Jan Lindhe. Clinical Periodontology

Подождите немного. Документ загружается.

ENDODONTICS AND PERIODONTICS • 333

for direct visual examination (Fig. 14-19e,f; Walton et

al. 1984).

Data on prevalence of vertical root fractures are

scarce in the literature. While the prevalence appears

to be low, vertical root fractures probably occur more

often than clinicians are able to diagnose (Tamse et al.

1999b). There seems to be an overrepresentation of

endodontically treated teeth compared to teeth with

vital pulps (Fig. 14-21), with molars and premolars

more often affected than incisors and canines (Meister

et al. 1980, Testori et al. 1993). In longitudinal clinical

follow-up studies of patients treated with fixed pros-

theses, vertical root fractures were frequent in root-

filled teeth with posts and, in particular, among those

teeth serving as terminal abutments in cantilever

bridges (Randow et al. 1986).

It is of clinical interest to note that root fracture of

endodontically treated teeth may occur and/or be

diagnosed several years after the completion of endo-

dontic therapy and final restoration of the tooth (Fig.

14-19). In a study comprising 32 vertical root fractures,

the average time between the completion of endodon-

tic treatment and diagnosis of fracture was 3.25 years,

with a range varying between 3 days and 14 years (

Meister et al. 1980). In another study comprising 36

teeth, symptoms of root fracture developed on aver-

age more than 10 years after completion of treatment

(Testori et al. 1993).

Although the subject of considerable study, the eti-

ology of vertical root fractures is not well established.

In some situations the cause is undoubtedly iatrogenic

from pin and post placements, root canal filling pro-

cedures, and seating of intracoronal restorations. Re-

sults of experimental studies suggest that loss of tooth

structure from caries, trauma and restorative proce-

dure weakens teeth and makes them susceptible to

fracture from mastication forces (Reeh et al. 1989,

Sedgley & Messer 1992). The reason vertical root frac

tures appear to be associated with endodontically

treated teeth may be that the access opening prepara-

tion as well as overzealous root canal preparation

results in substantial loss of fracture resistance. It has

also been speculated that, along with loss of vital pulp

tissue, mechanoreceptive functions are lost concomi-

tantly, allowing larger loads to be placed during mas-

tication than the patient would normally tolerate (

Lowenstein & Rathkamp 1955, Randow & Glantz

1986). Suggestions that endodontically treated teeth

with time become brittle due to changes in the

biomechanical properties of dentin and, thus, less

resistant to mastication forces have not been substan-

tiated in careful analyses (Sedgley & Messer 1992).

Also, clinically intact teeth with no or minimal

restorations may be subjected to vertical root fracture (

Fig. 14-21). Traumatic occlusal forces may induce

fracture, and mandibular molars appear to be espe-

cially at risk (Yang et al. 1995, Chan et al. 1999). Sub-

sequent to these fractures typical pulpitis symptoms

may be initiated followed by breakdown of the pulp

and abscess formation, if the fracture involves the

pulp tissue directly.

Vertical root fractures that involve the gingival sul-

cus/pocket area usually have a hopeless prognosis

due to continuous bacterial invasion of the fracture

space from the oral environment. While there are re-

ports on successful management of fractured teeth by

reattaching the fragments with a bonding resin after

extraction and re-implantation, fractured teeth are

normally candidates for extraction. In multirooted

teeth a treatment alternative is hemisection and ex-

traction of the fractured root.

Conclusion

Symptoms and signs associated with vertical root

fractures show a varying character and may be diffi-

cult to distinguish from those associated with peri-

odontal and endodontic lesions. A variety of diagnos-

tic procedures should be considered. Except for the

leads obtained from anamnestic findings and pocket

probing depths in buccal or lingual positions or both,

clinical examination should include measures to make

fracture lines visible: application of dye solutions, the

use of fiberoptic light, inspection in the surgical mi-

croscope or endoscope and by a surgical flap. Pain on

selective loading of cusps may be an indication of root

fracture. A vertical root fracture should be anticipated

in root-filled teeth, which, after a long history of being

asymptomatic and without signs of endodontic infec-

tion, suddenly present with tenderness, pain symp-

toms and radiographic bone destruction (Fig. 14-20).

Roots with vertical root fracture usually have a hope-

less prognosis and should be extracted.

INFLUENCE OF EXTERNAL ROOT

RESORPTIONS

External resorption of roots normally progresses with-

out clinical symptoms and without causing periodon-

tal defects that can be mistaken for endodontic or

periodontal disease. However, in their advanced

stages they may interfere with the gingival sulcus and

cause the development of a periodontal abscess (Fig.

14-22). Since such lesions may be associated with both

increased pocket probing depths and drainage of pus

upon probing, this section of the chapter addresses

various forms of external root resorptions, their

mechanisms, clinical features and management.

