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Periapical diseases ranges from mild granulomatous lesions to large cystic ones, with the treatments corresponding to their respective pre-operative diagnoses. However, the determination of cause of periapical radiolucency is impossible on pre-operative clinical and radiographic examinations. We present a case highlighting the difficulties encountered in treating a periapical cyst using the current evidence in literature. It demonstrates the uncertainty involved in treating such lesions, owing to the impossible nature of determining the histopathological nature of the cyst, i.e., being either true cysts or pocket cysts. This case includes orthograde re-treatment; decompression of the cystic lesion, followed by peri-apical surgery of two teeth over a course of three years; and the uncertain outcomes encountered after each phase of the treatment. Keywords: Granuloma, periradicular lesion, apical cyst, periapical surgery, non-surgical retreatment.

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Copyright of Serbian Dental Journal / Stomatološki Glasnik Srbije is the property of National Library of Serbia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Endodontic therapy has a high success rate. However, failed endodontic therapy with persistent periapical lesions may indicate the presence of an apical cyst that requires surgical apical intervention. The present case involved a 70-year-old woman who was referred after initiation of nonsurgical root canal treatment (NSRCT) in the upper left lateral incisor (tooth #22); due to recurrent swelling and sinus tract. Periapical radiographs showed an apical radiolucency on tooth #22. In a clinical examination, tooth #22 showed a normal response to cold and the electric pulp tester (EPT), while the upper left canine (tooth #23) showed a negative response to cold and the EPT. NSRCT was performed for tooth #23. Eighteen months later, the patient presented with the same chief complaint of recurrent swelling, and cone-beam computed tomography was performed to examine the extent of the apical lesion and plan for surgical intervention. Apical surgery was performed using a dental operating microscope. At the 18-month follow-up assessment, the patient's radiographs showed good bone healing and symptom resolution. This case report indicates that some cases with large persistent periapical lesions may require surgical intervention.

Purpose: The aim of this study was to investigate the effectiveness of cone-beam CT (CBCT) findings and gray scale values (GSV) in the differential diagnosis of apical cysts and granulomas. Methods: Two independent researchers retrospectively analyzed the CBCT images of 21 teeth and histopathologically diagnosed them as having radicular cysts or apical granulomas. In the CBCT images, apical lesions were evaluated and categorized according to 7 criteria. These criteria were determined as relationship of lesions with dental roots, periphery of the lesion, shape, darker focus in the center, root resorption, displacement in related teeth, and cortical bone perforation. In addition, the minimum and maximum gray scale values of the lesions were measured and compared. Results: There was a statistically significant relationship between histopathological (HP) diagnosis and well-defined cortical border and lesion shape (p = 0.003, p = 0.014, respectively). According to the HP diagnosis, no statistically significant difference was found among other variables (p > 0.05) Conclusion: The presence of a well-defined cortical border or partial cortical border is a distinctive criterion for cysts. Additionally, the shape of the lesion was found to be a significant criterion for the separation of the two lesions. The shape of cystic lesions was circular and apical granulomas had a more curved shape. There was no relationship between the histopathological diagnosis of lesions and CBCT gray scale values. [ABSTRACT FROM AUTHOR]

Objective: The purpose of our study was to determine the level of correlation between histopathologic results after surgery for chronic apical periodontitis and the radiographic and clinical diagnosis. The status of gold standard technique of histologic examination was evaluated in the diagnosis of apical radiolucency in necrotic teeth. Methods: Out of 154 patients with incorrect root fillings and apical radiolucency included in an endodontic retreatment protocol, 87 patients (108 teeth) were scheduled for apical surgery at 3-6 months control recall. Clinical and radiographic exams were completed prior to surgery and compared to the histological results of apical biopsies. The collected data were statistically analyzed with the SPSS version 20.0 and the Chi-square test was used to determine the associations between clinical and histologic diagnosis. A value of p <0.05 was considered statistically significant. Results: There was a statistically significant difference between the number of cases diagnosed as granulomas or cysts during clinical and radiological evaluation compared to histologic evaluation of tissue samples, with 40.9% to 75.9% and 54.2% to 16.8% respectively (p<0.05). Conclusions: The final diagnosis was obtained only after histologic examination of apical tissue samples, which means that the observations made based on radiologic investigations must be confirmed by biopsy. [ABSTRACT FROM AUTHOR]

There is a high incidence of chronic periapical periodontitis of deciduous teeth, however, there is a low incidence of the apical cyst. This paper reports a 7-year-old child with deciduous periodontitis caused by chronic periapical periodontitis of deciduous teeth. Through literature review, the etiology, imaging characteristics, diagnosis, differential diagnosis, and treatment methods were discussed to provide the basis for clinical diagnosis and treatment.

