early studies reported significant reductions in sensi-

tivity to tactile and air stimuli, properly controlled

studies have shown that a significant placebo effect

operates (Orchardson & Gillam 2000), which also ap-

plies to clinical trials employing agents aimed to block

the dentinal tubules (Yates et al. 1998).

Any treatment approach to root dentin hypersensi-

tivity should be preceded by a careful analysis of

conditions that may be the cause of, or contribute to,

the symptoms. Cracked teeth including cusp frac-

tures, fractured or leaky restorations, caries, as well as

a variety of other exposures of dentin to the oral

environment, may cause pain sensations to the same

stimuli which cause root dentin hypersensitivity. An

area of exposed dentin may be more sensitive if there

is irritation of the pulp from other areas of the tooth,

for example from a leaky restoration (Narhi et al. 1994)

and enhanced treatment effect on root dentin hy-

persensitivity has actually been obtained if restora-

tions were replaced concomitantly (Hovgaard et al.

1991). Particular care should be taken to eliminate

traumatic occlusion. Furthermore, dietary advice

should be given to patients who admit excessive con-

sumption of citrus fruits, apples or any other food or

drinks that are acidic by nature.

Plaque control is an important integral part of the

prevention and treatment of root dentin hypersensi-

tivity. It has been observed clinically that, with time,

teeth in patients with excellent oral hygiene habits

develop hard, smooth and insensitive root surfaces.

Electron microscopic examination of the dentin of

such root surfaces has revealed that mineral deposits

obliterate the tubular openings (Hiatt & Johansen

1972). However, when severe symptoms of root hy-

persensitivity have emerged it is difficult to motivate

the patient to maintain the degree of plaque control

that is necessary to allow for a natural occlusion of the

dentinal tubules. In such situations an agent may be

beneficial which has a reasonable capacity to block the

tubular openings, at least temporarily, so that proper

oral hygiene measures can be reinforced. In severe

cases, where no remedy is achieved with any advice

or treatment approach, pulpectomy and root filling

may be the last resort.

Conclusion

Root dentin hypersentivity frequently develops as an

uncomfortable and sometimes difficult ailment to

treat, subsequent to scaling and root planing proce-

dures in periodontal therapy. Although the exact

mechanism is not well established, the condition is

clearly related to open dentinal tubules that allow

hydrodynamic mechanisms to elicit painful sensa-

tions upon external stimuli. Treatment planning

should consider contributory etiologic factors includ-

ing overconsumption of acidic food items. Root dentin

hypersensitivity should also be checked against other

conditions that can cause similar symptoms, e.g.

cracked teeth (Fig. 14-21). A large number of therapeu

tic techniques are available that seek to block the

tubular openings. Most of these agents induce at least

a temporary block so that proper oral hygiene meas-

ures can be reinforced for a natural occlusion of the

dentinal tubules.

344 • CHAPTER 14

Fig. 14-30. Gingival swelling at the buccal aspect of tooth #11 (a). Radiographic appearance of the area. Note the

advanced destruction of alveolar bone along the mesial aspect of the root (arrowheads) (b). Healing of the area

7 months following periodontal treatment (c). Courtesy of Dr Harald Rylander.

ENDODONTIC CONSIDERATIONS

IN ROOT RESECTION OF

MULTIROOTED TEETH IN

PERIODONTAL THERAPY

Treatment of periodontally diseased, multirooted

teeth may involve separation and extraction of one or

two roots (see Chapter 29). As a rule, endodontic

treatment of the root to be retained should be per-

formed prior to surgery. Information will thus be

gained regarding the effect of the endodontic treat-

ment before alternative roots are extracted. This rule

should be followed for teeth with both vital and non-

vital pulps. The root canals of molars are sometimes

difficult to prepare, in particular when the tooth has

been exposed to longstanding periodontal disease.

Such teeth may harbor mineralizations (pulp stones,

dystrophic calcifications, reparative dentin forma-

tions) that make proper endodontic treatment precari-

ous. In multirooted teeth with advanced periodontal

destruction, it is not always possible to decide before

surgery which root(s) can be preserved. As an alter-

nate to permanent filling of all root canals in such

teeth, pulpectomy may be performed and the canals

may be temporarily filled with calcium hydroxide.

