to Reduce the Risk of Reinfection in Endodontics

Poorer prognosis

Better prognosis

Secondary infection

Primary infection

Long-standing infection

 

Presence of fistulae

No historical or current oral/endodontic communication

Lack of coronal seal/insufficient residual tooth structure

Sufficient tooth structure allowing gap-free restoration

Hairline cracks

 

Endo/perio lesion

 

The duration of an infection has a very important role: long-standing infection are more difficult to be removed. Several studies confirmed that the maturation of biofilms allows an increased resistance to any antibacterial approach [8]. The nature of bacterial contamination and sources may play a major role too.

Several routes and chances of contamination of the root canal system are present:

  1. 1.
    De novo infections of the root canal space

    1. (a)

      Deep decays (with a prompter effect on younger patients with wider dentinal tubules).

       
    2. (b)

      Coronal leakage (faulty or missing coronal restoration, degradation of the hybrid layer).

       
    3. (c)

      Coronal and radicular micro-crack (craze lines, hairline cracks, microfractures).

       
    4. (d)

      Long-standing periodontal disease (acidic exposure and root surface instrumentation can lead to dentinal tubules exposure and retrograde dentinal infection).

       
    5. (e)

      Presence of fistulae can sustain extra-radicular and retrograde endodontic infections leading to the formation of extra-radicular biofilm, which are proven to be more aggressive and pathogenic.

       
     
  2. 2.
    Recurrent endodontic infection

    1. (a)

      Incomplete eradication of the microbial communities presents as biofilms in the main root canal lumen and can lead to a re-propagation of the infection with a delayed recolonisation even in the presence of satisfactory root canal filling.

       
    2. (b)

      Incomplete disinfection of inaccessible areas due to inadequate or short time of disinfection.

       
    3. (c)

      Insufficient operative skills and incomplete chemo-debridement and shaping protocols (missed canals).

       
    4. (d)

      Iatrogenic contaminations, a novel concept in endodontics, may help in understanding the endodontic infection stages and its origin: cross-contamination during the handling of non-sterile endodontic consumables can be a significant cause for refractory infections.

       
     

8.1.1 Medically Compromised Patients and Relapse of Endodontic Infections

The evidence regarding the contribution of the endodontic infection to systemic pathologies and diseases in endodontic research is still sparse [911], whereas conclusive evidence has been reached in the field of periodontology [12]. The host’s role in the establishment and evolution of the endodontic pathology, including the potential systemic effects of a low-grade chronic inflammation/infection, is now taken more seriously. The receiving end of the infection has a major role in terms of permissiveness to the spreading of endodontic infections: B and T cell deficiency can lead to increased spreading of endodontic infection [13].

Vice versa the continuous inflammatory stress of an infected root canal system that triggers the immune response may have systemic effects on the host [14]. The main areas of potential association of endodontic infection and systemic diseases include cardiovascular disease (CVD), diabetes mellitus (DM), chronic liver disease, blood disorders and bone mineral density. The linkage between CVD and endodontic pathology may be conceivable, in particular with a hypothesised role of the endodontic inflammatory mediators on the initiation and progression of CVD; however, further studies are required [14].

In terms of DM, the association of an increased disease prevalence and frequency of onset of periapical lesion for type 2 diabetic patients has been confirmed [15]. However, a delayed or hindered healing of periapical lesions following endodontic treatment in diabetic patients has not been proved yet [16, 17]. The risk of bias for these studies is high, and further investigations are required. Little evidence is currently present for chronic liver disease, blood disorders and bone mineral density [14].

Interestingly the fitness level of the patient apparently has little influence on the manifestation of the endodontic disease [18]. Whereas other studies seemed to point towards a certain association of certain gene polymorphisms that lead to an increased susceptibility to endodontic manifestation (periapical resorption presence and extent), however the evidence is still very limited [19].