Mechanisms of hard tissue resorption

The hard tissues of the body consist of two major

components, mineral and matrix. The ratio of these

two components varies between bone, cementum and

dentin, but the same tools — acids and enzymes — are

used by nature to monitor the degradation of these

tissues. Bone is normally remodeled to adapt to func-

334 • CHAPTER 14

Fig. 14-22. Series of radiographs taken at different time periods showing the appearance of an external root resorp-

tion in a young adult patient (a-c). At the age of 15 years there is no sign of resorption (a). Six years later a small ra

diolucency is seen (arrow) (b). In just 6 months the lesion had expanded considerably (arrow) (c) and

appeared clinically as a pink area (arrow) (d). Courtesy of Dr Anders Molander.

tional changes, but as far as dental hard tissues in

permanent teeth are concerned resorption should be

seen as an expression of a pathological process. Bone

as well as cementum and dentin and also enamel,

when applicable, are resorbed by clast cells (Hammar-

strom & Lindskog 1992). Osteoclasts are large, multi-

nucleated, motile cells emanating from hematopoietic

precursor cells in the bone marrow (Marks 1983, Vaes

1988, Pierce et al. 1991). Mononucleated cells are also

involved when dental hard tissue is resorbed (Weden-

berg & Lindskog 1985, Lindskog et al. 1987, Sasaki et

al. 1990).

Under normal conditions, hard tissues are pro-

tected from resorption by their surface layers of blast

cells. It appears that as long as these layers are intact,

resorption cannot occur. It is known that hormonal

regulation of bone resorption is mediated by

osteoblasts (Chambers 1988). Stimulation by parathy-

roid hormone will make osteoblasts contract to expose

the bone surface for the osteoclasts (Jones & Boyde

1976, Rodan & Martin 1981). However, parathyroid

hormone exerts no influence on cementoblasts (Lind-

skog et al. 1987). This may explain why bone and not

teeth are remodeled to adapt to functional changes.

A denuded hard tissue surface attracts resorbing

cells. It has been suggested that the removal of the

organic matrix of bone will make it possible for phago

cytic cells to recognize the mineral component (Cham-

bers 1981). Thus it appears that the blast cell layer on

hard tissues forms a protective barrier that has to be

broken down to trigger osteoclastic activity. Under

clinical conditions various forms of damage can affect

the blast cell layer, e.g. trauma or excessive scaling and

root planing in periodontal therapy (Andreasen 1981).

Subsequent to the injury, mobile osteoclasts come and

seal themselves to the exposed hard tissue surface and

excrete acids into the extracellular environment under

their ruffled border to demineralize the tissue. This

event further creates the necessary acid environment

essential for the function of lysosomal enzymes with

low pH optima, to degrade the tissue matrix (Vaes

1968).

Conclusion

Two mechanisms are involved in resorption of a hard

tissue:

1. a trigger mechanism

2. a reason for the resorption to continue.

The trigger mechanism in root resorption is a root

surface detached from its protective blast cell layer.

Detachment may follow any damage to the cemen-

toblastic cell layer. For the resorption to continue, a

stimulus is required, e.g. an infection or a continuous

mechanical force such as the one in orthodontic treat-

ment. Consequently, the treatment of root resorption

should be directed towards the cause for the continu-

ance of the resorption, e.g. removal of infected mate-

rial in a root canal, or the halt of an orthodontic tooth

movement.

Clinical manifestations of external root

resorptions

Root resorptions

per se

do not cause painful symp-

toms. Unless a resorptive process is located coronally

and is undermining the enamel, giving it a pinkish

appearance (Fig. 14-22d), the only way to detect and

diagnose a dental resorption is by means of radiogra-

phy (Fig. 14-22a-c). If only one radiograph is taken it

is usually not possible to exactly define a radiolucent

area found inside the confines of a root. It may be a

resorptive process inside the root canal, or a radiolu-

cent resorptive defect located buccally or lingually

and superimposed on the image of the root. It may also

just be an artifact. Therefore, one should always take

more than one radiograph and use different angula-

tions to observe whether the radiolucent area belongs

to the root or not.

ENDODONTICS AND PERIODONTICS • 335

Fig. 14-23. Painful condition associated with a peripheral inflammatory root resorption (PIRR). The 30-year-old

male patient had experienced pain and tenderness of the right maxilla for several weeks (a). Clinically, all teeth

were sensible to pulp testing. Periodontal probing revealed pus drainage from the lingual aspect of tooth #13 (b).

An angulated radiograph revealed the presence of a resorptive defect (c). The tooth was deemed beyond

recovery and was extracted. An extensive resorptive defect had undermined the clinical crown (d).

Root resorptions always start at a surface and are

termed external if emanating from the root surface

and internal if initiated in the root canal wall. If the

radiolucent area is situated within the confines of the

root, at least two angulations or tomography are use-

ful to determine whether it is related to the root canal

or the root surface. If the outline of the root canal space

is clearly visible within the radiolucency, as in Figs.

14-22c and 14-23, this is a strong case for an external

origin. Due to its relatively rare occurrence internal

resorptions will not be further discussed in this chap-

ter.

