If You Can’t Save The Tooth, Save The Bone

July 1, 2022
By Lisa Germain, DDS, MScD

When you consider the plethora of bacteria that colonize the oral cavity, it is a wonder that any procedure performed in the mouth could heal uneventfully.  Cultural and molecular studies have identified over 700 different species.  Over 400 of these have been isolated in the sulcus around the tooth and the remaining 300 have been found in other areas such as the tongue, mucous membranes, carious lesions, and endodontic infections.  Each person is thought to have approximately 100-200 of these species of intra oral bacteria indicating that there is a substantial diversity among different individuals. 1

An infection of the root canal system is the major etiological factor in apical periodontitis. 2,3 Scientific evidence indicates that microorganisms are essential for the progression and perpetuation of different forms of apical periodontitis. 4   The intention of endodontic therapy is to eradicate the infection in order to prevent these microorganisms from infecting or re-infecting the root canal system and in turn the periodontal tissues.  Endodontic disease occurs in a coronal to apical direction.  Apical periodontitis occurs once the microbes are in a position to stimulate the periapical tissues through the radicular portals of exit. Endodontic infections are polymicrobial by nature, however obligate anaerobic bacteria dominate the microbiota in primary infections.5

When a tooth is considered un-restorable for prosthetic reasons, is periodontally unsound, or has a complete fracture, extraction of the natural tooth is necessary and an endosseous implant is frequently planned as a replacement.   Post extraction socket preservation is commonly performed with the placement of avascular grafting material to scaffold the area in an effort to minimize volumetric contraction and maintain the dimension of the ridge.6

Placing grafting material in areas with ododontogenic infections is sited as a factor associated with increased risk of infection for dental implant procedures. 7

An entity referred to as an implant periodontal lesion has been described in the literature suggesting that one of the causes is potentially the presence of a preexisting infection or residual root fragments and foreign bodies in the bone.8,9  While there is no protocol for immediate grafting into sites with endodontic infections versus waiting until the infection has cleared up, a knowledge of how endodontic lesions affect the bone is helpful in the decision making process.

 

PULP DIAGNOSIS WITHOUT APICAL PERIODONTITIS

A diagnosis of normal pulp or reversible pulpitis does not affect the surrounding bone. The pulp tissue is vital and the tooth is either asymptomatic or the symptoms are not from pulpal changes. Teeth in this category should be extracted when they are not sound periodontally, or there is inadequate ferrule and hence unrestorable.   Since there has been no pathological change to the pulp, no bacterial contamination has occurred in the bone. 10

A diagnosis of irreversible pulpitis is a bit more complicated because this is a continuum that frequently leads to pulp necrosis.  For example, if severe lingering cold sensitivity is reproduced, and there is no sensitivity to heat, the diagnosis is irreversible pulpitis however changes in the bone are unlikely.  This is seen at the beginning of the continuum.  Conversely, if sharp pain to heat is reproduced with lack of cold sensitivity, pulp necrosis is imminent and there is likely the beginning of bacterial egress into the periradicular tissues. This is seen at the end of the continuum.

APICAL PERIODONTITIS

Chronic and acute apical periodontitis is a biofilm-induced disease that can occur with pulp necrosis, complete fracture, in teeth previously treated with root canal therapy and traumatic injury.  These types of endodontic problems have the potential to affect the periradicular bone and each has unique sequela that can affect grafting protocol.

-Pulp Necrosis

When pulp necrosis occurs, there is a dynamic encounter between host defenses and bacterial bi-products that occurs at the interface of the radicular pulp and the periodontal ligament. This results in local inflammation, resorption of hard tissues and destruction of other periapical tissues. The formation of various histopathological types of apical periodontitis are commonly referred to as periapical lesions.11 

Microbial root canal cultures have not been adequate to accurately determine the bacterial status of the root canal space.  They are technique sensitive which limits their predictive value often rendering false positive and false negative results. 12 The study of endodontic (and periodontal) microflora are more accurate when molecular methods such as DNA hybridization are used and samples are taken from the actual boney lesions.1

The asymptomatic (chronic) form of apical periodontitis is more common.  The symptomatic form – the acute apical abscess – can spread from the original site of infection to sinuses and other facial spaces of head and neck and cause serious life-threatening complications.  While there appears to be a significantly higher diversity of bacteria in acute alveolar infections when compared to asymptomatic chronic infections, both show significant quantities of microbial biofilm colonization. In addition, it is suggested that some species of bacteria are more related to lesions with acute symptoms.13,14    

Elimination of the necrotic contents of the root canal space, hence eliminating the source of the infection, is the intent of endodontic therapy and has a high, success rate if performed properly.  If, however the tooth cannot be saved, extraction will also remove the contents of the root canal space and eliminate the source of the infection.  The question here is, what happens to the remaining bacteria in the bone?  Is it safe to place avascular bone grafting materials at this time, or should grafting be delayed until a later date?  Unfortunately there is no single answer to these questions and critical thinking is essential to determine the best course of action for each individual case. Many clinical studies have shown that with meticulous debridement of the socket, infection is unlikely in a healthy patient. 15-22 In addition, premedication with antibiotics to eliminate acute symptoms of apical periodontitis should be considered prior to any surgical procedures.20

-Complete fracture and fracture necrosis

Teeth with complete longitudinal fractures are not candidates for root canal therapy and extraction is recommended.   The boney destruction from these lesions is rapid and frequently resorbs a narrow portion of the socket wall.  If an isolated pocket around the tooth can be probed, fracture is likely.  Not all teeth with complete fractures present in this way and diagnosis can be challenging.  Yet, it is essential to differentiate these lesions from those of apical periodontitis and radiographic interpretation alone is not enough.