8.1.2 The Microbiota of Refractory Endodontic Infection

The microbiota of refractory infection is very dissimilar from the primary endodontic infection. The initial formation of periapical lesion can occur with limited bacteria present in the dentino-pulpal complex [5]. Not rarely tubular dentine infection may be sufficient to trigger a cytokine cascade leading to the formation of the periapical lesion [20]. Primary endodontic infection may however mature with time leading to the development of a complex endodontic biofilm [8]. The endodontic niche provides a selective pressure due to the limited oxygen tension. The starvation of bacteria receiving limited amount of serum proteins or alternative metabolite is another reason for the survival and rise of the most resilient and aggressive pathogens among the endodontic biofilm. With cultural methods the most commonly isolated species in primary endodontic infection are Peptostreptococcus micros, Fusobacterium necrophorum, Fusobacterium nucleatum, Prevotella intermedia and Porphyromonas gingivalis [21]. In primary endodontic infection associated with periapical lesion, the microbiota is mixed with both gram-negative and gram-positive, mostly anaerobic microorganisms and including more than three species per canal. In secondary endodontic infection, facultative anaerobes and gram-positive bacteria prevail, and interestingly only one or two species are isolated. In secondary endodontic infection, certain species are cultured more frequently: Enterococcus faecalis, Streptococcus spp., P. micros and F. necrophorum [22]. More recent microbiological studies adopting molecular methods that bypassed the limits of cultural approaches revealed a different picture. The association of E. faecalis with failed root canal treatments has been noted in several papers [2327].

A recent study showed that gram-negative anaerobes previously considered related to symptomatic lesions were also present in asymptomatic cases. A novel hypothesis suggests that different compositions of the endodontic microbiota can result in similar disease outcome characteristics [28]. Another established hypothesis is that the root canal treatment per se may have a direct effect on the microbiota creating an imbalance and selecting certain species by modifying the ecology of the root canal space [29]. Current studies are re-evaluating the sole etiopathological role of E. faecalis in the development of refractory endodontic infection showing instead the presence of more complex polymicrobial infection [30, 31].

A further concept regards the possible contribution of the clinician in the establishment of secondary infections in the course of the primary treatment. The nosocomial infections, also defined as hospital-acquired infection (HAI), have been reported in different branches of medicine and affect the outcome of surgical and other operative procedures [32, 33]. The usage of non-sterile consumables and the contact with infected environmental surfaces may lead to the transmission into the root canal space of pathogens, that can subsequently establish a secondary infection [34]. In particular Staphylococcus epidermidis and Propionibacterium acnes are not present as common commensal in the oral cavity; however, these species have been isolated in endodontic refractory infections [35]. Increasing the asepsis/sterility during endodontic treatment may prevent nosocomial infections.

8.2 Diagnosis of the Refractory Endodontic Infection

The diagnosis of a refractory endodontic infection is important for the clinician to minimise the chances of failure [25]. A truly refractory endodontic infection may not be eradicated even utilising the most advanced non-surgical techniques [36].

The detection of strains specifically associated with persistent/refractory pathology is still not practical in everyday clinical settings. Culturing methods cannot grow non-cultivable and fastidious bacterial strains, often present in endodontic infections. Molecular methods are still expensive and require a certain turnaround impractical during a single treatment session. The clinician can only rely on the clinical signs of pathology that are usually related to the more established infection.

Clinical examination revealing presence of symptoms and radiographic signs of non-healing or expanding periapical lesion is indicative, by assumption, of presence of a refractory endodontic infection. Clinician rarely confirms clinically the presence of bacteria. Clinical microbiologic sampling is not commonly used. Novel devices based on fluorescence may be utilised chairside to confirm directly the presence of bacteria in failed root canal treatment. Chairside tests have been previously considered in periodontology (e.g. BANA test) [37]. Reports of contemporary usage of anaerobic tests in endodontology are very limited [38].

Refractory infections may have developed due to iatrogenic infection or persistence of bacteria at the time of the primary endodontic treatment or due to secondary recolonisation of the root canal space. Lack of coronal seal is the major reason for the reinfection of the root canal system. Even in the presence of a well-executed root canal free of voids, bacteria can slowly recolonise the root canal space through a percolation phenomenon [39, 40].

