Interaction of stromal and microvascular components in keratocystic odontogenic tumors.

OBJECTIVE: Little is known about the interaction of stromal components in odontogenic tumors. Thus, the aim of this study was to investigate mast cells (MCs), myofibroblasts, macrophages, and their possible association with angiogenesis and lymphangiogenesis in keratocystic odontogenic tumors (KCOTs). MATERIAL AND METHODS: Thirty cases of KCOTs were included and analyzed by immunohistochemistry for mast cell tryptase, α-SMA, CD34, CD163, and D240. For comparative purpose, 15 radicular cysts (CRs) and 7 pericoronal follicles (PFs) were included. RESULTS: There was an increase in MCs for RCs and this difference was significant when they were compared to KCOTS and PFs. A significant increase in the density of MFs was observed for KCOTs when compared to RCs and PFs (P = 0.00). No significant difference in CD163-positive macrophages (P = 0.084) and CD34-positive vessels (P = 0.244) densities was observed between KCOTs, RCs, and PFs, although KCOTs showed a higher density of all proteins. Significant difference in lymphatic vessel density was observed for KCOTs when compared to RCs and PFs (P = 0.00). Positive correlation was observed between mast cell tryptase and CD34 in KCOTs (P = 0.025). CONCLUSIONS: A significant interaction between the MC population and CD34-positive vessels in KCOTs supported the hypothesis that MCs and blood vessels contribute to the stromal scaffold of KCOT.

Transcriptional profiles of SHH pathway genes in keratocystic odontogenic tumor and ameloblastoma.

BACKGROUND: Sonic hedgehog (SHH) pathway activation has been identified as a key factor in the development of many types of tumors, including odontogenic tumors. Our study examined the expression of genes in the SHH pathway to characterize their roles in the pathogenesis of keratocystic odontogenic tumors (KOT) and ameloblastomas (AB). METHODS: We quantified the expression of SHH, SMO, PTCH1, SUFU, GLI1, CCND1, and BCL2 genes by qPCR in a total of 23 KOT, 11 AB, and three non-neoplastic oral mucosa (NNM). We also measured the expression of proteins related to this pathway (CCND1 and BCL2) by immunohistochemistry. RESULTS: We observed overexpression of SMO, PTCH1, GLI1, and CCND1 genes in both KOT (23/23) and AB (11/11). However, we did not detect expression of the SHH gene in 21/23 KOT and 10/11 AB tumors. Low levels of the SUFU gene were expressed in KOT (P = 0.0199) and AB (P = 0.0127) relative to the NNM. Recurrent KOT exhibited high levels of SMO (P = 0.035), PTCH1 (P = 0.048), CCND1 (P = 0.048), and BCL2 (P = 0.045) transcripts. Using immunolabeling of CCND1, we observed no statistical difference between primary and recurrent KOT (P = 0.8815), sporadic and NBCCS-KOT (P = 0.7688), and unicystic and solid AB (P = 0.7521). CONCLUSIONS: Overexpression of upstream (PTCH1 and SMO) and downstream (GLI1, CCND1 and BCL2) genes in the SHH pathway leads to the constitutive activation of this pathway in KOT and AB and may suggest a mechanism for the development of these types of tumors.

CD1a-positive Langerhans cells and their relationship with E-cadherin in ameloblastomas and keratocystic odontogenic tumors.

BACKGROUND: Ameloblastomas and keratocystic odontogenic tumors (KOTs) are lesions that are characterized by locally invasive growth and cause extensive bone destruction. In addition, it is known that E-cadherin influences the adhesion of Langerhans cells (LCs) to keratinocytes. OBJECTIVE AND METHODS: The aim of this study was to investigate, using immunohistochemistry, the distribution of CD1a-positive cells in ameloblastomas and KOTs and their relationship with E-cadherin, in comparison to calcifying cystic odontogenic tumor (CCOT). RESULTS: The CD1a-positive LCs were observed in 11 ameloblastomas and KOTs. All of the cases of CCOT showed CD1a-positive LCs and a significant difference was found when this tumor was compared with ameloblastomas (P < 0.05, Mann-Whitney test). A statistically significant difference was also noted when comparing CD1a-positive LCs between CCOTs and KOTs (P < 0.05, Mann-Whitney test). Lower expression of E-cadherin in ameloblastomas (AMs) in relation to KOTs and CCOTs (P < 0.05, Fisher test) was observed. There was no correlation between E-cadherin and CD1a-positive LCs between all odontogenic tumors that were studied (P > 0.05, Spearman test). CONCLUSION: A quantitative difference of CD1a-positive cells between AMs and KOTs in comparison to CCOTs was observed. This permits to speculate that a depletion of CD1a-positive LCs might influence the local invasiveness of ameloblastomas and KOTs. Furthermore, it is suggested that E-cadherin mediates cell adhesion in these tumors.

