Internal replacement (invasive) resorption

This type of resorption is relatively rare
and may appear clinically as a pink area in the crown of the
affected tooth as shown in Fig 20a. However, the
clinician should recognize that a pink appearance in the
crown of a tooth is indicative of highly vascular
resorbing tissue which has removed sufficient dentine
and enamel to allow it to be visible through the thin
overlying tooth substance. While this may be internal in
origin, particularly if there has been a history of recent
trauma, it more commonly arises from an external
periodontal source. The location of the pink spot is
more likely to be entirely within the crown of the tooth
in internal replacement (invasive) resorption.

Hyperplastic invasive resorptions

The third group of dental resorptions are insidious in

nature and generally present complex therapeutic

challenges. In these cases, resorbing tissue invades the

hard tissues of the tooth in a destructive, and apparently

uncontrolled fashion, akin to the nature of some fibro-osseous 

lesions such as fibrous dysplasia.

An important distinguishing factor for this third group of

resorptions is that, unlike the first two types of

resorption, simple elimination of the cause of the lesion

is ineffective in arresting their progress. Total removal

or inactivation of the resorptive tissue is essential if

recurrence (or concurrence) is to be avoided.

Concurrence indicates the incomplete removal of the

resorptive tissue at the time of treatment and recurrence

is the re-establishment of the resorptive process. The

reason for recurrence or concurrence is probably due to

the invasive nature of the resorptive tissue whereby

small infiltrative channels are created within the  dentine

and these may interconnect with the periodontal

ligament in positions more apical to the main resorptive

defect.

Unless the tissue in these infiltrative channels is

inactivated the resorptive process will continue. While

these resorptions are not considered to be neoplastic,

their aggressive characteristics can seem to be similar.

At the present time one proven therapy for inactivation

is chemical in nature but surgical and other

technological modalities may also be applied.

These hyperplastic invasive resorptions may have a

pulpal (internal) or a periodontal origin (external).

Critical to the clinical use of therapies aimed at

controlling internal and external invasive tooth

resorptions is the correct diagnosis of the type and

localization of the resorption.

Hyperplastic resorptions may be subdivided into

internal replacement (invasive) resorption, invasive

coronal resorption, invasive cervical resorption and

invasive radicular resorption.

Communicating internal-external inflammatory resorption

Where resorption has extended from an internal

inflammatory resorption to involve the external surface

a communicating lesion is created. This can be

recognized radiographically by a radiolucency within

the tooth structure extending to the exterior surface

and the surrounding bone. While treatment is possible,

it is complex and referral to an endodontist is suggested

or implant therapy could be considered.

External inflammatory root resorption

Classically, this type of external root resorption

occurs when infection is superimposed on a traumatic

injury – usually following replantation of an avulsed

tooth or a luxation injury. Nevertheless it can also be

induced in some cases of endodontic pathosis as shown

in Fig 15a. Despite the degree of external inflammatory

resorption, treatment can be successful (Fig 15b).

A prerequisite for external inflammatory root

resorption is damage to the normally protective

Internal inflammatory (infective) root resorption

Internal inflammatory resorptions may be 
classified according to location as: (1) apical and (2)
intraradicular.
(1) Apical
A recent study has shown that apical internal
inflammatory resorption is far more common in teeth
with various inflammatory periapical pathoses than
previously thought.

The study showed that 74.7 per
cent of teeth with periapical lesions had varying degrees
of apical internal resorption, ranging from slight 
(grade 1) to severe (grade 4). Radiographically, apical
internal resorption may be difficult to diagnose when
the resorptions are of the lower grades as described by
Vier and Figueiredo, but should be discernable in
grades 3 and 4 lesions. This study has important
clinical implications in root canal preparation.

Infection induced dental resorption

The response of the dento-alveolar apparatus to

infection is characterized by inflammation which may

result in tooth resorption. This may be a consequence

of infective endodontic pathosis alone or superimposed

on trauma induced resorption. These infection induced

resorptions, which are generally termed inflammatory

root resorptions, may occur as internal resorptions,

external resorptions or combined internal-external

lesions. These infection induced resorptions can vary

widely in complexity but will generally respond

favourably to therapy aimed primarily at removing the

infective agent. Additional impetus to resorption

control can be provided by the use of anti-clastic

therapeutic agents such as Ledermix Paste (Lederle

Pharmaceuticals Wolfratshausen Germany) used as

Replacement resorption

The most serious form of trauma induced non-infective 
root resorption is  replacement resorption
which, as the name suggests, involves the progressive
replacement of tooth structure by alveolar bone and
ultimately tooth loss. Replacement resorption follows
the death of viable periodontal ligament cells due to
factors such as compression or drying of the ligament
cells as in the case of delayed replantation of an avulsed
tooth. On rare occasions an intact cementum/