The presence of a large periapical lesion is not related to the bacterial load; however, it does reduce the chances of healing independently of the microbiological status. On the other hand, the existence of sinus tract (fistula) is associated with more complex biofilms which are proven to be more resilient [41] (Fig. 8.1a, b). P. acnes can be isolated in the presence of fistulae. This bacterial strain has been described as an aggressive pathogen that can lead to failure of orthopaedic implants, cardiac valve and other prosthetic surfaces prone to biofilm development [42]. The formation of fistulous tracts also facilitates the infection of the external surface of the roots leading to the formation of extra-radicular biofilm, which are inaccessible by the non-surgical root canal treatment [43, 44].

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Fig. 8.1

(a–b) Clinical photograph (a) and long cone periapical X-ray (b) showing an intra-radicular fistula. The chances of healing are diminished due to the possibility of oral bacteria to form an extra-radicular biofilm which is inaccessible by orthograde root canal treatment. The presence of hairline crack should be investigated with an operative assessment in the presence of shallow existing restoration which is not impinging on pulp space. Alternative pathway of bacterial contamination of the root canal space should be suspected

The development of extra-radicular biofilm is associated also with specific bacterial strains as Actinomyces actinomycetemcomitans that may be also related to intra-radicular polymicrobial biofilms [45]. Another important dimension of the endodontic infection is time: long-standing endodontic infections are more resilient and difficult to be eradicated [46]. The maturation of biofilms causes the formation of complex defence mechanisms, including extracellular matrices [47].

If the clinician is aware at the diagnostic phase of the effect of these parameters on the outcome, a more successful treatment can be planned, possibly including a plan for failure, of which the patient should be made aware at the outset (i.e. apicoectomy).

Where several detrimental parameters co-exist very large periapical lesion associated with a tooth with minimal residual coronal structure and with a long-standing fistula) a poor prognosis with high chances of failure can be predicted [48]. The patient should be informed of the risks and alternative treatment options. In certain clinical cases, true refractory endodontic affected may only be resolved with the extraction of the affected tooth.

8.3 Restorability and Coronal Seal

The amount of remaining tooth structure is related to the provision of a successful restoration that prevents coronal leakage. The presence of marginal gaps in the coronal restorations can lead to a prompt reinfection. The average bacterial cell size of 2 μm allows a prompt passage through failing or deficient restoration. Lack of coronal seal increases the odds of reinfection of the root canal system even in the presence of a satisfactory root canal filling [49].

Limited number of study envisioned an objective restorability index [50, 51]. More recent data revealed that when the residual coronal tooth structure is less than 30%, the outcome of the root canal treatment decreases significantly due to higher chances of reinfection [52].

The main principles to be considered when restoring an endodontically treated tooth are to protect completely the cusps in posterior teeth in order to retain the tooth integrity and to achieve a good peripheral coronal seal. The choice of type of restorative material (amalgam vs. composite) and type of cuspal coverage (onlay vs. full crown) does not affect the longitudinal survival.

Achieving a satisfactory level of coronal seal seems to be independent from the type of restorative material employed and more related to the existing dentinal substratum [53]. The use of resin-based restoration or intracanalar fibre post has been advocated to improve the hermetic seal of the root canal system by clinicians, but no evidence is present in the literature [54]. However, the limited evidence present in literature reveals no superior advantages compared with more traditional coronal and intracanalar restoration [55]. Previous approaches included the use of the Nayyar core technique that requires removing 2–3 mm of sub-orifice gutta-percha to create a dovel space to allow the extension of an amalgam core in these areas [56]. The evidence seems very scarce in terms of type of restoration to achieve the best possible coronal seal [49]. The amount of residual tooth structure is more important than the type of post or restorative material supporting single crowns [57].

