Here, we demonstrated the successful preservation of the vitality of teeth involved with a large radicular cyst in anterior maxilla that was managed by a direct surgical enucleation approach.
Various reports identified extra radicular sources of irritations in cases of persistent radicular cysts [10, 11]. Thus, both the radicular space and the cyst itself should be considered as individual potential sources of morbidity. Periapical surgery offers an unequivocal single occasion resolution for the patient, in which the two entities are treated simultaneously. Nevertheless, it requires a high level of operator skills and has a higher risk of complications including the possible injury to surrounding vital structures [12].
Magnification and improved visualization by the dental operating microscope (DOM) in endodontic microsurgery enhance the ability of the operator to critically assess the anatomical features of the surgical field, leading to accurate judgments and higher success [13]. Development of endodontic microsurgical armamentarium allowed a more precise control of the surgical procedure, reducing the incidence of complications [7]. Traditionally, vigorous removal of the cystic pathological tissue was advocated to rapidly establish haemostasis and reduce the operation time [14]. However, in our case, the magnification by the DOM permitted carful and controlled excision of the pathological tissue and meticulous execution of the surgical technique while avoiding injury to the surrounding structures. Furthermore, the detection of tooth 11 neurovascular bundle, immediately after enucleation of the cystic membrane (Fig. 2b) and before flap repositioning (Fig. 2d), allowed us to accurately predict the prognosis of vitality of one of the two vital teeth included in the cystic cavity. Response to sensibility testing in follow-up recalls and absence of periapical radiolucency, resorption, and coronal discoloration are ancillary evidence that support the maintenance of tooth 11 to vitality.
On the other hand, multiple studies discussed the fate of vital pulps when their apical neurovascular bundles were interrupted. Revascularization is possible following injury with various degrees of reparative and neurological events [15]. In our case, tooth 13 demonstrated partial calcific obliteration (PCO) at the follow-up investigations. In absence of other conditions, PCO is a sign of vascular repair following injury to the tooth supporting structure [16]. The deposited dentin is considered reparative, as it’s formed by newly differentiated mesenchymal cells following odontoblasts degeneration secondary to the injury [17]. We noticed a near obliteration of coronal pulpal space at the 1-year follow-up radiographs (Fig. 3b). However, over the course of the following three years, the rate of calcification was significantly reduced with only a slight narrowing of the radicular canal (Fig. 4c). The initial pronounced calcification of the coronal pulp may be attributed to the tendency of inflammation to localize coronally after injury [17]. While reinstatement of the neural regulatory control over the newly differentiated odontoblast following neural regeneration, and reversal of hypoxic conditions in the pulp might have been the reasons of the limitation of calcification [18, 19]. Lundeberg & Cvek study [20] on PCO of traumatized teeth concluded that pre-emptive endodontic treatment is not warranted, based on the histological status of pulps undergoing calcification. Anderson et al. [16] reported that secondary pulpal necrosis happened only to 1 % of teeth exhibiting PCO during a 1 to 10-year follow-up study, while Robertson et al. [21] calculated a 20-year pulp survival rate to be 84% for permanent teeth with calcified pulps secondary to dental trauma., As the tooth is vital, the case remains under follow-up.
Guided tissue regeneration techniques utilized in periapical surgeries, are intended to improve the healing outcome in large osseous defects with resorbed cortices [22]. Usually, a membrane is used to cover an osteogenic material packed in a bone cavity. Although placing a membrane barrier might have been beneficial in this case, packing the grafting material in the defect cavity could have jeopardized the integrity of the vital teeth neurovascular bundles. This sighting adds a new factor to consider for the use of regenerative techniques in periapical surgeries.
Teeth 13 and 11 lacked positive responses to initial sensibility tests done by EPT and cold test but regained and maintained normal responsiveness following treatment at 1 and 4-year follow-up recalls. This could be attributed to compression neuropathy [23]. Positive pressure is considered a key regulator of cystic growth [24]. It has been linked to initiation of bone resorptive mechanisms and to alterations in the physiology of the surrounding structures including the inferior alveolar nerve [4, 24]. Previous reports showcased recovery of inferior alveolar nerve’s sensory function following decompression of large cystic lesions and illustrated improved responsiveness of the innervated teeth [4, 25]. Similarly, in our case, the direct pressure exerted on the periapical neurovascular bundles by the growing cyst might have led to reduced sensation and numbness of the two vital teeth included in the cystic cavity, while eliminating the pressure following cyst enucleation recovered the normal neural function and sensibility.
In neurological studies, reported pressures of 50 mm Hg and 60 mm Hg completely inhibited axonal transport function and interneural blood flow in rabbit vagus and tibial nerves, respectively [26, 27]. In addition, a pressure value between 40 mm Hg and 50 mm Hg is considered a critical threshold for the disruption of peripheral nerves conduction and response to cutaneous sensibility tests in healthy patients [23, 28]. Those values lie well within the + 47 and + 70 mm Hg means of measured intracystic pressures for radicular cysts [29, 30], and a 51 mm Hg minimum continuous pressure necessary to induce bone resorption in the hard palate, based on animal experiment on rats [31].
Additionally, the patient sudden pain reaction while accessing tooth 11 further supports the compression theory. The larger myelinated A- type nerve fibres are pressure and hypoxia sensitive compared with C- type nerve fibres [32]. The response to electrical and cold sensibility tests mediated by A- fibres might have been suppressed, while the heat build-up and mechanical stimulation by the cutting bur caused a latent C- fibre pain response [33]. Ricuccui et al. [5] reported a similar incident when two premolars, whose apices were compressed by large radicular cyst, only gave faint responses to cold sensibility tests, and did not respond to EPT but demonstrated vital pulps when they were endodontically treated. However, due to chronic caries and restorations in the premolars, direct conclusion could not be made. Interestingly, at multiple occasions when similar cases of large cysts and cystic like lesions were presented to our clinic, adjacent vital pulps were accessed without anaesthesia, demonstrating complete lack of sensation, especially in cases of secondary infections.