Distribution of mast cells in benign odontogenic tumors.

The aim of this study was to investigate the presence of mast cells in a series of odontogenic tumors. Forty-five cases of odontogenic tumors were investigated using immunohistochemistry for mast cell triptase, and differences between groups were statistically evaluated. Mast cells were present in 96% of odontogenic tumors. Mast cells present in solid ameloblastoma were observed in the tumor stroma surrounding more solid and follicular epithelial islands, with or without squamous metaplasia. The odontogenic mixoma showed few mast cells. In odontogenic tumors with a cystic structure, the mast cells were distributed throughout all areas of the lesions, mainly in keratocystic odontogenic tumor. In addition, the total density of mast cells between all odontogenic tumors showed no significant difference (p > 0.05). A greater mast cells distribution was found in keratocystic odontogenic tumor in relation to adenomatoid odontogenic tumor (p < 0.01), and when the unicystic ameloblastoma and keratocistic odontogenic tumor were compared to the odontogenic myxoma (p < 0.05). Syndrome keratocystic odontogenic tumor showed a higher mean of mast cells when compared with the other tumors of the sample. Mast cells values presented by syndrome keratocystic odontogenic tumor were significantly greater than those of the sporadic keratocystic odontogenic tumor that were not associated with the syndrome (p = 0.03). Mast cells are probably one of the major components of the stromal scaffold in odontogenic tumors. We found significant differences of mast cells between syndrome nonsyndrome keratocystic odontogenic tumors, although their distribution did not seem to have any influence on the biologic behavior of benign odontogenic tumors.

Gingival cyst of the adult: a case report and immunohistochemical investigation.

A 42-year-old woman had a sessile swelling that involved the maxillary gingiva corresponding to the right canine and premolar area. Clinical examination showed a painless small nodule (10 mm in diameter) located between the right maxillary canine and premolar. The lesion was vesicular, sessile, and slightly compressible on palpation. Microscopic examination of the lesion (following an excisional biopsy) showed cystic spaces covered by an epithelium lining that consisted of cuboidal and squamoid cells intermingled with clear cells. These morphologic findings were consistent with gingival cyst of the adult. Immunohistochemical technique against cytokeratins revealed that the epithelial cells were positive for cytokeratins No. 7, 8, 13, 14, and 19. Two years after removal, no recurrence was reported.

Expression of Ki-67, p53 and p63 proteins in keratocyst odontogenic tumours: an immunohistochemical study.

AIM: To investigate the immunohistochemical expression of Ki-67, p53 and p63 in Keratocyst Odontogenic Tumours (KOTs) in order to contribute to the biological profile of this tumor. METHODS: Immunohistochemical technique was performed using the EnVision System in 37 cases of KOTs. RESULTS: Ki-67- and p53-immunostained cells were mainly located in the suprabasal layers. p63-positive cells were found throughout the lining cystic epithelium. No difference in the immunostaining for these proteins was observed between primary and recurrent KOTs (Ki-67: P = 0.5591; p53: P = 0.9847; p63: P = 0.9127), or between KOTs associated with Nevoid Basal Cell Carcinoma Syndrome (NBCCS) and sporadic KOTs (Ki-67: P = 0.7013; p53: P = 0.3197; p63: P = 0.2427). CONCLUSIONS: It is possible that biological behavior of KOTs may be related to suprabasal proliferative compartment in the cystic epithelium as observed by high levels of Ki-67, p53 and p63. In addition, p63 immunostaining may represent immaturity of keratinocytes in KOTs, and suggests that this protein may participate in the regulation of epithelial cell differentiation. Taken together, these data may favor tumorigenesis on KOTs.

Influence of laser therapy on the dynamic formation of extracellular matrix in standard second degree burns treated with bacterial cellulose membrane.