Another important parameter to be considered is the time of provision of the final restoration. Historically the tendency to wait for a full healing of the periapical lesion following root canal treatment was a common place [58]. Current approach dictates a prompt finalisation of the coronal restoration. The provision of a good coronal seal is a key aspect of maintaining the periapical health (Fig. 8.2). The final restoration should be provided as soon as practical: the survival of root canal-treated teeth that received a crown within 4 months and after 4 months following RCT was 85 and 68%, respectively. Endodontically treated teeth that received a crown 4 months after RCT were extracted at three times the rate of teeth that received a crown within 4 months after RCT [59]. The presence of symptoms is the only major contraindication to a prompt restoration. Waiting unnecessarily for the completion of the ongoing bone healing process (up to 4 years according to the ESE guidelines) may instead lead to the reoccurrence of the endodontic infection due to loss of the coronal seal.

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Fig. 8.2

Long cone periapical X-ray showing the co-existence of unsatisfactory root canal filling on the upper right first premolar associated with a satisfactory coronal seal. Conversely the upper right second premolar has a poor coronal seal in the presence of a well-executed root canal filling. The role of the coronal restoration in maintaining the periapical health should be emphasised

8.4 Operative Strategies to Eradicate Endodontic Infection

The chemo-debridement of the canal is based on the use of files (stainless steel or NiTi, manual or mechanised) to remove the infected dentine with the concomitant irrigation with adequate disinfectants. The resection of infected dentine operated by the endodontic instruments removes not only the surface of the dentine but also exposes the infected tubules. The subsequent action of the irrigants is based on a direct physical effect creating a shear stress that can detach the biofilm adhering on the root canal wall and on the direct antibacterial effect on the biofilm. Several steps can allow achieving a better outcome of the root canal treatment and minimise the risk of relapse of the endodontic infection (Table 8.2).

Table 8.2

Operative phases and their significance aimed at maximising the disinfection of the root canal system, preventing nosocomial cross-contamination and reducing the risk of reinfection

Clinical steps

Significance

Rubber dam isolation

Saliva cross-contamination elimination

Disinfection of the operative field

Decontamination of tooth surface to avoid introduction of oral bacteria into the root canal system

Removal of existing restorations (i.e. direct or indirect restorations)

Confirmation of restorability and future coronal seal

Removal of infected dentine

Reduces chances of reinfection of the root canal system

Confirmation of absence of hairline cracks

Prevention of bacterial leakeage

Coronal flare

Creates an irrigation reservoir and maximise the exchange of irrigants

Copious irrigation with NaOCl solution

Enough contact time to reach the infected non-instrumented areas

Patency filing

Closed system vs. open system and removal of vapour lock

Adequate shaping

Apical gauging to remove sufficient infected dentine

Removal of dentinal debris from instruments flutes

Avoids cross-contamination between canals

Activation of irrigants (sonic or ultrasonic)

Increased antibacterial activity

EDTA irrigation

Penultimate rinse to remove smear layer

Final irrigation with NaOCl

Disinfection of the exposed dentinal tubules

Drying the canal with sterile paper points

Avoiding iatrogenic infection

Dressing with CaOH (if used)

Maximisation of the disinfection in the presence of fistulae (debatable) or wide periapical lesions or drainage (pus/exudate) within the canal (weeping tooth syndrome)

Change of gloves at time of obturation

Reduction of environmental cross-contamination

Disinfection of gutta-percha points for 1’ in NaOCl

Reduction of nosocomial infection risk

Rapid provision of a final restoration and/or full cuspal coverage

Maximisation of the coronal seal

To date no objective measurement is available to the clinician to determine the level of disinfection achieved during the chemo-debridement. Even in the case of microbiological sampling with a turnaround of at least 2 weeks for slow-growing fastidious anaerobes, the information provided regards only the bacteria of the main canal lumen. Different areas that are not reached by sampling such as isthmuses, lateral canals, apical deltas and dentinal tubules may contain an unknown amount of bacteria. Many study questioned whether the presence of bacteria in these inaccessible areas may contribute to the reinfection of the root canal system following primary root canal treatment. No clear evidence has been given so far to the clinicians to determine the endpoint of root canal treatment, that is, the required level of cleanliness or maximum acceptable bacterial cells count that does not hinder a successful outcome. Classic study compared the different outcomes depending on the presence of bacteria (positive cultures) prior to obturation; the agreement is that presence of bacteria at the time of obturation has a detrimental effect on the healing of periapical lesions [6062]. Bacterial entombment, where a well-executed root canal would entrap bacteria within the dentinal tubules and devoid them of any metabolite and substratum to sustain the root canal infection, may not be sufficient to eradicate the infection [63]. Starvation modalities of bacteria can lead to high resistance and a lapse in the reappearance of the infection [64]. Bacteria in a dormant state and starvation may maintain a viable but non-culturable state that may still lead to reinfection of the endodontic niche [47, 65] (Fig. 8.3).