The initial stage of a resorptive process usually

passes undetected as radiographs can only demon-

strate a resorptive cavity after a certain size has been

reached (Fig. 14-23a-c; Andreasen et al. 1987). The

location of the lesion is also important for the detec-

tion. A facial or lingual root resorption cavity is more

difficult to visualize radiographically than a proximal

cavity. Be aware that in the cervical region it may be

difficult to differentiate radiographically between

cavities caused by caries and those caused by resorp-

tion. Resorptive processes and caries develop by dif-

ferent mechanisms, which is useful for distinguishing

these lesions. Bacterial acids, which demineralize

dentin, create carious defects, but the organic part

will remain and render the cavity soft on exploration.

A simultaneous removal of the mineral phase and the

organic matrix of the hard tissue forms the resorptive

defect. This results in a cavity floor, which is hard on

probing.

Different forms of external root resorption

There are different forms of external root resorption.

The underlying mechanism is understood for some of

these, whereas other forms still remain unexplained.

In some instances external root resorptions appear to

be genetically linked, as

they

run in families. There are

also instances when only the enamel of an unerupted

tooth is being resorbed. Furthermore, external resorp-

tions can be caused by precipitation of oxalate crystals

in the hard tissues of patients as a result of increased

concentration of oxalates in the blood due to kidney

failure (Moskow 1989).

Andreasen (1981) has proposed a classification of

those external root resorptions that have a known

mechanism:

• Surface resorption

• Replacement resorption associated with ankylosis

• Inflammatory resorption associated with inflam-

mation in the periradicular tissues adjacent to the

resorption site.

Subforms are:

• Peripheral inflammatory root resorption (PIRR)

• External inflammatory root resorption (EIRR)

336 • CHAPTER 14

Surface resorption

This type of resorption is common, self-limiting and

reversible (Harding 1878). In a microscopic study of

human teeth in individuals varying in age from 16 to

58, only 10% of the teeth showed neither active resorp

tion nor signs of healed resorption (Henry &

Weinman 1951). Resorptions were noted twice as

often in older than in young subjects. Other studies

have demonstrated up to 88% of teeth with active or,

in most instances, healed resorptions (Hotz 1967).

Reports on surface resorptions are sparse as most are

self-limiting and spontaneously repaired upon injury.

A surface resorption is initiated subsequent to in-

jury of the cementoblastic cell layer. Osteoclasts are

attracted by substances from the damaged tissue on

the denuded root surface and resorb the hard tissue

for as long as activating factors are released at the site

of injury, usually for a few days (Hammarstrom &

Lindskog 1992). The resorptive process stops follow-

ing the disappearance of the osteoclasts and the defect

will become populated with hard tissue repairing cells

leading to cementum repair (Lindskog et al. 1983a,b,

1987).

These resorptions may be caused by a localized

injury in conjunction with external trauma (An-

dreasen 1981) and by trauma from occlusion. Resorp-

tion may also result from excessive orthodontic forces.

The mechanism of the latter kind of resorption is

thought to be a function of the hyaline zone that is

formed subsequent to the orthodontic compression of

the periodontal ligament. Along with the resorption

of the hyaline layer, clast cells will resorb the root

surface for as long as the orthodontic force is in place.

Major loss of dental hard tissue giving root fore-

shortening may occur from this kind of iatrogenic

injury.

Conclusion

The large majority of teeth show signs of active or

healed surface resorptions or both. It is conceivable

that minor traumata caused by unintentional biting on

hard objects, bruxism, high fillings, etc., cause lo-

calized damage to the periodontal ligament and trig-

ger the initiation of this type of resorption. The process

is self-limiting and self-healing – no active treatment

is required. During orthodontic treatment caution

should be exercised in monitoring the forces to mini-

mize the risk of foreshortening of roots.

Replacement resorption

This type of resorptive process results in a replace-

ment of the dental hard tissues by bone, hence the

name (Andreasen 1981). When a surface resorption

stops, cells from the periodontal ligament will prolif-

erate and populate the resorbed area (Lindskog et al.

1983a,b, 1987). If the resorption is large it will take

some time for the PDL cells to cover the entire surface.

Cells from the nearby bone tissue may then arrive first

and establish themselves on the resorbed surface (An-

dreasen & Kristersson 1981, Gottlow et al. 1986). Bone

is thus being formed directly upon the dental hard

tissue. This results in a fusion between bone and tooth

which is known as ankylosis.

Replacement resorption and ankylosis are often

used as synonyms. While replacement resorption de-

scribes the active process during which the tooth is

resorbed and replaced by bony tissue, ankylosis is the

Greek word for immobile. It describes the situation of

a tooth lacking normal mobility due to the fusion

between tooth and bone. This fusion can be perma-

nent or transient and appears to depend on the size of

the resorbed area. If the ankylotic area is small, the

bone on the tooth surface can resorb and be replaced

with reparative cementum (Andreasen & Skougaard

1972, Andreasen & Kristersson 1981, Andersson et al.