Traditional periapical radiographs of these lesions are often mistaken for apical periodontitis.  However, root canal therapy has a hopeless prognosis if performed on these teeth so the accuracy of diagnosis is essential.  If the radiolucency is J-shaped or balloons around the root, it is most likely caused by a fracture. Often cupping or a widened PDL space is seen, many times incorporating the furcal area.  If a sinus tract is present, it is more likely to be close to the gingival margin rather than in the mucosal area in the vicinity of the apices of the tooth. 

CBCT images will show the bone loss that occurs as a result of the leakage from the fracture, but the voxel size is not small enough to visualize the actual fracture itself.  When evaluating these lesions using CBCT, they need to be aligned symmetrically with the saggital, frontal, and transverse planes to idealize the fracture line with the associated osseous defect.  Transillumination data and periodontal probing depths combined with associating these defects in all three planes gives the most accurate information for diagnostic purposes.  Otherwise, a false positive diagnosis is likely because the clinician is most likely viewing an artifact.23   

If a tooth has no restoration, has a necrotic pulp, and has not had a luxation injury, it is likely to have fracture necrosis.  Clinically there will be a longitudinal fracture extending from the occlusal surface into the pulp.  There is enormous potential for this lesion to cause extensive, rapid peri-radicular bone loss.  This alone makes it imperative that a proper diagnosis is made initially to minimize the amount of damage.  If a root canal is performed, and evaluated for healing 6 months later, not only will the lesion be present, it will be larger.  These teeth are not candidates for root canal therapy and should be extracted forthwith. 

There is good news and bad news when ridge preservation is planned for post extraction sites that have been affected by a tooth with a complete fracture.  The good news is that this type of infection is now a periodontal lesion, not an endodontic lesion.  The host response to bacteria and the formation of osteolytic lesions are common to both endodontic and periodontal lesions.  Both lesions exhibit inflammation that appears to inhibit bone formation.   However, lesions of endodontic origin pose a particular challenge since the bacteria exist in a protected reservoir that is not readily accessible to immune defenses.  Leakage from the fracture line creates an egress for bacteria, and therefore the infection source is no longer contained within the unyielding tooth structure. 24 The bad news is that grafting is a more challenging because the socket is now a 4 -wall defect instead of a 5- wall defect. 

-Previously treated teeth

Endodontic therapy has a very predictable success rate.  However, operator skill is variable and poorly filled root canals and/or bacterial invasion due to microleakage from coronal restorations can result in secondary infections. 27 Microbiota of primary infected canals with apical periodontitis differs in number and in species from secondary infected canals. In addition, E. faecalis was found to be the most prevalent species in previously treated teeth. 28   While this might not affect grafting in a healthy patient, delayed grafting should be considered in a patient with adverse risk factors.

-Traumatic Injury

While many forms of resorption are idiopathic, there is strong evidence that ankylosis, a form of replacement resorption, occurs as a result of traumatic injury to teeth.   The highest risk of ankylosis occurs with subluxation and avulsion injuries due to the severity of damage to the PDL.  An intrusion injury is particularly destructive because it crushes not only the PDL, but the alveolar bone as well.     

While not one test is indicative of ankylosis, some of the signs for diagnostic puposes include: lack of mobility, sharp solid sound when percussed, sometimes the CEJ is at a more apical position compared to adjacent teeth, and radiographic exam reveals absence of a PDL.

Replacement resorption does not usually affect the surrounding bone.

Most likely, the resorption will continue to replace the tooth structure with the bone.  The rate is variable and unpredictable.  The first inclination is to extract these teeth, however this decision is decidedly multidisciplinary.  The actual treatment decision should be based on the age of onset of the ankylosis as well as restorative implications of the defect that would be left if the tooth were extracted.   When ankylosis begins before the patient has finished growing, the growth of the alveolar bone can be arrested.  If the patient is finished growing, and the tooth is in the correct position, extraction is not necessary for biologic reasons.  While the pulp may be necrotic due to the injury, the resorption is caused by the disruption in the PDL and will not be arrested with root canal therapy.  The necrotic pulp is caused by infection.  The resorption is inflammatory in nature. 

If extraction is the treatment of choice, the challenge is removing the tooth atraumatically.  Care must be taken to separate the bone from the tooth to prevent removal of the cortical plate which is inconveniently now directly attached to the tooth.  In addition, decortication of the boney socket is essential to induce bleeding if the ankylosed tooth has compromised the blood supply in the area.

Conclusion:

Root canal therapy is a very predicticle procedure if done correctly.  If the tooth is severely periodontally involved, is unrestorable, or has a complete fracture, extraction is recommended to prevent further destruction to the bone.     

Grafting protocol in endodontic lesions needs to be made on a patient- by- patient basis.  Identification of the etiology of the lesion is essential for appropriate decision making.  If grafting is performed immediately post extraction, meticulous debridement of the socket is paramount.     

Treatment planning in dentistry should be multidisciplinary so that each clinician can offer their particular area of expertise.  It is important to consult with a specialist if diagnosis of an endodontic lesion is uncertain. 

References:

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