Each of the canal orifices is then sealed with a tempo-

rary, bacteria tight cement. Root separation can thus

be performed without bacterial contamination of the

root canals. Permanent root filling of the root(s)

retained is performed after surgery.

DIFFERENTIAL DIAGNOSTIC

CONSIDERATIONS

It is clear from the previous text that during treatment

of periodontal disease one is not infrequently pre-

sented with the dilemma of accurately assessing the

contribution of an endodontic infection to deep peri-

odontal pockets. In this chapter, several examples of

lesions in the periodontium have been presented

which are not associated with periodontal disease.

Two cases are described below showing clinical and

radiographic symptoms similar to those of an acute

endodontic condition. The cases demonstrate that di-

agnostic entities such as location, form and extension

of radiolucencies, clinical symptoms of pain or swel-

ling, and increased probing depths are not always

accurate diagnostic criteria for differentiating a peri-

odontal lesion from an endodontic disorder.

The clinical photograph in Fig. 14-30 shows swel-

ling of the marginal gingiva on the buccal aspect of

tooth #11. The swelling had for a few days been pre-

ceded by severe throbbing pain. Radiographic exami-

nation (Fig. 14-30a) disclosed the presence of an angu-

lar bony defect that involved the apical portions of the

tooth. In this case the pulp demonstrated vital signs

upon testing, indicating that the pathologic condition

was not of endodontic origin. Pocket debridement

was combined with irrigation with 0.2% chlor-

hexidine digluconate solution and systemic admini-

stration of an antibiotic. The lesion healed rapidly.

Seven months after treatment new bone had formed

around the apex and along the mesial root surface (

Fig. 14-30c). This case demonstrates that the peri-

odontal destruction observed was caused by peri-

odontal disease.

Fig. 14-31 illustrates another case of differential

diagnostic interest. A radiograph taken of the front

tooth region of the mandible demonstrates bone loss

associated with the apex of tooth #31 in addition to a

generalized horizontal loss of alveolar bone (Fig. 14-

31a). The form and extension of the apical radiolu-

cency around tooth #31 are similar to those resulting

from an endodontic lesion. Clinically, a deep peri-

odontal pocket could be probed along the distobuccal

root surface. The patient had been on a recall program

after treatment for periodontal disease and had pre-

viously shown excellent gingival conditions. Sensibil-

ity tests indicated that the pulp was vital. Therefore,

endodontic treatment was not performed. Following

ENDODONTICS AND PERIODONTICS • 345

Fig. 14-31. Advanced destructions of alveolar bone including an angular bone defect simulating an endodontic

periapical lesion around tooth #31 (a). The pulp responded vital on testing and the tooth was therefore not

subjected to endodontic therapy but only to periodontal treatment. On raising a flap (d) the lesion was at the

buccal aspect and obviously had not destroyed the neuro-vascular supply of the pulp as evidenced by the

healing of the lesion in 6 months (b) and deposition of hard tissue in the pulp, which became obvious 2 years

after therapy (c). Courtesy of Dr Ingvar Magnusson.

elevation of a mucoperiosteal flap, an angular bone

defect was found at the buccal aspect of the root but

without involving the root tip. The wound area was

debrided along with scaling of the root surface. Rapid

bone fill followed after surgery (Fig. 14-31b) and the

pulp maintained its vitality, although later the root

canal became obliterated by hard tissue repair, most

likely as a consequence of the surgical procedure (Fig

14-31c). The mechanism behind the apically posi-

tioned radiolucency in Fig 14-31a is explained by su-

perimposition of the buccal loss of alveolar bone on

the root tip of tooth #31, which went beyond its most

apical level (Fig. 14-32).