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Fig. 8.3

SEM photomicrograph depicting an infected smear layer covering the root canal walls following shaping with insufficient irrigation. The clinical relevance of entombed bacteria is not clear; however, recent studies described the dormant state of bacteria embedded in the smear layer. Refractory endodontic infection may occur due to the recolonisation of the root canal system starting from these sparse bacteria

The traditional indications for reaching the clinical endpoint in endodontic treatment are based on subjective or dogmatic approaches. Clinicians referred to presence or absence of smell from dentinal shavings as an indicator of persistence or eradication of the infection; others observed the shade of the dentinal shaving collected on the file flutes [66]. More rigorous and dogmatic approaches indicated certain protocols to achieve dentinal cleanliness: it has been recommended to instrument at least three sizes bigger of the first file to bind at the apex to remove sufficient infection at the apical level [67]. Alternatively, protocols dictating a minimal dressing time with CaOH implied that the biofilm could be eradicated after a sufficient time of exposure to an alkaline environment [68]. However, both methods can be easily proved fallacious: tubular infection may infect the dentine to a depth of 1000 μm which is beyond the three sizes increase; on the other hand, bacteria such as E. faecalis have been shown to survive in alkaline environment [69, 70].

8.5 Access Cavity and Infection Prevention

The clinician needs to follow certain operative procedure to maximise the level of disinfection of the root canal system. The use of the rubber dam should be considered as the primary means to avoid the relapse of primary endodontic treatment. Despite the evidence that carrying out root canal treatment without rubber dam nullify the attempt to achieve a clean root canal, the adoption by general practitioner is extremely limited (<5%) [71, 72]. Furthermore, in absence of rubber dam, sodium hypochlorite is sparingly used due to potential ingestion [72]. Mastering the placement of the rubber dam is essential. Single tooth isolation with winged clamps and OraSeal (Ultradent, St. Louis, MO, USA) used as an adjuvant to increase the peripheral seal around the tooth to be treated improves significantly the ability to achieve complete sterility of the operative field. In case a sufficient isolation cannot be achieved (often due to the lack of residual coronal tooth structure), the feasibility of the root canal treatment should be questioned unless pre-endodontic restoration cannot be placed to improve seal. Still the provision of pre-endodontic restorations should not override the restorative consideration where a tooth is not restorable if the sound dentine is subgingival [73].

A good practice is to use surface disinfectants once the rubber dam is placed prior to accessing the endodontium. This simple step minimises the risk of introduction of further plaque bacteria into the root canal system especially in cases with limited endodontic bacteria load (i.e. irreversible pulpitis).

Following the essential step of a leakage-free rubber dam isolation, a thorough removal of carious infected dentine is recommended, despite minimal invasive approaches recommended in pulp vitality preservation cases say otherwise [74]. A convenient access cavity needs to be considered avoiding key-hole approaches (ninja, truss, calla lily, etc.) that limit the visibility and ability to fully disinfect the root canal system. Subsequently a thorough examination of the pulp chamber under magnification will rule out the presence of hairline cracks or other defects that would lead to a prompt reinfection of the endodontium via periodontal space. Hairline cracks visible under magnification can have a width of 40 μm, which are readily accessible by bacteria of 2 μm size [75]. The consensus regarding the management of visible hairline crack within the root canal system is still limited. Zero tolerance to hairline crack present on the floor of the pulp chamber is recommended to increase the outcome of the root canal treatment [76]. Other authors consider problematic only the hairline cracks that reach the canal orifice level, and others would consider unsalvageable only teeth with hairline crack penetrating into the canal below the orifice level [77].