1985, Hammarstrom et al. 1986). If the ankylotic area

is large, a sufficient amount of bone will be formed on

the root surface to make the fusion between bone and

tooth permanent (Andreasen 1981, Andreasen & Kris-

tersson 1981, Hammarstrom et al. 1986). It has been

shown that long-term rigid splinting following exter-

nal trauma results in a higher incidence of dentoalveo-

lar ankylosis than with a short-term, less rigid fixa-

tion. The latter allows for some movement during the

splinting period and probably prevents ankylosis (

Andreasen 1975).

Clinically, ankylosis is diagnosed by absent tooth

mobility and by a percussion tone that is higher than

in a normal tooth (Andreasen 1975, Andersson et al.

1985). Radiographically, a local disappearance of the

periodontal ligament contour may show an initial

stage of fusion. However, even in non-ankylosed teeth

it is not always possible to observe the entire contour

of the periodontal ligament. Percussion and tooth mo-

bility testing appear therefore more sensitive diagnos-

tic tools than radiography in the early stages of re-

placement resorption (Andersson et al. 1985). When

dentoalveolar ankylosis occurs at a young age, the

tooth will not erupt but will follow the growth pattern

of the bone resulting in so-called infra-occlusion (An-

dreasen & Hjorting-Hansen 1966, Kiirol 1984, Malm-

gren et al. 1984).

The formation of bone on a dentin surface is not

necessarily a pathological process, but one to be re-

garded as a form of repair. The bone has accepted the

dental hard tissue as a part of itself and the tooth

becomes involved in the normal skeletal turnover (

Loe & Waerhaug 1961, Hammarstrom et al 1986). The

turnover phase is fast in the growing child, but slower

in the adult individual. Hence, the rate of bone re-

placement follows this pattern. However, the detailed

mechanism of the resorptive process is not clearly

understood.

Conclusion

Ankylosis is a prerequisite for replacement resorption.

It may be seen as a form for repair of root surface

ENDODONTICS AND PERIODONTICS • 337

Fig. 14-24. Radiograph from a 78-year-old lady who presented herself to the clinic after an episode of severe pain

and with a lingual periodontal abscess (a). The medical history was unremarkable. Radiograph revealed external

root resorption on the lingual aspect of both the central incisors (a). The patient was initially managed by antibiotic

treatment. Upon flap elevation and accessing the resorbing area and removing the granulation tissue an exposure

to a necrotic pulp of tooth #31 was noted (b). Endodontic treatment was carried out during the surgery

procedure (c). Tooth #41 was left without any further treatment and the case was followed clinically and

radiographically. No recurrence of resorption occurred on either tooth and the patient has remained comfortable.

Radiograph at the last follow-up 8 years after treatment (d). Note that there is no obvious progression of the

resorptive process associated with tooth #41.

resorptions, which from a clinical standpoint is not

desirable. No treatment for this condition is available.

External inflammatory resorption

The term external inflammatory resorption suggests

the presence of an inflammatory lesion in the peri-

odontal tissues adjacent to a resorptive process (An-

dreasen 1985). There are two main forms — peripheral

inflammatory root resorption (PIRR) and external in-

flammatory root resorption (EIRR). Both forms are

triggered by a destruction of the cementoblasts and the

cementoid. In PIRR the factors activating osteoclasts

are thought to be provided by an inflammatory lesion

in the adjacent periodontal tissues (Andreasen 1985,

Gold & Hasselgren 1992). EIRR, on the other

hand, receives its stimulus from an infected necrotic

pulp (Andreasen 1985, Andreasen & Andreasen 1992).

Peripheral inflammatory root resorption (PIRR)

The outstanding feature of this type of resorption is its

cervical location and invasive nature (Heithersay

1999a). It has therefore been termed invasive cervical

root resorption. However, in the adult, the periodontal

tissue may have receded apical to the cervical area.

Therefore, other names have been used for this lesion

such as subosseous resorption (Antrim et al. 1982) and (

the complete opposite) supraosseous extra-canal in-

vasive resorption (Frank & Bakland 1987). The differ-

ent names reflect the confusion that has surrounded

this type of resorptive lesion. Since the resorptive

process extends into the dentin peripherally towards

338 • CHAPTER 14

the pulp, and the clast activating factors seem to ema-

nate from a periodontal inflammatory lesion, a name

which reflects the etiology of this phenomenon, pe-

ripheral inflammatory root resorption (PIRR), was

proposed (Gold & Hasselgren 1992).

The clinical features of PIRR include granulation

tissue formation that bleeds freely on probing. Occa-

sionally, a periodontal abscess may develop due to

marginal infection, which may mimic a periodontal or

endodontic condition (Fig. 14-23). When the lesion is

located more apically or proximally, probing is usu-

ally difficult. Radiographically the lesion may only be

seen after a certain size has been reached (Fig 14-22).