The present study aims to assess the influence of Aluminum-Gallium-Indium-Phosphide laser (AlGaInP laser, λ = 660 nm), whether or not in association with the application of a membrane of bacterial cellulose (Nexfill™), during recovery from induced second-degree burns at the dorsum of Wistar rats. (Rattus norvegicus, Wistar). Forty-eight animals have been distributed into four groups: Control (burns remained untreated), Group I (laser-treated), Group II (treated with Nexfill), and Group III (laser + Nexfill™). In addition to a morphological analysis, immunohistochemical analysis has been performed for type I collagen, type III collagen, fibronectin, and laminin. The Fisher's Test was used to assess differences among groups (p < 0,05). A larger amount of collagen type III was observed in Control, Group II and Group III when compared with Group I (p < 0,05). Group I and Group III have shown a greater collagen deposition when compared with Group II (p < 0,05), but the amount of collagen was similar in Group I, Group III, and Control. Group III has shown larger fibronectin amounts in comparison with Group II (p < 0,05). As regards laminin, Group I has shown a predominant discontinuity pattern on the basal lamina in comparison with Control, Group II, and Group III (p < 0,05). It is concluded that in this current study the laser when used alone (Group I) hasn't influenced collagen deposition neither has it acted on fiber pattern (fibril and/or reticular). Moreover, laser application hasn't accelerated the repair of wounds caused by inflicted second-degree burns.

Immunohistochemical detection of Langerhans cells in dental granulomas and radicular cysts.

OBJECTIVE: Dental granulomas (DGs) and radicular cysts (RCs) are chronic periapical lesions frequently involving the jaws. Langerhans cells (LCs) are dendritic cells responsible for the presentation of antigens to T lymphocytes. This study examined the expression of LCs in DG and RCs by immunohistochemical staining. STUDY DESIGN: Eighteen cases of DGs and 26 cases of RCs were analyzed using anti-CD1a marker. RESULTS: CD1a-labeled LCs were observed in 11.1% of DGs and in 69.2% of RCs, showing a significant correlation (P < 0.0001; Fisher's test). In DGs, LCs were only observed in granulation tissue, showing discrete immunostaining density. In RCs, LCs exhibited both a round and a dendritic shape in all epithelial layers. Although a correlation was observed between immunostaining density and epithelial thickness, as well as between immunostaining and inflammatory intensity, the differences were not significant in radicular cysts. CONCLUSION: Langerhans cells provide important insight into the immunopathogenesis of chronic periapical lesions.

Actinomycosis is not Frequent in the Periapex But is a Persistent Lesion.

Periapical actinomycosis caused by a gram-positive anaerobic pathogen characterizes a typical extra-radicular infection. This study determined the frequency and correlated the content of bacteria colonies with the of periapical actinomycosis size. The study comprised a total of 218 periapical lesions (PL) (cysts, granulomas or abscess). The specimens embedded in paraffin were sliced into 4-µm sections and stained with hematoxylin-eosin, Gram, Periodic Acid-Schiff (PAS) and Grocott's stain. The presence of bacterial colonies composed of filamentous structures labeled with the histochemical stains were described as Actinomyces, and for each case, the bacterial colonies were counted and measured. The correlation between the number and size of bacterial colonies and the size of PL was tested using Pearson's adjusted correlation coefficient. From 218 PL, bacterial colonies were identified in 64 biopsies. Seven cases (0.3%) fulfill the criteria for diagnosis of periapical actinomycosis. All of cases were therapy-resistant and did not showed periapical repair after 12 months of follow-up. Periapical surgery or dental extraction was performed. The correlation test indicated no correlation between the number of bacterial colonies and the lesion size (p=0.752, r=-0.148). However, a larger bacterial colony size generally resulted in a larger periapical lesion (P=0.000, r=0.657). The frequency of periapical actinomycosis was low, and this lesion should be included in the differential diagnosis of PL. The size of the Actinomyces colonies seemed to contribute to increase the size of the periapical lesion.

Oral mucoceles: a clinical, histopathological and immunohistochemical study.