Operatively the main advices are to prevent hairline propagation by taking the tooth off the occlusion (cusp trimming) and/or cement orthodontic bands. Alternatively, an acrylic temporary crown can be considered for similar reasons. The evidence for repair of dentine with bonding and resin composite is limited, and this technique should be avoided. Whereas deep apical root cracks cannot be detected at the diagnostic stage, the presence of deep single-spot (tubular) probing associated with hairline crack should discourage from any attempt to provide root canal treatment [78].

Once the integrity of the pulp chamber is confirmed, all existing canal orifices need to be detected. The overlooking of the endodontic anatomy may lead to prompt failure. The use of CBCT at the treatment planning phase may greatly reduce the occurrence of missed anatomy and iatrogenic errors [79]. In certain clinical condition in elderly patients or with previous history of pulpal irritation, secondary and/or tertiary dentine may have caused a significant reduction of the patency of the canals and size of the pulp chamber [80]. Canals that are not patent macroscopically can still be patent to microorganism that can freely colonise the niche and reach the apex. At this stage it is extremely important to have a good knowledge of the textbook anatomy of each type of tooth. This knowledge should be backed up by the use of high magnification and illumination to fully comprehend the canal orifice position and relationship. Missed canal is still one of the main reasons for root canal treatment failure [81, 82]. On this account, again, minimal access cavities (ninja, truss, calla lily) leaving undercuts and not allowing visual and tactile exploration of the pulp chamber may cause failure to treat the whole root canal system. At this stage the use of ultrasonic tips or of long shank rose-head burs as the gooseneck or Meisinger can aid the task to remove calcifications within the pulp chamber. Pulp stones can be present and obstruct the access to the orifice and leave a false bottom at the furcation level; the virtual space between the furcation floor and pulp stones can be rife with bacteria, and even in the absence of an existing infection, pulp remnants may represent a future substrate for bacteria infecting the root canal space. For these reasons leaving pulp stones in situ may cause future relapse of the endodontic treatment.

8.6 Shaping with Stainless Steel and NiTi Instruments

The next operative stage following initial patency confirmation and manual scouting of the root canal system is the establishment of a coronal flare. With the advent of double flare techniques and modified step back, a great emphasis on avoiding rushing to the apex has been recommended to minimise the extrusion of bacteria and debris through the apex together with the formation of blockages [83]. A premature shaping of the apical third without coronal flare is bound to have limited effectiveness as the irrigant penetration is limited.

Prior to the NiTi revolution, predicting the amount of dentine removed during the shaping was difficult [84]. Stainless steel files have a 2% taper to retain enough flexibility. To achieve a sufficient preparation taper, as per the Schilder’s technique, the step back technique was utilised. Depending if stepping back 1 or 0.5 mm, a taper of 5 or 10% would be achieved. The advent of more flexible alloy allows increased tapers that can lead to a predictable and standardised removal of dentine. Still to date no study provided sufficient evidence regarding the effect of different shaping tapers on the success of root canal treatment. The microscopic anatomy of dentinal tubules varies among the different levels of the canal with wider tubules and increased density per square μm at the coronal level with respect to the apical. For these reasons the permeability of dentine to endodontic irrigant may be very efficient independently of an increased removal of dentine dictated by an increased taper instrument. Very few studies analysed the contribution to removal of the infection of instruments independently of the irrigation [85]. Clinically hand or mechanised instruments should never be used without irrigants. The presence of a prematurely enlarged coronal third improves the fluid dynamics of irrigants and increases the volume entering in the root canal system [86]. Nonetheless one of the main limitations of root canal shaping is the difficulty of any type of instrument to contact the full extent of the root canal wall surface [87]. The effect of an incomplete disinfection of the root canal system will have a major effect if larger amount of bacteria is left behind, in particular in the main canal lumen as demonstrated by the cultural studies [60].