Sometimes the appearance is mottled due to forma-

tion of hard tissue within the resorptive defect (Se-

ward 1963). The outline of the root canal can often be

seen within the radiolucent area (Fig. 14-22c). The

presence of a profuse bleeding upon probing and

granulation tissue in combination with a hard cavity

bottom confirm the diagnosis. Electric pulp test and

cold tests are usually positive, but will not distinguish

this condition from caries or internal resorption,

which are the two major differential diagnostic op-

tions (Frank & Bakland 1987).

The mechanism for this form of resorption is far

from completely understood. Predisposing factors

seem to be orthodontic treatment, trauma and intra-

coronal bleaching, while periodontal therapy took a

low incidence among 222 examined cases (Heithersay

1999b). The reason for the low incidence following

periodontal treatment could be that even upon exces-

sive scaling and root planing, the damaged area of the

root surface usually becomes covered by junctional

epithelium. Yet, it appears that in the presence of a

periodontal inflammatory lesion the onset of a resorp-

tive process is triggered and that its continuance has

an infectious cause (Brosjo et al. 1990, Gold & Hassel-

gren 1992).

Unmineralized, newly formed tissue in cementum (

Gottlieb 1942), in osteoid (Chambers et al. 1985), and

in predentin (Stenvik & Mjor 1970) has been observed

to be resistant to resorption. This seems to explain the

pattern of progression this form of resorption nor-

mally takes as it avoids invasion of the pulp and

expands laterally instead. Yet, this peripheral exten-

sion can markedly undermine the tooth structure (Fig.

14-23). If there is a non-vital pulp and thus no resorp-

tion inhibition in the form of odontoblast supported

predentin, PIRR will go straight to the pulpal space (

Fig. 14-24). In root-filled teeth, which have been sub-

jected to intracoronal bleaching, tissue toxic bleaching

agents such as hydrogen peroxide have been found to

be capable of penetrating through dentin and cemen-

turn (Fuss et al. 1989). If this occurs under clinical

conditions, damage will be inflicted upon the peri-

odontal ligament cells and cause resorption (Har-

rington & Natkin 1979, Montgomery 1984). Sub-

sequently, bacteria may colonize the chemically emp-

tied dentinal tubules and maintain inflammation and

the resorptive process (Cvek & Lindvall 1985).

The most common form of treatment for PIRR is

surgical exposure of the area, including removal of the

granulation tissue. A base material is subsequently

placed followed by a permanent filling and suturing

of the flap. Other treatment forms include reposition-

ing of the flap apical to the filling or orthodontic

extrusion of the tooth (Gold & Hasselgren 1992). Re-

cently, it has been suggested that guided tissue regen-

eration can be used, after surgical removal of the

granulation tissue, to promote ingrowth of periodon-

tal ligament cells into the resorbed area (Rankow &

Krasner 1996). This kind of resorption may also be

approached from within the tooth structure. Usually

pulpectomy is required. To aid in removal of the resor

bing tissue the use of 90% aqueous solution of

trichloracetic acid has been proposed (Heithersay

1999c).

External inflammatory root resorption (EIRR)

This type of resorption is usually a complication that

follows a dental trauma. It begins as a surface resorp-

tion due to damage of the periodontal ligament and

the root surface in conjunction with the traumatic

injury. The stimulus for EIRR is infectious products

released into the adjacent tissues by way of the denti-

nal tubules exposed by the resorption (Bergenholtz

1974, Andreasen 1985, Andreasen & Andreasen 1992).

The bacterial components will then maintain an in-

flammatory process in the adjacent periodontal tis-

sues that in turn will trigger the continuance of the

resorption. The osteoclastic resorption, basically

aimed at eliminating the irritants, will thus move in

the direction of the infected pulp tissue. As dentin is

being further resorbed, more infectious and inflam-

matory byproducts are released into the surrounding

area, thus perpetuating the inflammatory reaction and

the resorptive process (Andreasen 1985).

The earliest stages are usually hard to detect as the

resorptive cavity needs to reach a certain size to be-

come radiographically visible. The first radiographic

signs of resorption following trauma cannot usually

be seen for several weeks (Andreasen et al. 1987).

Treatment will be directed towards the cause of the

resorption, that is, the root canal infection (Cvek 1993).

In this context the use of calcium hydroxide has been

advocated (Cvek 1993) as it is a useful antibacterial

intracanal medicament (Bystrom et al. 1985). Calcium

hydroxide also aids the cleaning of the canal by its soft

tissue dissolving capability (Hasselgren et al. 1987),

thus eliminating sources for bacterial nutrition. How-

ever, the positive effect of any medicament appears to

be secondary to the elimination of root canal infection.

Hence, clinical follow-ups suggest no difference in

outcome between teeth treated long-term with cal-

cium hydroxide and teeth subjected to instrumenta-

tion and filling with gutta-percha (Cvek 1973).

