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 »  Home  »  Endodontic Articles 11  »  Supplementary routes to local anaesthesia
Supplementary routes to local anaesthesia
Advantages and disadvantages of intraligamentary anaesthesia.

Advantages of intraligamentary anaesthesia.
  1. Smaller doses are required compared to conventional infiltration and block anaesthesia.
    As mentioned earlier the normal dose is 0.2 mL per root. It has been suggested that the use of computerized delivery systems will allow the administration of a greater dose per root (Williams 2001).
  2. This method overcomes failed conventional anaesthesia.
    Walton & Abbott (1981) looked at a series of 120 failed conventional local anaesthetic injections for conservative and endodontic procedures. They found that after one periodontal ligament injection 63%of the teeth were successfully anaesthetized and a second intraligamentary injection was effective in 71% of the rest. In other words, a success rate of 92% in teeth in which conventional anaesthetic methods failed. In a similar study, Smith et al. (1983) reported an overall success of 93% for periodontal ligament injections in patients in whom conventional techniques had failed.
  3. There is limited soft tissue anaesthesia.
    The elimination of unwanted soft tissue anaesthesia can be of considerable benefit, particularly in the mandible. Apart from the obvious advantages in relation to four-quadrant dentistry, this can be especially useful for procedures in permanent teeth in children by eliminating the self inflicted trauma to the lower lip which can occur after mandibular block anaesthesia (Bedi et al. 1984). Loss of soft tissue anaesthesia, however, is not absolute. Matthews & Stables (1985) recorded that 27% of patients reported lower lip anaesthesia after periodontal ligament injections to mandibular molars. Similarly, intraligamentary injections for lower premolars can produce a mental anaesthesia (Kaufman et al.1983).
  4. This technique can be used for mandibular anaesthesia in patients with bleeding diatheses.
    Intraligamentary anaesthesia injections have been shown to be effective when used for restorative procedures in haemophiliac patients. In studies reported by Ah Pin (1987) and Spuller (1988), no complications related to haemorrhage or haematoma formation were recorded in haemophiliac patients who had received periodontal ligament injections for restorative dentistry without administration of Factor VIII.

Disadvantages of intraligamentary anaesthesia.
  1. Intraligamentary injections produce a bacteraemia.
    Roberts et al. (1997) reported that a significant bacteraemia occurred following over 95% of intraligamental injections in children. Thus the injection represents a potential cause of endocarditis in‘at-risk’groups.
  2. There is rapid entry of local anaesthetic and vasoconstrictor into circulation.
    Although direct entry of the needle into the lumen of a blood vessel is unlikely; using the periodontal ligament technique, the solution does reach the vasculature via the socket walls (Smith & Walton 1983, Dreyer et al.1983, Garfunkel et al.1983). Rawson & Orr (1985) presented results of the injection of mercury into cadavers using the periodontal ligament route and demonstrated extensive entry of the solution into vessels in a distribution that was suggestive of a universal entrance into the vascular tree rather than simple diffusion into the alveolar tissue.
    Smith & Pashley (1983) investigated the systemic effects of injecting various solutions (0.3 mL) into different anatomical sites in dogs and found that with adrenaline-containing solutions the qualitative and quantitative effects on blood pressure (20-25% fall) and heart rate (10-20% rise) after intraligamentary, intraosseous and intravenous injections were similar. Pashley (1986) claims that patients with cardiovascular disease should receive infiltration or nerve block anaesthesia rather than intraligamental injections when catecholamine- containing solutions are used as systemic spread is so rapid with the latter technique.
  3. Peri- and post injection discomfort can occur.
    The discomfort of intraligamentary injection varies between individuals (D’Souza et al. 1987); some recipients finding the method painful (Meechan & Thomason 1999). In Faulkner’s (1983) studyof100periodontal ligament injections for conservative procedures in 85 patients, 5 returned complaining of pain within 24 h. One had a region of necrotic gingiva as did one of the five patients (out of 187) who returned complaining of pain in the sample of Kaufman et al. (1983). In Miller’s (1983) series, six (out of 70) patients returned in pain within 24 h. Walton (1986) suggests that postinjection pain is owing to the insertion of the needle as pain occurs whether or not a solution is injected. However, the incidence of after pain may be related to the speed of injection as slow injection seems to be associated with less postinjection discomfort (Sykes1991).
    Some of the postoperative discomfort may be owing to tooth extrusion. Complete extrusion of a lower premolar tooth as a result of intraligamentary anaesthesia has been reported (Nelson1981). In addition a case of emphysema has occurred following an intraligamentary injection (Antenucci et al.1990).