The aim of study was to evaluate the clinicopathological features of oral mucoceles and the immunohistochemical expression of cellular and extracellular matrix components in these lesions. One hundred cases of oral mucoceles were examined for clinicopathological features. The expression of mast cell tryptase, CD68, MMP-1 (matrix metalloproteinase-1), MMP-9 (matrix metalloproteinase-9) and CD34 was investigated immunohistochemically in 32 cases. The lesions arose as nodules or blisters of variable color. The mean age was 23.2 years and a higher male frequency was observed. The most common locations were the lower lip (92%), followed by the floor of the mouth (7%), and palate (1%). The lesion size ranged from 0.4 to 3.0cm. Unusual histopathological findings as superficial mucoceles (n=16, 16%), pseudopapillary projections (n=3, 3%), epithelioid histiocytes (n=4, 4%), multinucleated giant cells (n=1, 1%) and myxoglobulosis (n=9, 9%) were also seen. Mast cells and CD68-positive macrophages, MMP-1, MMP-9 and CD34-positive blood vessels were seen in all cases. A significant association was seen between mast cells and MMP-1 (p=0.03) and between macrophages and MMP-1 (p=0.01). This study provided important insight into the demographic and histopathological occurrence of oral mucoceles. The tissue remodeling seen in these lesions mainly involved the migration and interaction of mast cells, macrophages and MMP-1.

Actinomycosis is not Frequent in the Periapex But is a Persistent Lesion

Abstract Periapical actinomycosis caused by a gram-positive anaerobic pathogen characterizes a typical extra-radicular infection. This study determined the frequency and correlated the content of bacteria colonies with the of periapical actinomycosis size. The study comprised a total of 218 periapical lesions (PL) (cysts, granulomas or abscess). The specimens embedded in paraffin were sliced into 4-µm sections and stained with hematoxylin-eosin, Gram, Periodic Acid-Schiff (PAS) and Grocott's stain. The presence of bacterial colonies composed of filamentous structures labeled with the histochemical stains were described as Actinomyces, and for each case, the bacterial colonies were counted and measured. The correlation between the number and size of bacterial colonies and the size of PL was tested using Pearson's adjusted correlation coefficient. From 218 PL, bacterial colonies were identified in 64 biopsies. Seven cases (0.3%) fulfill the criteria for diagnosis of periapical actinomycosis. All of cases were therapy-resistant and did not showed periapical repair after 12 months of follow-up. Periapical surgery or dental extraction was performed. The correlation test indicated no correlation between the number of bacterial colonies and the lesion size (p=0.752, r=-0.148). However, a larger bacterial colony size generally resulted in a larger periapical lesion (P=0.000, r=0.657). The frequency of periapical actinomycosis was low, and this lesion should be included in the differential diagnosis of PL. The size of the Actinomyces colonies seemed to contribute to increase the size of the periapical lesion.

Resumo A actinomicose periapical causada por um patógeno anaeróbio Gram positivo caracteriza uma infecção extra-radicular típica. Esse estudo determinou a frequência e correlacionou o conteúdo das colônias bacterianas com o tamanho das actinomicoses periapicais. O estudo compreendeu um total de 218 lesões periapicais (LPs) (cistos, granulomas ou abscessos). Os espécimes embebidos em parafina foram cortados em secções de 4-µm e corados com hematoxilina-eosina, Gram, ácido periódico de Schiff (PAS) e coloração de Grocott. A presença de colônias bacterianas compostas por estruturas filamentosas marcadas com os corantes histoquímicos foram descritas como Actinomyces, e para cada caso, as colônias bacterianas foram contadas e mensuradas. A correlação entre o número e tamanho das colônias bacterianas e o tamanho das LPs foi testado usando o coeficiente de correlação ajustado de Pearson. De 218 LPs, colônias bacterianas foram identificadas em 64 biópsias. Sete casos (0,3%) preencheram os critérios para o diagnóstico de actinomicose periapical. Todos os casos foram resistentes à terapia e não mostraram reparo periapical após 12 meses de acompanhamento. Cirurgia periapical ou extração dental foi realizada. O teste de correlação indicou nenhuma correlação entre o número de colônias bacterianas e o tamanho da lesão (p=0.752, r=-0.148). Entretanto, uma maior colônia bacteriana geralmente resultou em uma maior lesão periapical (p=0.000, r=0.657). A frequência de actinomicose periapical foi baixa e esta lesão deve ser incluída no diagnóstico diferencial das LPs. O tamanho das colônias de Actinomyces pareceu contribuir para o aumento no tamanho da lesão periapical.

Keratocystic odontogenic tumour: an experience in the Northeast of Brazil.