Pressure resorption and orthodontic resorption

More extensive trauma induced non-infective root
resorption may be induced by the pressure of a crypt of
an unerupted/erupting tooth or some neoplasms and
more commonly during orthodontic treatment. The
resorption is often extensive and easily observable
radiographically. Figure 6 shows the radiographic
appearance of extensive resorption of a maxillary

Surface resorption

From a treatment management point of view, the

simplest form of trauma induced (non-infective)

resorption is surface resorption which, as the name

suggests, is a shallow resorption of cementum often

with involvement of a small amount of underlying

dentine. This type of resorption is self-limiting and

transient and can follow some traumatic injuries or

Trauma induced tooth resorption

In this category using a broader interpretation of the

term “trauma”, resorptions may have resulted from

pressure from unerupted or erupting teeth or some

neoplasms, from biomechanical forces involved in

orthodontics, mechanical trauma (luxation and avulsion

injuries) and surgical, thermal or chemical trauma.

Classification of dental resorptions

Classifications play an important role for the
clinician in the process of diagnosis and treatment
planning. Andreasen has over the past 40 years made
an unique contribution to the understanding of tooth
resorption following dental trauma and his original
classification which follows (Fig 1) remains the most
widely accepted.

Management of tooth resorption

A correct diagnosis and an understanding of the

aetiology and dynamics of the processes involved in

tooth resorption is critical to effective management.

Tooth resorptions can be classified as: (1) trauma

induced; (2) infection induced; or (3) hyperplastic

invasive. Some transient trauma induced resorptions

require no treatment but must be carefully

monitored to check that there are no complicating

issues such as infection. In cases of trauma induced

replacement resorption, a multidisciplinary approach

is usually necessary to ensure an optimal long-term

solution. Infection induced tooth resorptions require

the removal of the invading micro-organisms by

endodontic therapy including intra-canal medication

which can also facilitate repair of the resorbed tooth

structure. The hyperplastic invasive tooth resorptions

pose considerable challenges in management due to

the complexity and aggressive nature of the

resorptive process. With careful case selection and

complete inactivation of resorptive tissue successful

management can be achieved.

Management of pulp and root canal conditions

The ultimate decision the practitioner must make is

whether to treat or not to treat the tooth, and if treat-ment is indicated, 

whether to treat the pulp or the root

canal system. The alternative management is to extract

the tooth and then to consider a prosthesis to replace it.

Accurate diagnosis and identification of the cause(s) of

the problem(s) will lead to effective management of the

offending tooth. Table 5 

summarizes the treatment strategies for the management of the various pulp

diseases.

Management strategies vary considerably for the

various pulp conditions which emphasizes the need for

an accurate diagnosis before considering any treatment.

Conditions such as a pulp with atrophy or pulp canal

calcification do not require any treatment (unless the

pulp has become necrotic and the canal has been

infected). A conservative approach should be adopted

when dealing with conditions such as pulp necrosis

without infection since pulp tests are not entirely

Examination and diagnostic procedures to assess the status of the pulp and root canals

The importance of gathering all the relevant

information for making a correct diagnosis cannot be

over-emphasized. An accurate diagnosis is imperative in

all cases so appropriate treatment can be provided in a

timely manner.

A current medical and dental health history is

important, not only for preventing health problems

during treatment but also to help reach a thorough

diagnosis.

For example, pain medication taken within

6–12 hours prior to examination may alter the

responses to pulp sensibility tests or other clinical tests.

One tablet of pain medication may be sufficient to

reduce the pulp or periapical inflammation, or the

analgesic may alter the patient’s perception of pain by

lowering the pain threshold.

Periapical diseases

A discussion about pulp diseases would be

incomplete without discussing the periapical tissues and

their disease processes since periapical diseases are

usually a direct result of pulp diseases. It is beyond the

scope of this paper to discuss periapical diseases in

detail and such diseases have been fully discussed in

other publications.

Unfortunately, there is also

considerable confusion amongst authors and clinicians

regarding the classifications and terminology used for

periapical conditions.

However, Abbott has 

outlined a classification for periapical diseases that is

based on the same principles as the above classification

for pulp diseases and root canal conditions and

therefore the two classifications can be used

concurrently.

When a tooth is being examined for pulp disease, the

condition of the periapical tissues must also be

assessed, and vice versa, since apical periodontitis is

usually associated with inflammatory conditions of the

pulp (i.e., reversible and irreversible pulpitis), or

infection of the pulp space following necrosis of the

pulp or after previous endodontic treatment. That is,

periapical diseases are usually a direct consequence of,

and/or a sequel to, interaction with the root canal

system.

Examples of some typical diagnoses are:

• Acute irreversible pulpitis with primary acute apical

periodontitis due to caries.

• Acute irreversible pulpitis with primary acute apical

periodontitis due to breakdown of a restoration 

(Fig 3).

