目的研究口腔粘膜良性淋巴组织增生病(benign lymphoadenosis of oral mucosa,BLOM)中增生的淋巴细胞的性质。方法采用免疫组化SP法检测14例口腔粘膜良性淋巴组织增生病、9例粘膜良性淋巴组织增生病伴上皮异常增生、11例口腔粘膜良性淋...目的研究口腔粘膜良性淋巴组织增生病(benign lymphoadenosis of oral mucosa,BLOM)中增生的淋巴细胞的性质。方法采用免疫组化SP法检测14例口腔粘膜良性淋巴组织增生病、9例粘膜良性淋巴组织增生病伴上皮异常增生、11例口腔粘膜良性淋巴组织增生病发生癌变者及10例正常口腔粘膜组织中淋巴细胞CD20和CD45RO的表达。结果正常粘膜中有8例出现CD45RO阳性染色,且染色强度和阳性细胞数并不均一;未见CD20阳性染色。口腔粘膜良性淋巴组织增生病发生癌变组中有一例CD20阴性,其余各组均可见CD20和CD45RO阳性染色,细胞分布呈现出明显的规律性,CD20主要见于淋巴滤泡内或呈灶性聚集的淋巴细胞中,在周围的组织中阳性细胞较少,CD45RO则主要出现在固有层,淋巴滤泡内也可见部分阳性细胞。结论BLOM中浸润的淋巴细胞既有T细胞,亦有B细胞,属于多克隆增生。展开更多
Vascular birthmarks are the most common disease.The morbidity is about 2.5%,most of the lesions occur in oral and maxillofacial regions which accounts for 40%-60% of the total lesions.In 1982,Mulliken and Glowacki pro...Vascular birthmarks are the most common disease.The morbidity is about 2.5%,most of the lesions occur in oral and maxillofacial regions which accounts for 40%-60% of the total lesions.In 1982,Mulliken and Glowacki proposed a biologic classification of vascular birthmarks on the basis of their clinical manifestations,histopathological features,and natural history.They defined hemangiomas as vascular tumors with a growth phase,marked by endothelial proliferation and hypercellularity,and an involutional phase.They recognized that many entities referred to as hemangiomas are actually structural malformations of the vasculature,derived from capillaries,veins,lymph vessels,or arteries or from a combination of these sources.The classification was confirmed and issued by International Society for the study of vascular anomality(ISSVA) in 1988.Waner and Suen amended the above category in 1995.This paper presents the new classification of vascular birthmarks and the developments in this field in re-cent years,including the pathology,clinical features and the therapy.For example,the classification of venular malformation categorized by Waner in 1989;the classification of lymphous malformation by Waner and Suen in 1995;and the treatments according to above classifications.展开更多
Keratocystic odontogenic tumors(KCOTs,previously known as odontogenic keratocysts) are aggressive,noninflammatory jaw lesions with a putative high growth potential and a propensity for recurrence.This article puts tog...Keratocystic odontogenic tumors(KCOTs,previously known as odontogenic keratocysts) are aggressive,noninflammatory jaw lesions with a putative high growth potential and a propensity for recurrence.This article puts together a summary of the serial studies related to KCOTs undertaken by the author’s research group in recent years.Intraosseous jaw cysts with a solely orthokeratinized lining epithe-lium have been suggested to differ from the typical KCOTs.We report 20 cases of such cyst type under the term of ’orthokeratinized odontogenic cyst(OOC)’.Apart from the presence of a keratinizing epithelial lining,the OOC lacks the other histological features of KCOT,exhibits little if any tendency to recur,has no apparent association with NBCCS,may be cured by simple enucleation,and may thus constitute its own clinical entity.Mutations in PTCH1 gene are responsible for NBCCS and are related in tumors associated with this syndrome.We have so far detected 26 PTCH1 mutations(2 mutations occurred twice) in 10 out of 34(29.4%) sporadic and 14 out of 16(87.5%) NBCCS-associated KCOTs.The 26 mutations consisted of 10 frameshift,2 nonsense,3 aberrant splicing,4 in-frame insertion/deletion/ duplication and 7 missense mutations.Two missense mutations in PTCH2 were also detected in 2 out of 15 NBCCS related KCOT patients.By contrast,no pathogenic mutation was detected in SMO.Thus,our data,together with reports from ther groups,indicate that defects of PTCH1 are involved in the pathogenesis of syndromic as well as sporadic KCOTs.The pathogenic role of PTCH2 requires further investigation.A series of in vitro studies on bone resorption of KCOTs and ameloblastomas were undertaken by this group.The results indicate that odontogenic lesions could promote bone resorption in vitro and it is likely to be related to some of the cytokines secreted by the lesions.展开更多