INTRODUCTION: Keratocystic odontogenic tumours raise particular interest, because of their high recurrence rate and association with nevoid basal cell carcinoma syndrome. OBJECTIVE: To analyze the clinical and histopathological features of all cases diagnosed as keratocystic odontogenic tumour in a Brazilian population. METHODS: A total of 64 keratocystic odontogenic tumours, arising in forty-six patients, were evaluated using the following parameters: association with nevoid basal cell carcinoma syndrome, gender, age at first diagnosis, race, anatomical location, symptoms, radiographic features, history of recurrence, association with teeth, and treatment. RESULTS: Keratocystic odontogenic tumours were more frequent among women than men (1:0.84). The mean patient age was 31.5 years (SD: +/- 16.6). Ten tumours (16.4%) involved the maxilla and 51 (83.6%) the mandible. Swelling (n = 12; 46.1%), followed by pain and swelling (n = 4; 15.3%), were most common clinical manifestations. A unilocular radiotransparency with well-defined margins was the main radiographic finding (n = 29; 87.8%). A significant association was observed between the multilocular radiographic pattern and recurrence (p < 0.05, Fisher's Test). Sixty-one (95.3%) tumours were treated by surgical enucleation followed by bone curettage, and the recurrence rate was 13% (n = 6). This study showed that the keratocystic odontogenic tumours relapsed within a mean period of 25-36 months. CONCLUSION: Despite the results of this study being similar to previous reports found in the literature, it provides an important insight about keratocystic odontogenic tumours in a Brazilian population.

Histopathological study of radicular cysts diagnosed in a Brazilian population.

The aim of this study was to investigate the histopathological features of radicular cysts (RCs) diagnosed in a Brazilian population. Seventy-three cases of RCs, from a total of 1480 biopsies diagnosed between 2001 and 2008 at the Laboratory of Oral Surgical Pathology of the Dental School of the Federal University of Bahia were investigated regarding their histopathological features. Morphological results showed that exocytosis (n = 50), spongiosis (n = 40), acanthosis (n = 28), atrophic epithelium (n = 27) and apoptotic bodies (n = 21) were the most common findings. Other morphological findings included: foamy macrophages (n = 10), Russell's bodies (n = 7), cholesterol crystals (n = 7) and glandular-like odontogenic epithelial rests (n = 1). Evidence of exogenous material was seen in 16 samples. It was concluded that the clinical and histopathological findings observed in Brazilian patients were comparable with those described for other populations.

Altered expression of cytokeratins in primary, recurrent and syndrome keratocystic odontogenic tumors.

Keratocystic odontogenic tumor (KOT) is a benign cystic tumor that affects the jaw bones and may be associated with the nevoid basal cell carcinoma syndrome (NBCCS). Twenty-five cases diagnosed as KOT, including primary and recurrent tumors and those associated with NBCCS, were submitted to immunohistochemical study for analysis of cytokeratins (CKs) 7, 8, 10, 13, 14, 18 and 19. The results showed CK13 immunostained on the intermediate layers and upper cells. CK14 was expressed in all epithelial layers and in those areas where inflammation and subepithelial splits were present; this protein was preserved within the basal cells. CK 18 was expressed mainly in the basal layer, whereas CK19 was expressed mainly on the intermediate and superficial layers. The remaining CKs tested were not immuoreactive. The status of maturation of cytokeratin seems to be altered on KOTs, and this is not distinct when different tumors are compared.

Russell body apical periodontitis: an unusual case report.

Russell bodies (RBs) changes in chronic apical lesions have rarely been reported in the literature. We describe a case of a periapical lesion abundantly and extensively composed of RB. Microscopic examination showed accumulation of plasma cells containing globular, spherical, polygonal, and eosinophilic structures against fibrous connective tissue. Initial diagnostic considerations based on a smaller magnification included hypersecretory plasmocytoma, although there was no evidence of infiltrative growth, mitotic activity, nuclear atypia, or cellular pleomorphism. Then, a panel of immunohistochemical markers was applied and the cells showed positivity with both kappa and lambda chains demonstrating their polyclonal origin. The extensive accumulation of RBs involving the periapical region represents an unreported and significant histologic change, as it was mimicking a malignant neoplasm.

Histopathological study of radicular cysts diagnosed in a Brazilian population

The aim of this study was to investigate the histopathological features of radicular cysts (RCs) diagnosed in a Brazilian population. Seventy-three cases of RCs, from a total of 1480 biopsies diagnosed between 2001 and 2008 at the Laboratory of Oral Surgical Pathology of the Dental School of the Federal University of Bahia were investigated regarding their histopathological features. Morphological results showed that exocytosis (n=50), spongiosis (n=40), acanthosis (n=28), atrophic epithelium (n=27) and apoptotic bodies (n=21) were the most common findings. Other morphological findings included: foamy macrophages (n=10), Russell’s bodies (n=7), cholesterol crystals (n=7) and glandular-like odontogenic epithelial rests (n=1). Evidence of exogenous material was seen in 16 samples. It was concluded that the clinical and histopathological findings observed in Brazilian patients were comparable with those described for other populations.