Conclusion

Peripheral inflammatory root resorption (PIRR) and

external inflammatory root resorption (EIRR) are two

ENDODONTICS AND PERIODONTICS • 339

Fig. 14-25. Radiographs from a 27-year-old woman, showing the left maxillary canine which had been autotrans

planted into a surgically prepared socket 2 months earlier. External inflammatory root resorption (EIRR) is

visible on the distal aspect of the root (a). Endodontic treatment was initiated (b) and following the preparation

of the canal, calcium hydroxide was placed as a long-term dressing. Radiograph following root filling (c) shows

that the external resorption cavity is more rounded and a periodontal contour can be seen between the root and

bone which has grown into the prepared socket.

forms of progressing external root resorption associ-

ated with inflammation in the periodontal tissues. The

mechanism of EIRR is thought to be the release of

bacterial elements from an infected pulp devitalized

in conjunction with trauma. By focusing the treatment

on the endodontic infection the resorption can usually

be stopped as this takes away the reason for the con-

tinuance of the resorption (Fig. 14-25). In the sub-

sequent healing phase there is risk of ankylosis. The

greater the resorbed area, the greater is the risk for this

complication (Andreasen & Kristersson 1981, Gottlow

et al. 1986).

INFLUENCE OF PERIODONTAL

DISEASE ON THE CONDITION OF

THE PULP

The formation of bacterial plaque on detached root

surfaces following periodontal disease has the poten-

tial to induce pathologic changes in the pulp along the

very same pathways as an endodontic infection can

affect the periodontium in the opposite direction.

Thus, bacterial products and substances released by

the inflammatory process in the periodontium may

gain access to the pulp via exposed lateral canals and

apical foramina, as well as dentinal tubules.

A clearcut relationship between progressive peri-

odontal disease and pulpal involvement, however,

does not invariably exist. In fact, while inflammatory

alterations as well as localized necrosis of pulp tissue

have been observed adjacent to lateral canals in teeth

exposed by periodontal disease (Seltzer et al. 1963a,

Rubach & Mitchell 1965), a number of clinical studies

Fig. 14-26. Histologic section of a monkey tooth ex-

posed to experimental periodontal tissue breakdown.

Beneath resorptive defects in the external root surface a

slight infiltrate of inflammatory cells and a small rim of

reparative dentin are observed in the pulp. From Ber-

genholtz & Lindhe (1978).

have failed to confirm a direct correlation between

periodontal disease and pulp tissue changes (Mazur &

Massler 1964, Czarnecki & Schilder 1979, Torabine-

jad & Kiger 1985). In a study in monkeys, Bergenholtz

& Lindhe (1978) observed the nature and frequency of

tissue changes in the pulp of teeth following an experi-

mentally induced breakdown of the attachment appa-

ratus. They found that the majority of the root speci-

mens examined (70%) exhibited no pathologic pulp

tissue changes, despite the fact that approximately

30-40% of the periodontal attachment was lost. The

remaining roots (30%) displayed only small inflam-

matory cell infiltrates and/or formations of reparative

dentin in areas of the pulp subjacent to root areas

exposed through the periodontal tissue destruction.

340 • CHAPTER 14

Fig. 14-27. Case of a lower second molar with severe periodontal tissue breakdown and furcation involvement (

a) that was extracted and subjected to histologic examination. Upon extraction substantial amounts of calculus is

seen on the distal root surface (b). While there was bacterial accumulation on the cementum layer (c), the pulp

tissue has remained functional and without inflammatory involvement (d). Courtesy of Dr Domenico Ricucci.

These tissue changes were frequently associated with

root surface resorption (Fig. 14-26), suggesting that

dentinal tubules have to be uncovered before irritation

can be transmitted. This observation further suggests

that the presence of an intact cementum layer is im-

portant for the protection of the pulp from injurious

elements produced by the plaque microbiota (Fig. 14-

27). Consequently, the lack of correlation found in

clinical observations between periodontal disease and

pulp tissue alterations may simply depend on the fact

that few open pathways exist in many periodontally

involved teeth. Furthermore, once the dentin/pulp

complex has been exposed to a bacterial challenge,

repair and healing will often be instituted, leaving the

remaining tissue relatively unaffected (Warfvinge &

Bergenholtz 1986, Bergenholtz 2000).

In the study by Bergenholtz & Lindhe (1978), de-

structive periodontal disease was produced experi-

mentally during a comparatively short period (5-7

months), while in humans a similar degree of destruc-

tion of periodontal tissue normally requires several

years. It has been reported that the pulp of teeth with

long-standing periodontal disease develops fibrosis

and various forms of mineralizations (Fig. 14-1;

Bender & Seltzer 1972, Lantelme et al. 1976). The

number of blood vessels and nerve fibers can also be

reduced. It seems reasonable that tissue changes of

this nature represent the accumulated response of the

pulp to the relatively weak, but repeatedly occurring,

insults of the tissue via exposed dentinal tubules and

lateral canals.

Conclusion

It seems that periodontal disease rarely jeopardizes

the vital functions of the pulp. In teeth with moderate

breakdown of the attachment apparatus, the pulp

usually remains in proper function. Breakdown of the

pulp presumably does not occur until the periodontal

disease process has reached a terminal state, i.e. when

bacterial plaque involves the main apical foramina

(Langeland et al. 1974). Apparently, as long as the

blood supply through the apical foramen remains

intact, the pulp is capable of withstanding injurious

elements released by the lesion in the periodontium.