These two cases demonstrate that neither clinical

symptoms nor radiographic findings invariably lead

to a correct diagnosis. The only significant observation

for the differential diagnosis was pulp vitality. Pulp

vitality means that the pulp chamber is occupied by

connective tissue supplied by nerves and blood ves-

sels. Sensory nerve function is normally present. Vital

pulp tissue may or may not be subjected to inflamma-

tory and degenerative tissue changes. In most situ-

ations its vitality must be determined by indirect

means and such measures are based on the assump-

tion that a vital pulp is able to respond to sensory

stimuli such as mechanical, thermal and electric

stimulation. This means that the sensibility of the pulp

is tested rather than the

vitality

of the tissue. There is

ample documentation to support the concept that a

tooth which responds to sensory stimuli has vital

functions. Conversely, if a tooth does not respond to

sensory stimuli, the pulp may be non-vital. It must be

recognized that both false positive and false negative

readings occur (Seltzer et al. 1963b, Mumford 1964,

Peters et al. 1994). Therefore, a combination of differ-

ent test methods should always be used to ensure a

correct diagnosis. Pulpal sensibility can be examined

by thermal stimulation with the use of ethyl chloride,

carbon dioxide snow, ice, or heated gutta-percha sticks

and by the use of electric stimulation with a pulp

tester.

Conclusion

It is important to remember that the recognition of

pulp vitality is essential for a differential diagnosis

and for the selection of primary measures for treat-

346 • CHAPTER 14

Fig. 14-32. The drawing attempts to picture a potential

mechanism for the radiographic radiolucency in Fig 14

-31a. Due to the periodontal infection a substantial

amount of the supporting tissue was broken down. Yet

the neuro-vascular supply of the pulp was not en-

gaged. The appearance of an apical lesion is explained

by the superimposition of the alveolar bone destruc-

tion at the buccal aspect of the tooth. Courtesy of Dr

Mats Joatell.

ment of inflammatory lesions in the marginal and

apical periodontium. Deep restorations, dental

trauma, endodontic treatment, previous pulp cap-

ping, etc., are factors to consider when assessing the

need for endodontic treatment as a part of the overall

periodontal therapy. Location, form and extension of

radiolucencies, as well as clinical symptoms of pain,

tenderness, abscess formation, increased probing

depth, etc., may not always distinguish a periodontal

lesion from an endodontic lesion.

TREATMENT STRATEGIES FOR

COMBINED ENDODONTIC AND

PERIODONTAL LESIONS

Occasionally, endodontic and periodontal lesions may

affect one and the same tooth. Lesions may be totally

separated from each other and present no extraordi-

nary therapeutic consideration. In a few other situ-

ations there is no obvious demarcation between the

two lesions, which both radiographically and clini-

cally appear as one lesion (see Figs. 14-5 and 14-12b,c).

This type of combined lesion defect may be identified

by probing along the root to the apical region of the

tooth.

Treatment of combined endodontic and periodon-

tal lesions does not differ from the treatment given

when the two disorders occur separately. The part of

the lesion sustained by the root canal infection can

usually be expected to resolve after proper endodontic

treatment (Figs. 14-5b,14-12d-f). The part of the lesion

caused by the plaque infection may also heal follow-

Table 14-1. Treatment strategies

Cause

Condition

Treatment

of the pulp

Non-vital

Endodontic

Vital

Periodontal

Non-vital

Endodontic - first observe

the

result of this therapy and

institute periodontal therapy

later if necessary

ing periodontal therapy, although little or no regen-

eration of the attachment apparatus can be expected

(see Chapter 28). This suggests that the larger the part

of the lesion caused by the root canal infection, the

more favorable the prognosis is for regeneration of the

attachment apparatus. It is important to realize that it

is clinically not possible to determine the extent to

which one or the other of the two disorders (endodon

tic or periodontal) has affected the supporting

tissues. Therefore, the treatment strategy must be first

to focus on the pulpal infection and to perform

debridement and disinfection of the root canal

system. The second phase includes a period of

observation whereby the extent of periodontal

healing resulting from the endodontic treatment is

followed. Reduced probing depth can usually be

expected within a couple of weeks while bone

regeneration may require several months before it

can be radiographically detected. Thus, periodontal

therapy including deep scaling with and without

periodontal surgery should be postponed until the

result of the endodontic treatment can be properly

evaluated (Figs. 14-5, 14-12).