O propósito desse estudo foi investigar os aspectos histopatológicos de cistos radiculares diagnosticados em uma população brasileira. Setenta e três casos de cistos radiculares entre 1480 biópsias diagnosticadas na Faculdade de Odontologia da Universidade Federal da Bahia, entre 2001 e 2008, foram investigados, considerando os seus aspectos histopatológicos. Os resultados morfológicos mostraram que os achados mais comuns foram a exocitose (n=50), espongiose (n=40), acantose (n=28), epitélio atrófico (n=27) e células apoptóticas (n=21). Outros achados encontrados incluíram macrófagos espumosos (n=10), corpúsculos de Russell (n=7), imagens negativas de colesterol (n=7) e restos epiteliais odontogênicos semelhantes à tecido glandular (n=1). Material exógeno foi observado em 16 casos. Concluiu-se que os aspectos histopatológicos e clínicos observados foram comparáveis a outros descritos em outras populações.

Density of Langerhans cells in the keratocystic odontogenic tumor / Densidade das células de Langerhans no tumor odontogênico queratocístico

INTRODUCTION: Keratocystic odontogenic tumors (KOTs) are distinct odontogenic lesions commonly affecting the mandible bones. Langerhans cells (LCs) are specialized dendritic cells responsible for the presentation of antigens to T lymphocytes in mucosal and cutaneous surfaces. OBJECTIVE: This study analyzed the immunohistochemical expression of LCs in KOTs. MATERIALS AND METHODS: Fifteen cases of KOTs were studied using the anti-CD1a marker. Results: LCs were observed in all 15 cases analyzed. They were found to be concentrated in areas of cystic epithelial hyperplasia, mainly in those areas presenting higher concentration of inflammatory cells. Furthermore, a significant association between the number of LCs and areas of cystic epithelium presenting hyperplasia (Mann-Whitney test, p = 0.0223) was observed. The shape and location of these cells in KOTs epithelium were variable. CONCLUSION: The lower number of LCs observed on atrophic cystic epithelium of KOTs may be due to decreased epithelial immunosurveillance and this may result in locally aggressive invasiveness.

INTRODUÇÃO: Tumor odontogênico queratocístico (TOQ) é uma lesão odontogênica de caráter distinto que afeta frequentemente ossos maxilares. Células de Langerhans (CLs) são células dendríticas especializadas, responsáveis pela apresentação de antígenos aos linfócitos T nas superfícies cutânea e mucosa. OBJETIVO: Este estudo analisou a expressão imuno-histoquímica das CLs em lesões de TOQ. MATERIAIS E MÉTODOS: Quinze casos de TOQ foram estudados utilizando o marcador anti-CD1a. RESULTADOS: As CLs foram observadas em todos os 15 casos analisados. Essas células estavam concentradas em áreas de hiperplasia do epitélio cístico, especialmente naquelas que apresentavam alta concentração de células inflamatórias. Em adição, foi encontrada associação significativa entre número de CLs e áreas do epitélio cístico que apresentavam hiperplasia (Mann-Whitney test, p = 0.0223). O formato e a localização dessas células no epitélio dos TOQs foram variáveis. CONCLUSÃO: O menor número de CLs encontrado no revestimento cístico atrófico dos TOQs pode ser atribuído à imunovigilância deficiente e isso pode resultar em comportamento biológico localmente agressivo.

Etiopatogenia do cisto radicular: parte II / Pathogenesis of radicular cyst

Os cistos odontogênicos são muito comuns na clínica diária, sendo também uma das principais lesões maxilofaciais causadores de destruição desses ossos. Diferentes células e mediadores inflamatórios estão envolvidos na formação desses cistos. Dentre esses influenciadores moleculares pode-se citar alguns fatores de crescimento como o PDGF, TGF, VEGF e o CTGF. Este artigo discute brevemente sobre tais fatores de crescimento, citocinas inflamatórias e suas relações com metaloproteinases de matriz no desenvolvimento de lesões periapicais crônicas.