INFLUENCE OF PERIODONTAL

TREATMENT MEASURES ON THE

PULP

Scaling and root planing

Scaling and root planing are indispensable procedures

in the treatment of periodontal disease. However, not

only will bacterial deposits be removed from the root

surface but so also may cementum and superficial

parts of dentin. Therefore, by this instrumentation,

dentinal tubules will be exposed and normally left

unprotected to the oral environment. Subsequent mi-

crobial colonization of the exposed root dentin may

result in bacterial invasion of the dentinal tubules (

Adriaens et al. 1988). As a consequence, inflamma-

tory lesions may develop in the pulp (Bergenholtz &

Lindhe 1978). Yet, the vitality of the pulp is not nor-

mally put at risk (Bergenholtz & Lindhe 1978, Nilveus

& Selvig 1983, Hattler & Listgarten 1984), even though

root dentin hypersensitivity frequently develops fol-

lowing such measures, presenting an uncomfortable

and difficult problem to manage (see below).

During the maintenance phase of periodontal ther-

apy, scaling and planing of roots are frequently re-

peated procedures. At each recall session, the root

surfaces are debrided and some dentin is removed.

This therapy can result not only in weakening of the

tooth structure but also in extensive reparative dentin

formation in the pulp (Fig. 14-28). Whether such repair

processes impair pulp functions on a long-term basis

is not well studied. In a patient material subjected to

ENDODONTICS AND PERIODONTICS • 341

Fig. 14-28. Clinical photograph of a patient, who has been in the maintenance phase after treatment for periodontal

disease (a). While there are excellent gingival conditions and no pocket probing depths, there is substantial loss of

cervical root dentin. One of the lower incisors later fractured off, but without a pulpal exposure due to accumula

tion reparative dentin in the coronal portion of the pulp chamber (b). Courtesy of Dr Sture Nyman.

maintenance therapy for over 4-13 years, pulp tissue

necrosis was a rare finding (3%), and, when occurring,

it was attributed to caries and progression of peri-

odontal disease rather than to the periodontal treat-

ment

per se

(Bergenholtz & Nyman 1984). On rare

occasions deep periodontal scaling may expose lateral

canals that in turn can induce severe painful symp-

toms of pulpitis.

Conclusion

Results of clinical observations and animal experi-

ments support the view that scaling and root planing

procedures normally do not threaten the vitality of the

pulp. Adjacent to instrumented root surfaces localized

inflammatory alterations may on occasion emerge,

but in most instances these will be followed by repair

processes. (Figs. 14-1, 14-28b).

Root dentin hypersensitivity

Patients subjected to scaling and root planing in peri-

odontal therapy may after the instrumentation proce-

dure experience increased sensitivity of the treated

teeth to evaporative, tactile, thermal and osmotic stim-

uli (Fischer et al. 1991, Kontturi-Narhi 1993, Chaban-

ski et al. 1996). Usually, the symptoms, when occur-

ring, develop and peak during the first week to sub-

side or disappear within the subsequent weeks and

are, although uncomfortable, most often a temporary

and sustainable complication. However, occasionally

the condition may become a chronic pain problem and

may persist for months or years. Patients appear to be

especially at risk after periodontal surgery. In a com-

prehensive questionnaire survey, severe painful

symptoms were reported to prevail in 26% of the

subjects 6 months to 5 years after the completion of

treatment, while 16% treated non-surgically had pain

symptoms (Kontturi-Narhi 1993). In a clinical trial

comprising 35 patients, Tammaro et al (2000) observed

that, while a majority of patients subjected to non-sur-

gical periodontal instrumentation developed sensi-

tive teeth, only a few teeth in a small number of the

patients developed highly sensitive root surfaces.

The main initial symptom is sharp pain of rapid

onset that disappears once the stimulus is removed. In

more severe, long-standing cases, shorter or longer

periods of lingering, dull or aching pain symptoms

may be provoked. Even a minimal contact of a tooth-

brush with the root dentin surface may result in in-

tense pain – a condition not only uncomfortable but

one likely to hinder proper oral hygiene measures.

The pain condition is termed dentin hypersensitiv-

ity (Holland et al. 1997). But the ailment has also been

given many other names such as sensitive dentin,

cervical dentinal sensitivity and root sensitivity,

which reflect the confusion that still exists regarding

its etiologic background (Orchardson et al. 1994). The

fact that root surfaces become sensitive to a variety of

externally derived stimuli after periodontal instru-

mentation is not surprising as dentinal tubules be-

come uncovered to the oral environment and subject

to hydrodynamic forces. Hence, a variety of pain-

evoking stimuli including evaporative, tactile, ther-

mal and osmotic stimuli may elicit sudden fluid shifts

in the exposed tubules thereby inducing a painful

sensation according to the hydrodynamic theory of

dentin sensitivity (Brannstrom 1966, Pashley 1996).