Introduction: The mechanism of the formation of apical cyst has been elusive. Several theories have long been proposed and discussed speculating how an apical cyst is developed and formed in the jaw bone resulting from endododontic infection. Two popular theories are the nu-tritional deficiency theory and the abscess theory. The nutri-tional deficiency theory assumes that the over proliferated epithelial cells will form a ball mass such that the cells in the center of the mass will be deprived of nutrition. The abscess theory postulates that when an abscess cavity is formed in connective tissue, epithelial cells proliferate and line the preexisting cavity because of their inherent tendency to cover exposed connective tissue surfaces. Based on the nature of epithelial cells and the epithelium, nutri-tional theory is a fairy tale, while abscess theory at best just indi-cates that abscess may be one of the factors that allows the stratified epithelium to form but not to explain a mechanism that makes the cyst to form. The hypothesis: Apical cyst formation is the result of proliferation of resting epithelial cells, due to inflammation, to a sufficient number such that they are able to form a polarized and stratified epithelial lining against dead tissues or foreign materials. These stratified epi-thelial lining expands along the dead tissue or foreign materials and eventually wrap around them as a spherical sac, i.e. a cyst. The space in the sac is considered the external environment separating the internal (tissue) environment – the natural function of epithelium. Evaluation of the hypothesis: This theory may be tested by introducing a biodegradable device able to slowly release epithelial cell mitogens in an in vivo environment implanted with epithelial cells next to a foreign object. This will allow the cells to continuously proliferate which may form a cystic sac wrapping around the foreign object.

Abstract: Introduction: This article reports on the morphologic features and the frequency of ciliated epithelium in apical cysts and discusses its origin. Methods: The study material consisted of 167 human apical periodontitis lesions obtained consecutively from patients presenting for treatment during a period of 12 years in a dental practice operated by one of the authors. All of the lesions were obtained still attached to the root apices of teeth with untreated (93 lesions) or treated canals (74 lesions). The former were obtained by extraction and the latter by extraction or apical surgery. Specimens were processed for histopathologic and histobacteriologic analyses. Lesions were classified, and the type of epithelium, if present, was recorded. Results: Of the lesions analyzed, 49 (29%) were diagnosed as cysts. Of these, 26 (53%) were found in untreated teeth, and 23 (47%) related to root canal–treated teeth. Ciliated columnar epithelium was observed partially or completely lining the cyst wall in 4 cysts, and all of them occurred in untreated maxillary molars. Three of these lesions were categorized as pocket cysts, and the other was a true cyst. Conclusions: Ciliated columnar epithelium-lined cysts corresponded to approximately 2% of the apical periodontitis lesions and 8% of the cysts of endodontic origin in the population studied. This epithelium is highly likely to have a sinus origin in the majority of cases. However, the possibility of prosoplasia or upgraded differentiation into ciliated epithelium from the typical cystic lining squamous epithelium may also be considered. [Copyright &y& Elsevier]

Large periapical lesions, regardless of whether they are granulomas, abscesses or cysts, are primarily caused by root canal infection. Thus the treatment protocol should be elimination of etiological factors in the root canal system rather than their product, apical true cyst. A 10 year old female patient reported to the Department of Pedodontics and Preventive Dentistry, Dr R Ahmed Dental College & Hospital, Kolkata, with the chief complaint of pain and swelling in relation to upper front fractured teeth. Clinical and radiological findings were suggestive of periapical radicular cyst. Non-surgical endodontic therapy was performed using 1% sodium hypochlorite solution irrigant and Calcium hydroxide intra canal medicament. A 12 months follow-up radiographic examination revealed progressive involution of periapical radiolucency without any clinical symptoms. Periapical cysts respond favorably to non-surgical endodontic treatment and should be considered as primary treatment modality. [ABSTRACT FROM AUTHOR]

Abstract: Irreversible pulpitis and apical periodontitis are inflammatory diseases caused by opportunistic bacteria with possible co-infection with latent herpesviruses. The objectives of this study are to identify herpesviruses, including human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV-1), and Varicella zoster virus (VZV) in patients with irreversible pulpitis (n = 29) or apical periodontitis, either primary (n = 30) or previously treated (n = 23). Using primary and nested polymerase chain reaction (PCR) and reverse transcription-PCR, EBV DNA and RNA were present in endodontic pathoses in significantly higher percentages (43.9% and 25.6%, respectively) compared with healthy pulp controls (0% and 0%, respectively). HCMV DNA and RNA were found in measurable numbers in both endodontic patients (15.9% and 29.3%, respectively) and in healthy pulp controls (42.1% and 10.5%, respectively). HSV-1 DNA was found in low percentages in endodontic patients (13.4%), and only one patient showed the presence of VZV. In conclusion, EBV may be associated with irreversible pulpitis and apical periodontitis. [Copyright &y& Elsevier]