Endodontic

Periodontal

Endodontic/

periodontal

ENDODONTICS AND PERIODONTICS • 347

Conclusion

It should be understood that periodontal disease may

be responsible for the entire loss of the supporting

apparatus around a tooth (see Fig. 14-30) and may in

addition be the cause of the breakdown of the pulpal

tissue. In such cases endodontic treatment will not

contribute to periodontal healing and the problem

will have to be solved by a periodontal treatment

approach (Fig. 14-30). When there is doubt as to

whether a lesion in the periodontium is of endodontic

or periodontal origin, or both, the treatment strategy

listed in Table 14-1 may be followed.

REFERENCES

Absi, E.G., Addy, M. & Adams, D. (1987). Dentine hypersensitiv-

ity A study of the potency of dentinal tubules in senstitive and

non-sensitive cervical dentin.

Journal of Clinical Periodontology

14, 280-284.

Addy, M., Absi, E.G. & Adams, D. (1987). Dentine hypersensitiv-

ity. The effects in vitro of acids and dietary substances on

root-planed and burred dentine.

Journal

Periodontology

14,

274-279.

Adriaens, P.A., De Boever, J.A. & Loesche, W.J. (1988). Bacterial

invasion in root cementum and radicular dentin of periodon-

tally diseased teeth in humans.

Journal

Periodontology

59,

222-230.

Alhadainy, H.A. (1994). Root perforations. A review of literature.

Oral Surgery 78,

368-374.

Andersson, L., Blomlof, L., Lindskog, S., Feiglin, B. & Hammar-

strom, L. (1984). Tooth ankylosis. Clinical, radiographic and

histological assessments.

International Journal of Oral Surgery

13, 423-431.

Andersson, L., Lindskog, S., Blomlof, L., Hedstrom, K-G. &

Hammarstrom, L. (1985). Effect of masticatory stimulation on

dentoalveolar ankylosis after experimental tooth replanta-

tion. Endodontics and Dental Traumatology 1, 13-16.

Andreasen, J.O. (1975). Periodontal healing after replantation of

traumatically avulsed human teeth. Assessment by mobility

testing and radiography. Acta Odontologica Scandinavica 33,

325-335.

Andreasen, J. O. (1981). Relationship between surface and in-

flammatory resorption and changes in the pulp after replan-

tation of permanent incisors in monkeys.

Journal of Endodon-

tics 7, 294-301.

Andreasen, J.O. (1985). External root resorptions: its implication

in dental traumatology, paedodontics, periodontics, ortho-

dontics and endodontics.

International Journal

Endodontics 8,

109-118.

Andreasen, J.O. & Andreasen, F.M. (1992). Root resorption fol-

lowing traumatic dental injuries.

Proceedings of the Finnish

Dental Society 88, Suppl. 1, 95-114.

Andreasen, J.O. & HjOrting-Hansen, E. (1966). Replantation of

teeth. I. Radiographic and clinical study of human teeth

replanted after accidental loss. Acta Odontologica Scandinavica

24, 263-286.

Andreasen, J.O. & Kristerson, L. (1981). Evaluation of different

types of autotransplanted connective tissues as potential peri-

odontal ligament substitutes.

International Journal of Oral Sur-

gery 10, 189-201.

Andreasen, F.M., Sewerin, I., Mandel, U. & Andreasen, J.O.

(1987). Radiographic assessment of simulated root resorption

cavities. Endodontics and Dental Traumatology 3, 21-27.

Andreasen, J.O. & Skougaard, M. (1972). Reversibility of surgi-

cally induced dental ankylosis in rats.

International Journal of

Oral Surgery

1, 98-102.

Antrim, D.D., Hicks, M.L. & Altaras, OF. (1982). Treatment of

subosseous resorption: a case report.

Journal of Endodontics 8,

567-569.

Arens, D.E. & Torabinejad, M. (1996). Repair of furcal perfora-

tions with mineral trioxide aggregate: two case reports.

Oral

Surgery 82, 84-88.

Babal, P., Soler, P., Brozman, M., Jakubovsky, J., Beyly, M. &

Basset, F. (1987). In situ characterization of cells in periapical

granuloma by monoclonal antibodies.

