The pathogenesis of odontogenic cysts: a review

Browne, R.M.

doi:10.1111/j.1600-0714.1975.tb01738.x

Cited by 137 publications

(86 citation statements)

References 53 publications

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“…However, recent work characterizing the cytokeratin profile of the pocket wall found a more similar pattern to that found in odontogenic rests normally resident in the periodontal ligament than in the sulcular epithelium ). This raises the possibility that pocket deepening is due to transient proliferations of periodontal odontogenic rests Spouge, 1984) and it is important to note that proliferation of these rests in response to bacterial irritants from infected teeth is the basis for development of radicular dental cysts in chronic periapical infections (Browne et al, 1975). Although most of the venules draining the gingival sulcus lead to the deeper gingival soft tissues and the alveolar mucosa, some venules are known to drain to collecting venules in the periodontal ligament so that this may provide an important route of access for bacterial agents stimulating proliferation of odontogenic epithelial rests during pocket deepening.…”

Section: Characteristics Of Periodontitis That Are Unexplained But Mmentioning

confidence: 99%

Microvasculature in gingivitis and chronic periodontitis: Disruption of vascular networks with protracted inflammation

Zoellner

Chapple

Hunter

2002

Microscopy Res & Technique

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Gingivitis occurring when bacterial plaque accumulates in the gingival crevice provides a convenient and interesting model for chronic inflammation in humans. In some patients, gingivitis progresses to the destructive lesion of periodontitis, involving the formation of periodontal pockets. The basis for pocket formation and progression is not as yet clear, although neutrophilic polymorphonuclear leukocytes (PMN) appear to play a protective role. Vascular changes appear to either facilitate or inhibit PMN function with the effect of either protecting from, or stimulating, periodontitis. Contrary to most circumstances, high endothelial cells in periodontitis are involved with PMN rather than lymphocyte emigration. Expansion of the microvasculature through increased vascular diameter and tortuosity as well as the development of high endothelial cells appears to protect from periodontitis by increasing the supply of both plasma defense factors and PMN to the tissues. Vascular changes that may oppose this and promote periodontitis are the formation of perivascular hyaline material and accumulation of basement membrane rests. The inadequate tissue turnover that accumulation of these vascular products represents can be argued as a vascular response to a chronic inflammation that has failed to eliminate the irritant. It is suggested that these vascular changes may account for the highly localized and burst-like pattern of pocket formation in periodontitis. Finally, it is possible that the recent observation that periodontitis is an independent risk factor for systemic vascular disease may reflect stimulation of acute phase protein synthesis by cytokines released by periodontal high endothelial cells.

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Section: Characteristics Of Periodontitis That Are Unexplained But Mmentioning

confidence: 99%

Microvasculature in gingivitis and chronic periodontitis: Disruption of vascular networks with protracted inflammation

Zoellner

Chapple

Hunter

2002

Microscopy Res & Technique

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“…Along with the epithelial lining, the fibrous walls of odontogenic cysts may be involved in tumor expansion and aggressiveness (Browne, 1975). The epithelial lining in the more aggressive NBSCC-associated syndromic KCOTs (S-KCOTs) has higher expression of the heparanase gene and protein compared with that in sporadic, non-syndromic KCOTs (NS-KCOTs), which is closely correlated with a higher capacity for invasion (Katase et al, 2007); expression of the proliferation marker Ki67 is also higher in S-than in NS-KCOTs (Ba et al, 2010).…”

Section: Fibroblasts Regulate Aggressiveness Of S-kcots and Ns-kcotsmentioning

confidence: 99%

Fibroblasts Regulate Variable Aggressiveness of Syndromic Keratocystic and Non-syndromic Odontogenic Tumors