Abstract: There is continuing controversy regarding the potential for inflammatory apical cysts to heal after nonsurgical endodontic therapy. Molecular cell biology may provide answers to a series of related questions. How are the epithelial cell rests of Malassez stimulated to proliferate? How are the apical cysts formed? How does the lining epithelium of apical cysts regress after endodontic therapy? Epithelial cell rests are induced to divide and proliferate by inflammatory mediators, proinflammatory cytokines, and growth factors released from host cells during periradicular inflammation. Quiescent epithelial cell rests can behave like restricted-potential stem cells if stimulated to proliferate. Formation of apical cysts is most likely caused by the merging of proliferating epithelial strands from all directions to form a three-dimensional ball mass. After endodontic therapy, epithelial cells in epithelial strands of periapical granulomas and the lining epithelium of apical cysts may stop proliferating because of a reduction in inflammatory mediators, proinflammatory cytokines, and growth factors. Epithelial cells will also regress because of activation of apoptosis or programmed cell death through deprivation of survival factors or by receiving death signals during periapical wound healing. [Copyright &y& Elsevier]

Aim To report the repair of an extensive periapical lesion of endodontic origin, following nonsurgical treatment. Clinical and radiographic examination revealed an extensive periapical lesion related to tooth 22, extending from the distal surface of tooth 21 to the mesial surface of 26. The patient reported a previous history of dental trauma involving this quadrant and had been under orthodontic treatment for a year. Intraoral examination revealed an asymptomatic bony hard swelling, mainly confined to the palate. During root canal exploration irregular walls associated with 3 mm of apical calcification were noted. After apical patency was obtained 1 mL of bloody serous exudate was drained. Intracanal aspiration provided a further 2 mL of yellow serous exudate. Following biomechanical preparation, a dressing of calcium hydroxide with anaesthetic solution was applied and replaced four times over a period of 12 months. The clinical–pathological picture demonstrated resolution of the lesion during this period of time. The 14-month clinical and radiographic examinations revealed normal bony contour and a significant resolution of the maxillary radiolucency. Key learning points • Periapical lesions of endodontic origin may develop asymptomatically and become large. • Proper biomechanical preparation followed by calcium hydroxide medication renewed periodically represents a nonsurgical approach to resolve extensive inflammatory periapical lesions. [ABSTRACT FROM AUTHOR]

Periradicular curettage is a part of the treatment procedure of periradicular surgery. Its main purpose is to remove pathological periradicular tissues for visibility and accessibility to facilitate the treatment of the apical root canal system, or sometimes for the removal of harmful foreign materials present in the periradicular area. Inflammatory periradicular lesions (granuloma and cysts) are the responses of the periradicular tissues to irritants from the root canal and not from the periradicular area unless medicaments and/or filling materials have been forced through the apical foramina or perforations into the periodontium. Histologically, the inflammatory periradicular lesion is similar to healing granulation tissue, which is composed of cells which have natural and specific immunological defence capability and cooperate by means of cytokines to amplify the protective mechanisms ofthe host. Accordingly, it is not necessary to completely curette out all the inflamed periradicular tissues during surgery, since this granulation- like tissue will be incorporated into the new granulation tissue as part of the healing process. To control the source of irritants in the root canal is far more important than to remove all periradicular tissues affected by the irritants. The successful removal of all irritants from the root canal system results in resolution of pulpally induced periradicular lesions. In the case where the periradicular lesion is caused by endodontic instruments or cytotoxic filling materials placed in the periradicular tissues, removal of these foreign objects is required for resolution of the lesion. [ABSTRACT FROM AUTHOR]

Introduction: The mechanism of the formation of apical cyst has been elusive. Several theories have long been proposed and discussed speculating how an apical cyst is developed and formed in the jaw bone resulting from endododontic infection. Two popular theories are the nutritional deficiency theory and the abscess theory. The nutritional deficiency theory assumes that the over proliferated epithelial cells will form a ball mass such that the cells in the center of the mass will be deprived of nutrition. The abscess theory postulates that when an abscess cavity is formed in connective tissue, epithelial cells proliferate and line the preexisting cavity because of their inherent tendency to cover exposed connective tissue surfaces. Based on the nature of epithelial cells and the epithelium, nutritional theory is a fairy tale, while abscess theory at best just indicates that abscess may be one of the factors that allows the stratified epithelium to form but not to explain a mechanism that makes the cyst to form., The Hypothesis: Apical cyst formation is the result of proliferation of resting epithelial cells, due to inflammation, to a sufficient number such that they are able to form a polarized and stratified epithelial lining against dead tissues or foreign materials. These stratified epithelial lining expands along the dead tissue or foreign materials and eventually wrap around them as a spherical sac, i.e. a cyst. The space in the sac is considered the external environment separating the internal (tissue) environment - the natural function of epithelium., Evaluation of the Hypothesis: This theory may be tested by introducing a biodegradable device able to slowly release epithelial cell mitogens in an in vivo environment implanted with epithelial cells next to a foreign object. This will allow the cells to continuously proliferate which may form a cystic sac wrapping around the foreign object.