Oral Surgery 64,

348-

352.

Baumgartner, J.C. & Falkler, W.A. (1991). Bacteria in the apical 5

mm of infected root canals.

Journal of Endodontics

17, 380-383.

Beavers, R.A., Bergenholtz, G. & Cox, C.F. (1986). Periodontal

wound healing following intentional root perforations in

permanent teeth of

Macaca mulatto. International Journal of

Endodontics 19, 36-44.

Bender, I.B. & Seltzer, S. (1972). The effect of periodontal disease

on the pulp.

Oral Surgery 33,

458-474.

Bergenholtz, G. (1974). Micro-organisms from necrotic pulp of

traumatized teeth. Odontologick Reny 25, 347-358.

Bergenholtz, C. (2000). Evidence for bacterial causation of ad-

verse pulpal responses in resin-based dental restorations.

Critical Reviews in Oral Biology and Medicine 11, 467-480.

Bergenholtz, G., Lekholm, U., Liljenberg, B. & Lindhe, J. (1983).

Morphometric analysis of chronic inflammatory periapical

lesions in root filled teeth.

Oral Surgery 55,

295-301.

Bergenholtz, G. & Lindhe, J. (1975). Effect of soluble plaque

factors on inflammatory reactions in the dental pulp. Scandi-

navian Journal of Dental Research 83,

153-158.

Bergenholtz, G. & Lindhe J. (1978). Effect of experimentally

induced marginal periodontitis and periodontal scaling on the

dental pulp.

Journal of Clinical Periodontology 5,

59-73.

Bergenholtz, G. & Nyman, S. (1984). Endodontic complications

following periodontal and prosthetic treatment of patients

with advanced periodontal disease.

Journal of Periodontology

55, 63-68.

Bissada, N.F. (1994). Symptomatology and clinical features of

hypersensitive teeth.

Archives

Oral Biology 39, Suppl., 113S-119S.

Orchardson, R., & Peacock, J.M. (1994). Factors affecting nerve

excitability and conduction as a basis for desensitizing den-

tine.

Archives of

Oral Biology 39, Suppl., 81S-86S.

Oyama, T. & Matsumoto, K. (1991). A clinical and morphological

study of cervical hypersensitivity.

Journal

of Endodontics 17,

500-502.

Pashley, D.H. (1996). Dynamics of the pulpo-dentin complex.

Critical Reviews in Oral Biology & Medicine 7, 104-133.

Perlich, MA., Reader, A. & Foreman, D.W. (1981). A scanning

electron microscopic investigation of accessory foramens on

the pulpal floor of human molars.

Journal

of Endodontics 7,

402-406.

Peters, D.D., Baumgartner, J.C. & Lorton L. (1994). Adult pulpal

diagnosis. I. Evaluation of the positive and negative re-

sponses to cold and electrical pulp tests.

Journal

of Endodontics

20, 506-511.

Petersson, K., Hasselgren, G. & Tronstad, L. (1985). Endodontic

350 • CHAPTER 14

treatment of experimental root perforations in dog teeth.

Endodontics and Dental Traumatology 1, 22-28.

Pierce, A.M., Lindskog, S. & HammarstrOm, L.E. (1991). Osteo-

clasts: structure and function. Electron Microscopical Revue 4,

1-5.

Pineda, F. & Kuttler, Y. (1972). Mesiodistal and buccolingual

roentgenographic investigation of 7,275 root canals.

Oral

Sur

gery 33, 101-110.

Pitts, D.L. & Natkin, E. (1983). Diagnosis and treatment of verti-

cal root fractures.

Journal of Endodontics

9, 338-346.

Randow, K. & Glantz, E-O. (1986). On cantilever loading of vital

and non-vital teeth. An experimental clinical study.

Acta

Odontologica Scandinavica

44, 271-277.

Randow, K., Glantz, P.O. & Zoger, B. (1986). Technical failures

and some related clinical complications in extensive fixed

prosthodontics. An epidemiological study of long-term clini-

cal quality. Acta Odontologica Scandinavica 44, 241-255.