Hong

et al. 2014

J Dent Res

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Keratocystic odontogenic tumors (KCOTs) are jaw lesions that can be either sporadic or associated with nevoid basal cell carcinoma syndrome, which typically occurs as multiple, aggressive lesions that can lead to large areas of bone destruction and resorption and cause major impairment and even jaw fracture. To clarify the role of fibroblasts in the aggressivness of syndromic (S-) as compared with non-syndromic (NS-) KCOTs, we assessed fibroblasts derived from 16 S- and NS-KCOTs for differences in cell proliferation, multilineage differentiation potential, alkaline phosphatase activity, and osteoclastogenic potential. S-KCOT fibroblasts had proliferative and osteoclastogenic capacity higher than those from NS-KCOTs, as evidenced by higher numbers of tartrate-resistant acid-phosphatase-positive multinuclear cells, expression of cyclooxygenase 2, and ratio of receptor activator of nuclear factor–kappa B ligand to osteoprotegerin. The osteogenic potential was higher for S- than for NS-KCOT fibroblasts and was associated with lower mRNA expression of runt-related transcription factor 2, collagen type I α1, osteocalcin, and osteopontin as well as reduced alkaline phosphatase activity. These results suggest that the distinct characteristics of fibroblasts in KCOTs are responsible for the greater aggressiveness observed in the syndromic subtype. Abbreviations: AP, alkaline phosphatase; CK, cytokeratin; COL1A1, collagen type I α1; COX-2, cyclooxygenase-2; GM-CSF, granulocyte-macrophage colony-stimulating factor; IL-1α, interleukin 1α; KCOT, keratocystic odontogenic tumor; NBCCS, nevoid basal cell carcinoma syndrome; NS-KCOT, non-syndrome-associated KCOT; OCN, osteocalcin; OPG, osteoprotegerin; OPN, osteopontin; RANKL, receptor activator of nuclear factor-kappa B ligand; Runx2, runt-related transcription factor 2; S-KCOT, syndrome-associated KCOT; TAF, tumor-associated fibroblast; and TRAP, tartrate-resistant acid phosphatase.

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“…Since it occurs with out particular clinical symptom, if a DC is found late, the cyst can increase considerably and invade into the nasal cavity, maxillary sinus, orbital fl oor, coracoid, condyle, and mandibular ramus. If the mandibular molar is included in the cyst, it can cause the displacement of the mandibular inferior border or ascending ramus, expansion of cortical bone through invasion into neighboring tissue, and, even worse, malocclusion and facial asymmetry through tooth displacement 3) . Moreover, the second infection of the cyst can destroy neighboring structure and cause a serious problem through the variation to malignant tumor from the cyst wall 3) .…”

Section: Casementioning

confidence: 99%

“…If the mandibular molar is included in the cyst, it can cause the displacement of the mandibular inferior border or ascending ramus, expansion of cortical bone through invasion into neighboring tissue, and, even worse, malocclusion and facial asymmetry through tooth displacement 3) . Moreover, the second infection of the cyst can destroy neighboring structure and cause a serious problem through the variation to malignant tumor from the cyst wall 3) . In these cases, unicystic radiolucent lesion related to unerupted permanent tooth or impacted mandibular third molar was found, and its boundary was clear.…”

Section: Casementioning

confidence: 99%

“…There is little gender differentiation, but it occurs a bit more frequently in men. It develops anywhere in the jaw but occurs frequently in the mandible; mandibular third molar, maxillary canine, maxillary third molar, and mandibular second premolar are the more affected areas 3) . Radiologically, it is a unicystic radiolucent lesion including the crown of unerupted tooth; its boundary is clear, with sclerotic border with bone shown sometimes.…”

Section: Introductionmentioning

confidence: 99%

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Conservative Treatment Using Marsupialization for Cysts Occurring in the Jaw of Adolescents: A Case Report

Yun¹,

Jung²,

Cho³

et al. 2014

Journal of Korean Dental Science

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cc This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/ by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.Dentigerous cyst (DC) is an odontogenic cyst associated with the crown of an impacted, embedded, unerupted, or developing tooth. It is the second most common type of odontogenic cysts, accounting for 14% to 24% of all jaw cysts. Although these cysts occur more frequently during the second and third decades of life, they can also be found in children and adolescents in the mixed dentition stage. Treatment of the odontogenic cyst involves enucleation or marsupialization/decompression methods. The latter approach is preferred for larger cysts, and it is especially helpful in adolescent patients in conserving the unerupted permanent successors. The aim of treatment for DC is the complete elimination of pathology and maintenance of dentition with minimal surgical intervention. Recently defined criteria for the selection of treatment modality include the cyst size and location of the cyst, patient age, dentition involved, stage of root development, position of the tooth involved in the jaw, and relationship with the surrounding vital structure. Marsupialization or decompression technique has been advocated by several authors for treating DCs among young patients. In this conservative technique, the creation of an accessory cavity helps relieve intra-cystic pressure and accelerate the healing of cystic lesion. This technique has been successfully performed and is indicated for growing children and adolescents. Here, we report a large cyst lesion in the mandible treated by marsupialization for conservative management. In conclusion, successful reduction in size was achieved, and intraoperative complication could be prevented.

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The pathogenesis of odontogenic cysts: a review

Cited by 137 publications

References 53 publications

Microvasculature in gingivitis and chronic periodontitis: Disruption of vascular networks with protracted inflammation

Microvasculature in gingivitis and chronic periodontitis: Disruption of vascular networks with protracted inflammation

Fibroblasts Regulate Variable Aggressiveness of Syndromic Keratocystic and Non-syndromic Odontogenic Tumors

Conservative Treatment Using Marsupialization for Cysts Occurring in the Jaw of Adolescents: A Case Report

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