Among the different envelopes of movement of hand files, the balanced force together with circumferential and anticurvature filling is the best combination to maximise the contact with the dentinal walls to remove the adhering biofilm. Similarly, in de novo cases where the root canal is minimally infected, great care should be paid to remove effectively all the pulpal tissue as this may represent a future substratum for bacteria leading to a prompt bacterial regrowth. The collagen component of the ground substance of the pulp and of the dentine can favour the early adhesion of biofilms [88].

Instead mechanised NiTi instrument (both rotary and reciprocating) have a fixed envelope of motions (rotation associated with pecking or with brushing movement or progressive reciprocation associated with pecking or with brushing). Furthermore, the NiTi alloy is characterised with a self-centring ability especially in curved canals. These features lead to the presence of untouched areas of the canal that can reach up to 49% of the total surface [87].

The current mechanised NiTi instrument sequences, usually based on a fewer number of files, are based on a preliminary enlargement of the coronal third of the canal. Even single file techniques recommend to approach the shaping of the root canal in thirds, usually focusing on the coronal third first. The removal of the bulk of infection present within the pulp chamber underneath decays and in the coronal third of the canal can reduce further cross-contamination from the coronal third to the middle and the apical thirds [85]. During mechanised shaping the production of infected dentinal shavings cut from the root canal walls is increased compared with manual filing [89]. The operator will remove the infected dentinal debris from the flutes of the NiTi instruments after each passage. The use of a sponge may facilitate this task. Using different sponges may reduce the chances of cross-contamination between thirds of each individual canal and among different canals. In multi-rooted teeth different levels of contamination and inflammation may be present in each individual canal; for this reason cross-contamination should be avoided with a thorough cleaning of the file after each passage: ten strokes of an “in and out” movement of the file in a dense sponge saturated in NaOCl or chlorhexidine achieve 85–100% cleaning [90].

8.7 Irrigation

The shaping action of endodontic instruments is complemented by the use of irrigation. Its main purposes are the direct eradication of the endodontic biofilm and the removal of organic and inorganic debris produced during the shaping [91]. The selection of the best irrigant solutions and the optimisation of their usage required several trials and errors. One of the important aspects is also the biocompatibility of irrigants to be used in the root canal system. Irrigation efficacy is based on the type of irrigant, the volume, the delivery method and other activation methods, which will be later discussed.

Three main categories of irrigants are used in endodontics: tissue-dissolving agents, antibacterial agents and chelating agents.

Currently, solution combining all activities together, although being developed, did not acquire a widespread use [92]. The irrigant needle allowing the best fluid dynamic of the irrigant within the root canal system is the side-vented ones. Compared to flat or bevelled one, the risk of irrigant extrusion is limited. As previously discussed taper and apical preparation may affect the effectiveness of the irrigants. The creation of a coronal flare increases the volume and exchange rate of the irrigant to the middle and apical third. An increased taper increases shear stress on the root canal walls, still maintaining a limited risk of apical extrusion. The shear stress can detach adhering biofilm allowing their dislodgment and complete removal from the coronal aspect by means of aspirating the irrigant outflowing from the root canal orifice [86, 93].

The gauge of the needle used for irrigation is affecting the level of irrigation within the shaped canal (Table 8.3). Several studies reported the presence of a stagnation plane beyond the tip of irrigation needles under which the exchange of irrigants is limited. Knowing the diameter of the needle allows to determine the exact level reached by the irrigants effectively. To obtain a continuous exchange of irrigants, the side-vented needle should be ideally positioned within 2 mm of the working length [93]. The irrigation needs to be carried out by expressing the plunger of the syringe gently with the index finger and maintaining a continuous in and out movement to avoid locking of the needle.

Table 8.3

Correspondence between irrigation needle gauge and their lumen calibre in mm and the corresponding ISO files considering their external diameter

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Oct 21, 2018 | Posted by in Endodontics | Comments Off on to Reduce the Risk of Reinfection in Endodontics
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