Rankow, H.J. & Krasner, P.R. (1996). Endodontic applications of

guided tissue regeneration in endodontic surgery

Journal of

Endodontics 22, 34-43.

Reeh, E.S., Messer, H.H. & Douglas, W.H. (1989). Reduction in

tooth stiffness as a result of endodontic and restorative pro-

cedures.

Journal of Endodontics

15, 512-516.

Rod an, G.A. & Martin, T.J. (1981). Role of osteoblasts in hormo

nal control of bone resorption. A hypothesis. Calcified Tissue

Research 33, 349-355.

Rubach, W.C. & Mitchell, D.F. (1965). Periodontal disease, acces

sory canals and pulp pathosis.

Journal of Periodontology

36,

34-38.

Sasaki, T., Shimizu, T., Watanabe, C. & Hiyoshi, Y. (1990). Cellular

roles in physiological root resorption of deciduous teeth in the

cat.

Journal of Dental Research

69, 67-74.

Schwartz, R.S., Mauger, M., Clement, D.J. & Walker, W.A. 3rd

(1999). Mineral trioxide aggregate: a new material for endo-

dontics. Journal of American Dental Association 130, 967-975.

Sedgley, C.M. & Messer, H.H. (1992). Are endodontically treated

teeth more brittle.

Journal of Endodontics

18, 332-335.

Seltzer, S., Bender, I.B. & Ziontz, M. (1963a). The interrelationship

of pulp and periodontal disease.

Oral Surgery

16, 1474-1490.

Seltzer, S., Bender, I.B. & Ziontz, M. (1963b). The dynamics of

pulp inflammation: correlations between diagnostic data and

actual histologic findings in the pulp.

Oral Surgery

16, 1846-

1871.

Sessle, B.J. (2000). Acute and chronic craniofacial pain: Brainstem

mechanism of nociceptive transmission and neuroplasticity,

and their clinical correlates. Critical Reviews in Oral Medicine

and Biololgy 11, 962-981.

Seward, G.R. (1963). Periodontal disease and resorption of teeth.

British Dental Journal

34, 443-449.

Stashenko, P. (1990). Role of immune cytokines in the pathogene-

sis of periapical lesions. Endodontics and Dental Traumatology

6, 89-96.

Stashenko, P., Teles, R. & D'Souza, R. (1998). Periapical inflam-

matory responses and their modulation. Critical Reviews in

Oral Biology and Medicine 9, 498-521

Stashenko, P, Wang, C.Y., Riley, E., Wu, Y, Ostroff, G. & Nieder

man, R. (1995). Reduction of infection-stimulated periapical

bone resorption by the biological response modifier PGG

Glucan.

Journal of Dental Research

74, 323-330.

Stashenko, P. & Yu, S.M. (1989). T-helper and T suppressor cell

reversal during the development of induced rat periapical

lesions.

Journal of Dental Research

68, 830-834.

Stenvik, A. & Mjor, I.A. (1970). Pulp and dentin reactions to

experimental tooth intrusion. American Journal of Orthodontics

57, 370-385.

Stromberg, T., Hasselgren, G., Bergstedt, H. (1972). Endodontic

treatment of traumatic root perforations in man.

Swedish Den-

tal Journal

65, 457-466.

Sundqvist, G. (1976). Bacteriologic studies of necrotic dental pulps.

Umea University Odontological Dissertation #7.

Sundqvist, G. (1990). Endodontic microbiology. In: Spangberg,

L.S.W., ed. Experimental endodontology. Boca Raton, FL: CRC

Press, pp. 131-153.

Sundqvist, G. (1994). Taxonomy, etiology, and pathogenecity of

the root canal flora.

Oral Surgery

78, 552-530.

Syed, S.A., Bergenholtz, G., Cox, C.F. & Loesche, W.J. (1982).

Microbiological and histopathological correlation of induced

periapical lesions in monkeys.

Journal of Dental Research

61,

IADR Abstract 251.

Tammaro, S., WennstrOm, J. & Bergenholtz, G. (2000). Root

dentin sensitivity following non-surgical periodontal treat-

ment.