• Necrotic and infected pulp with primary acute apical

periodontitis due to caries and restoration break-down.

• Pulpless, infected root canal system with secondary

acute apical periodontitis due to breakdown of the

restoration.

• Pulpless, infected root canal system with a chronic

apical abscess due to breakdown of the restoration

(Fig 5).

• A pulpless, infected root canal system with secondary

acute apical periodontitis due to breakdown of the

restoration (Fig 6).

• A root-filled tooth with an infected root canal system

and chronic apical periodontitis due to breakdown

of the restoration (Fig 6).

• Pulpless, infected root canal system with chronic

apical periodontitis due to a crack in the tooth and

caries.

• A clinically normal pulp with pulp canal calcification

but no signs of apical periodontitis (Fig 7a).

Endodontically-treated teeth

Many teeth that are examined by dentists will have

had previous pulp therapy or endodontic treatment.

Such treatments include pulp capping, partial pulpotomy,

pulpotomy, partial pulpectomy and pulpectomy. These

teeth may or may not have signs or symptoms, and they

may or may not have apical periodontitis associated

with them. The technical standard of the previous

treatment may also vary considerably and this can only

be partly assessed by the radiographic appearance of

the material(s) placed in the pulp space or root canal(s).

Essentially, the radiographic appearance of a root

filling only indicates the radiodensity of the material

and where the material has been placed. Radiographs

do not provide any indication of whether or not the

root canal system was disinfected during the previous

treatment, how effectively the canal was sealed,

whether the seal has been maintained, whether any

bacteria survived the previous treatment and whether

any new bacteria have entered the root canal system

since the treatment was completed.

Degenerative changes

The pulp will usually respond to noxious stimuli by

becoming inflamed, but it may also respond by

degeneration which includes atrophy and fibrosis,

calcification, root resorption, or hyperplasia.

Atrophy

Atrophy is a normal physiologic process that occurs

with age and is asymptomatic. Pulp sensibility tests

responses may be normal or delayed. No significant

radiographic or clinical signs are present. As the pulp

atrophies, there will also likely be fibrosis of the pulp

tissue and the extent of this will be largely determined

by the number of irritant episodes suffered by that

particular pulp throughout its history. The size of the

pulp chamber may be reduced. No treatment is

required.

Pulpless and infected root canals

Pulpless canals will always be infected. There will be
no pain from the tooth itself when it has a pulpless
canal, although some patients may give a history of
occasional vague discomfort over a period of time.
However, pain may arise from the periradicular tissues
that become inflamed because of the presence of
bacteria in the pulp space. The only clinical sign
suggesting the condition may be the lack of response to
pulp sensibility tests. No significant changes can be
detected on the radiograph in the early stages of this
condition but within 2–10 months there will be a
radiolucency suggesting periapical involvement.

As there is the potential for erroneous pulp sensibility test
responses, corroborating the clinical findings, radio-graphs 
and patient information is necessary for a
definitive diagnosis.

Pulp necrosis

A necrotic pulp should be suspected when the tooth

does not respond to pulp sensibility tests. However, this

will not always be the case since teeth with pulp canal

calcification, previous root fillings or pulpotomies will

also not respond to pulp sensibility tests. Likewise,

some teeth or patients just do not respond to such tests

for no apparent reason. When pulp necrosis is present,

the history may reveal past trauma, previous episodes

of pain or history of restorations and caries.

Radiographically, a tooth with a necrotic pulp may

have signs (such as untreated caries, an extensive

restoration, previous pulp capping) or there may be no

such signs (e.g., following trauma). Trauma to a tooth

may cause pulp necrosis as a result of severing the

apical blood supply if the tooth has been displaced

from its normal position (e.g., luxations, avulsion) or if

there has been significant damage and inflammation to

the apical periodontal ligament (e.g., subluxation).

No significant radiographic changes are evident at

the root apex unless there is also periapical involve-ment, 

and this only occurs once the necrotic tissue

becomes infected. It is important to realize that a

necrotic pulp  per se does not cause apical periodontitis

unless it is infected.

Necrobiosis

A tooth with necrobiosis has both inflamed and

necrotic (usually infected) pulp tissue.

Many dentists use the term “partial necrosis” for this stage of the

disease process; however, “necrobiosis” was suggested

by Grossman

because it more accurately indicates the

condition – the key factor to the spread of the disease

process is the presence of bacteria within the necrotic

part of the pulp rather than the necrosis itself of part of

the pulp. The necrotic tissue may be in the coronal

portion of the pulp (e.g., pulp chamber) with the

inflamed tissue apically, or the different tissue states

may exist in different canals of a multi-canal tooth.

Teeth with this condition can be quite difficult to

diagnose since they usually present with a mixture of

the signs and symptoms of both pulpitis and necrosis

with infection. The symptoms may be mild with