  4. Intraligamentary injections may damage periodontal tissues.
    Histological studies in animal models have reported varying degrees of periodontal destruction ranging from no damage to some areas of irreversible damage. Brannstrom et al. (1982) looked at the periodontal tissue changes in monkeys subjected to periodontal ligament anaesthesia. One hour after injection they found disruption of collagen and lesions in the root surface and alveolar wall. The following day, there was loss of cementoblasts, osteoblasts and osteocytes and there were areas of necrosis. One week following the injection- damaged tissue was being replaced by a cell-rich vascular granulation tissue and osteoclastic activity was apparent. At 2 weeks, the appearance was returning to normal with new bone and young collagen and cementoblasts at the sites of root repair. One area of possible irreversible damage was noted, this being the interdental septal crest when periodontal ligament injections were administered to adjacent teeth. In such cases, sloughing of the interdental papilla occurred and the crestal bone became necrotic. Walton & Garnick (1982), using a similar model, also reported some bone resorption in the crestal region. On the other hand, Galili et al. (1984) noted no damage to bone or cementum in monkeys who had received intraligamentary injections. These workers found that the damage produced was localized, minor and reversible. They found no damage apical to the needle penetration site and in most cases all signs of damage had gone by 8 days. Similarly, Walton & Garnick (1982) noted no damage apical to the needle insertion point. Fuhs et al. (1983) could find no evidence of damage to the periodontium in dogs sacrificed within 28 days of intraligamentary anaesthesia. Pertot & Dejou (1992) noted osteoclastic activity and bone resorption in dogs 7 days after intraligamental injections. This had healed by 25 days. These authors correlated the degree of resorption with the force of injection. List et al. (1988) measured the gingival crevicular fluid flow before and following intraligamentary injections in volunteers. They concluded that the amount of inflammation was minimal.
    Roahen&Marshall (1990) demonstrated external root resorption in dogs following intraligamentary injections. Saroff et al. (1986) reported a case of external root resorption in a lower left second permanent molar in a 40-year-old patient which arose following the administration of a periodontal ligament injection. Lovsund- Johannessonet al. (1986) reported reversible root-surface changes in children’s teeth subject to intraligamentary anaesthesia. These authors concluded that the technique was safe in children.
  5. Intraligamentary anaesthesia may damage pulp.
    Kim (1986) reported a dramatic reduction in pulpal blood flow when vasoconstrictor-containing solutions were administered via the periodontal ligament in dogs. However, histological studies (also in dogs) performed by Plamondon et al. (1990) and Roahen & Marshall (1990) revealed no long-term deterioration in the pulp following periodontal ligament injections. Similarly, Lin et al. (1985) reported no histological changes in the pulps of cat teeth subjected to intraligamental injections of 2% lignocaine with 1: 50 000 and 1:100 000 adrenaline and Peurach (1985) found no deterioration in pulpal tissue after intraligamental injections in the monkey model. Plamondon et al. (1990) investigated the additive effects of cavity preparation and intraligamental injections of lidocaine with adrenaline and found no more serious reaction in teeth treated this way compared to those subjected to cavity preparation alone. Torabinejad et al. (1993) in an electron microscopy study, noted no deleterious effects in pulpal tissue of human teeth subjected to intraligamentary injections of 2% lidocaine with1:100 000 adrenaline.
  6. Intraligamentary anaesthesia may damage unerupted teeth.
    The pressure used during periodontal ligament injections can force the anaesthetic solution into underlying tooth germs (Brannstrom et al.1982). Brannstrom et al. (1984) investigated this possibility in monkeys. Permanent teeth whose deciduous predecessors had received intraligamentary injections exhibited defects in enamel. In addition, in both treatment groups, other permanent teeth in the same quadrants as the treated teeth (but not in control uninjected quadrants) showed areas of enamel hypomineralization. However, such effects have never been reported in humans.
  7. Injection equipment may be damaged.
    Local anaesthetic cartridge fracture has been reported by a number of authors (Malamed 1982, Miller 1983, Status Report 1983). This occurs because the specialized syringes allow the application of more force during intraligamentary injections than traditional equipment. Pressures of around 5 MPa can be produced within the cartridge during intraligamentary anaesthesia (Walmsley et al. 1989). This will fracture around 1% of glass cartridges but will cause about 75% of plastic cartridges to fail at room temperature (Meechan et al. 1990). Plastic cartridges stored at body temperature will be more susceptible to failure (Meechan et al. 1995). The solution to the problem is to avoid the use of plastic cartridges and to inject slowly. Grundy (1984) recommends the rate employed should be at least 20 s for each 0.2 mL injected.