Journal of Clinical Periodontology

27, 690-697.

Tamse, A., Fuss, Z., Lustig, J., Ganor, Y. & Kaffe, I. (1999a).

Radiographic features of vertically fractured, endodontically

treated maxillary premolars.

Oral Surgery

88, 348-352.

Tamse, A., Fuss, Z., Lustig, J & Kaplavi, J. (1999b). An evaluation

of endodontically treated vertically fractured teeth.

Journal of

Endodontics 25, 506-508.

Taylor, PE., Byers, M.R. & Redd, P.E. (1988). Sprouting of CGRP

nerve fibers in response to dentin injury in rat molars. Brain

Research 461, 371-376.

Ten Cate, A.R. (1972). The epithelial cell rests of Malassez and

the genesis of the dental cyst.

Oral Surgery

34, 956-964.

Testori, T., Badino, M. & Castagnola, M. (1993). Vertical root

fractures in endodontically treated teeth.

Journal of Endodon-

tics 19, 87-90.

Thilo, B.E., Baehni, P. & Holz, J. (1986). Dark-field observation of

the bacterial distribution in root canals following pulp ne-

crosis.

Journal of Endodontics

12, 202-205.

Torabinejad, M. & Kettering, J.D. (1985). Identification and rela

tive concentration of B and T lymphocytes in human chronic

periapical lesions.

Journal of Endodontics

11, 122-125.

Torabinejad, M. & Kiger, R.D. (1985). A histologic evaluation of

dental pulp tissue of a patient with periodontal disease.

Oral

Surgery 59, 198-200.

Torabinejad, M., Pitt Ford, T.R., McKendry, D.J., Abedi, H.R.,

Miller, D.A. & Kariyawasan, S.P. (1997). Histologic assess-

ment of mineral trioxide aggregate as a root-end filling mate-

rial in monkeys.

Journal of Endodontics

23, 225-228.

Waltimo, T.M., Siren, E.K., Torkko, H.L., Olsen, I. & Haapasalo,

M.P. (1997). Fungi in therapy-resistant apical periodontitis.

International Endodontic Journal

30, 96-101.

Walton, R.E., Michelich, R.J. & Smith, G.N. (1984). The his-

topathogenesis of vertical root fractures.

Journal of Endodontics

10, 48-56.

Warfvinge, J. & Bergenholtz, G. (1986). Healing capacity of hu-

man and monkey dental pulps following experimentally in-

duced pulpitis. Endodontics and Dental Traumatology 2, 256-

262.

Wasfy, M.O., McMahon, K.T., Minah, G.E. & Falker Jr., W.A. (

1992). Microbiological evaluation of periapical infections in

Egypt. Oral Microbiology and Immunology 7, 100-105.

Wedenberg, C. & Lindskog, S. (1985). Experimental internal

resorption in monkey teeth.

Endodontics and Dental Traumatol-

ogy

1, 221-227.

Vaes, G. (1968). On the mechanism of bone resorption: the action

of parathyroid hormone on the excretion and synthesis of

lysosomal enzymes and the extracellular release of acid by

bone cells. Journal of Cell Biology 39, 676-697.

Vaes, G. (1988). Cellular biology and biochemical mechanism of

bone resorption.

Clinical Orthopedics

23, 239-271.

Vertucci, F.J. & Williams, R.G. (1974). Furcation canals in the

human mandibular first molar.

Oral Surgery

38, 308-314. Yang,

S.F., Rivera, E.M. & Walton, R.E. (1995). Vertical root

fracture in nonendodontically treated teeth.

Journal of Endo-

dontics 21, 337-339.

Yates, R., Owens, R., Jackson, R., Newcombe, R.G. & Addy M. (

1998). A split mouth placebo-controlled study to determine

the effect of amorphous calcium phosphate in the treatment

of dentine hypersensitivity.

Journal of Clinical Periodontology

25, 687-692.

Yoshiyama, M., Masada, A., Uchida, A. & Ishida, H. (1989).

ENDODONTICS AND PERIODONTICS • 351

Scanning electron microscopic characterization of sensitive

vs. insensitive human radicular dentin.