This mechanism alone can certainly explain the sensi-

tivity patients experience immediately after the in-

strumentation procedure and during a short period

afterwards, while it does not make clear why the

symptoms increase over time and why the pain con-

dition may prevail in certain patients and in certain

teeth.

The increase in pain intensity may have one or both

of the following two explanations. Firstly, the smear

layer formed on the root surface by the scaling proce-

342 • CHAPTER 14

Fig. 14-29. Scanning electron microscopic images of specimens of hypersensitive (a, b) and non-sensitive root

dentin areas of human teeth (c, d). In (a) there are numerous wide tubular apertures. These tubules show no

evidence of hard tissue depositions after being fractured open (b). Most tubules are occluded (c) and below the

surface rhombohedral crystals of from 0.1-0.3 µm are present (d). The images are kindly provided by Dr

Masahiro Yoshiyama and published with permission of the

Journal of Dental Research.

dure will be dissolved within a few days (Kerns et al.

1991). This in turn will increase the hydraulic conduc-

tance of the involved dentinal tubules (Pashley 1996)

and thus decrease the peripheral resistance to fluid

flow across dentin. Thereby pain sensations are more

readily evoked. Secondly, open dentinal tubules serve

as pathways for diffusive transport of bacterial ele-

ments in the oral cavity to the pulp, which is likely to

cause a localized inflammatory pulpal response (Ber-

genholtz & Lindhe 1975, 1978). Indeed, experiments

in dogs have shown that pulpal inflammation greatly

enhances the sensitivity of responding nerve fibers (

Narhi et al. 1994). A large number of intradental A-

delta fibers, normally inactive, are now able to re-

spond upon stimulation (Nth-hi et al. 1996). It has

furthermore been shown that the receptive field of

individual fibers gets wider (Narhi et al. 1996). In

addition, shallow oral exposures of root dentin in the

rat are accompanied by sprouting of new terminal

branches from pulpal axons in areas subjacent to the

root surface injury (Taylor et al. 1988). Sprouting of

nerves is a temporary event and will subside if inflam-

mation disappears – a feature consistent with their

involvement in root dentin hypersensitivity (Byers &

Narhi 1999). In other words, an essential component

of the increasing root sensitivity that patients experi-

ence after an instrumentation procedure in periodon-

tal therapy is likely to be related to a peripheral sensi-

tization of pulpal nociceptors due to release of inflam-

matory mediators.

The fact that root dentin hypersensitivity often dis-

appears a few weeks after the scaling procedure is best

explained by the development of a natural occlusion

of the exposed dentinal tubules by mineral deposits (

Fig. 14-29; Yoshiyama et al. 1989, 1990). The hydrody-

namic mechanism for dentinal pain will thereby be

inactivated. Furthermore, the potential for an inward

diffusion of bacterial elements to the pulp will be

substantially reduced. The observations of few if any

open tubules in non-sensitive radicular dentin (Hiatt

& Johansen 1972, Absi et al. 1987, Yoshiyama et al.

1989, Cuenin et al. 1991, Oyama & Matsumoto 1991,

Kontturi-Narhi 1993), while hypersensitive root areas

show large numbers of tubular apertures on their

surfaces (Absi et al. 1987, Yoshiyama et al. 1989,

Cuenin et al. 1991, Oyama & Matsumoto 1991,

Kontturi-Narhi 1993), support this view.

The fact that only certain individuals become seri-

ously affected may be related to local factors in the oral

cavity, as well as to the level of the subjects' pain

perception. Certain dietary factors, in particular fruit

juices, yoghurt and wines, have been implicated in the

pathogenesis of dentin hypersensitivity (Addy et al.

1987). By their acidity and ability to etch dentin, natu

ral occlusions of dentinal tubules by mineralizations

may thus be dissolved or prevented from forming. It

needs also to be recognized that pain is not only an

expression of injury and noxious stimuli, but also a

psychobiological phenomenon having both a physi-

ological and psychological basis for its perception and

reaction to it. Indeed, a variety of emotional elements

may influence the subjective interpretation of pain (Eli

1992), and anxiety, fear and depression are factors that

are known to affect pain perception and the subject's

ability to identify coping methods (McGrath 1994).

A further factor that is potentially involved in the

symptomatology associated with root dentin hy-

persensitivity is the enhancement of the responsive-

ness of the central nervous system. Indeed it has been

shown that neuroplastic changes in the central no-

ciceptive pathways, including expanded receptive

fields and heightened excitability, may occur follow-

ing peripheral injury and inflammation (see review by

Sessle 2000). Such changes may be maintained even if

peripheral sensitization phenomena are bypassed and

seem to become more prominent in long-lasting pain

conditions (Sessle 2000).

In cases of severe root dentin hypersensitivity, ac-

tive treatment is urgent. However, the methods pres-

ently available provide an unpredictable remedy and

only temporary relief is at best attained (Orchardson

et al. 1994, Ikola 2001). Since tubular patency seems to