Journal of Dental Re-

68, 1498-1502.

Yoshiyama, M., Noiri, Y, Ozaki, K., Uchida, A., Ishikawa, Y. &

Ishida, H. (1990). Transmission electron microscopic charac-

terization of hypersensitive human radicular dentin. Journal of

Dental Research 69, 1293-1297.

Yu, S.M. & Stashenko, P. (1987). Identification of inflammatory

cells in developing rat periapical lesions.

Journal of Endodon-

tics 13, 535-540.

Zappa, U.

(1994).

Self-applied treatments in the management of

dentine hypersensitivity. Archives of Oral Biology 39, Suppl.,

107S-112S.

CHAPTER 15

Trauma from Occlusion

JAN LINDHE, STURE NYMAN AND INGVAR ERICSSON

Definition and terminology

Trauma from occlusion and

plaque-associated periodontal disease

Analysis of human autopsy material

Clinical trials

Animal experiments

Conclusions

DEFINITION AND TERMINOLOGY

Trauma from occlusion

is a term used to describe

pathologic alterations or adaptive changes which de-

velop in the periodontium as a result of undue force

produced by the masticatory muscles.

Trauma from

occlusion

is only one of many terms that have been

used to describe such alterations in the periodontium.

Other terms often used are:

traumatizing occlusion,

occlusal trauma, traumatogenic occlusion, periodontal

traumatism, overload,

etc. In addition to producing

damage in the periodontal tissues, excessive occlusal

force may also cause injury in, for example, the tern-

poromandibular joint, the masticatory muscles, the

pulp tissue. This chapter deals exclusively with the

effects of

trauma from occlusion

on the periodontal

tissues.

Trauma from occlusion

was defined by Stillman

(

1917) as "a condition where injury results to the

supporting structures of the teeth by the act of bring-

ing the jaws into a closed position". WHO in 1978

defined

trauma from occlusion

as "damage in the peri-

odontium caused by stress on the teeth produced

directly or indirectly by teeth of the opposing jaw". In

"Glossary of Periodontic Terms" (American Academy

of Periodontology 1986),

Occlusal Trauma

was defined

as "An injury to the attachment apparatus as a result

of excessive occlusal force".

Traumatizing forces may act on an individual tooth

or on groups of teeth in premature contact relation-

ship; may occur in conjunction with parafunctions

such as clenching and bruxism, in conjunction with

loss or migration of premolar and molar teeth with an

accompanying, gradually developing spread of the

anterior teeth of the maxilla, etc.

In the literature, the tissue injury associated with

trauma from occlusion

is often divided into

primary

and

secondary.

The

primary

form includes a tissue reaction

(

damage), which is elicited around a tooth with nor-

mal height of the periodontium, while the

secondary

form is related to situations in which occlusal forces

cause injury in a periodontium of reduced height. The

distinction between a

primary

and

a secondary

form of

injury —

primary

and

secondary occlusal trauma —

serves

no meaningful purpose, since the alterations which

occur in the periodontium as a consequence of trauma

from occlusion are similar and independent of the

height of the target tissue, i.e. the periodontium. It is,

however, important to understand that symptoms of

trauma from occlusion

may develop only in situations

when the magnitude of the load elicited by occlusion

is so high that the periodontium around the exposed

tooth cannot properly withstand and distribute the

resulting force with unaltered position and stability of

the tooth involved. This means that in cases of severely

reduced height of the periodontium even compara-

tively small forces may produce traumatic lesions or

adaptive changes in the periodontium.

TRAUMA FROM OCCLUSION AND

PLAQUE-ASSOCIATED

PERIODONTAL

DISEASE

Ever since Karolyi (1901) postulated that an interac-

tion may exist between

"trauma from occlusion"

and

alveolar pyrrohea"

different opinions have been pre-

sented in the literature regarding the validity of this

claim. Already in the 1930s Box (1935) and Stones

(

1938) reported experiments in sheep and monkeys,

the result of which seemed to indicate that "trauma

from occlusion is an etiologic factor in the production

of that variety of periodontal disease in which there is