文摘目的研究口腔粘膜良性淋巴组织增生病(benign lymphoadenosis of oral mucosa,BLOM)中增生的淋巴细胞的性质。方法采用免疫组化SP法检测14例口腔粘膜良性淋巴组织增生病、9例粘膜良性淋巴组织增生病伴上皮异常增生、11例口腔粘膜良性淋巴组织增生病发生癌变者及10例正常口腔粘膜组织中淋巴细胞CD20和CD45RO的表达。结果正常粘膜中有8例出现CD45RO阳性染色,且染色强度和阳性细胞数并不均一;未见CD20阳性染色。口腔粘膜良性淋巴组织增生病发生癌变组中有一例CD20阴性,其余各组均可见CD20和CD45RO阳性染色,细胞分布呈现出明显的规律性,CD20主要见于淋巴滤泡内或呈灶性聚集的淋巴细胞中,在周围的组织中阳性细胞较少,CD45RO则主要出现在固有层,淋巴滤泡内也可见部分阳性细胞。结论BLOM中浸润的淋巴细胞既有T细胞,亦有B细胞,属于多克隆增生。
文摘Vascular birthmarks are the most common disease.The morbidity is about 2.5%,most of the lesions occur in oral and maxillofacial regions which accounts for 40%-60% of the total lesions.In 1982,Mulliken and Glowacki proposed a biologic classification of vascular birthmarks on the basis of their clinical manifestations,histopathological features,and natural history.They defined hemangiomas as vascular tumors with a growth phase,marked by endothelial proliferation and hypercellularity,and an involutional phase.They recognized that many entities referred to as hemangiomas are actually structural malformations of the vasculature,derived from capillaries,veins,lymph vessels,or arteries or from a combination of these sources.The classification was confirmed and issued by International Society for the study of vascular anomality(ISSVA) in 1988.Waner and Suen amended the above category in 1995.This paper presents the new classification of vascular birthmarks and the developments in this field in re-cent years,including the pathology,clinical features and the therapy.For example,the classification of venular malformation categorized by Waner in 1989;the classification of lymphous malformation by Waner and Suen in 1995;and the treatments according to above classifications.
文摘Keratocystic odontogenic tumors(KCOTs,previously known as odontogenic keratocysts) are aggressive,noninflammatory jaw lesions with a putative high growth potential and a propensity for recurrence.This article puts together a summary of the serial studies related to KCOTs undertaken by the author’s research group in recent years.Intraosseous jaw cysts with a solely orthokeratinized lining epithe-lium have been suggested to differ from the typical KCOTs.We report 20 cases of such cyst type under the term of ’orthokeratinized odontogenic cyst(OOC)’.Apart from the presence of a keratinizing epithelial lining,the OOC lacks the other histological features of KCOT,exhibits little if any tendency to recur,has no apparent association with NBCCS,may be cured by simple enucleation,and may thus constitute its own clinical entity.Mutations in PTCH1 gene are responsible for NBCCS and are related in tumors associated with this syndrome.We have so far detected 26 PTCH1 mutations(2 mutations occurred twice) in 10 out of 34(29.4%) sporadic and 14 out of 16(87.5%) NBCCS-associated KCOTs.The 26 mutations consisted of 10 frameshift,2 nonsense,3 aberrant splicing,4 in-frame insertion/deletion/ duplication and 7 missense mutations.Two missense mutations in PTCH2 were also detected in 2 out of 15 NBCCS related KCOT patients.By contrast,no pathogenic mutation was detected in SMO.Thus,our data,together with reports from ther groups,indicate that defects of PTCH1 are involved in the pathogenesis of syndromic as well as sporadic KCOTs.The pathogenic role of PTCH2 requires further investigation.A series of in vitro studies on bone resorption of KCOTs and ameloblastomas were undertaken by this group.The results indicate that odontogenic lesions could promote bone resorption in vitro and it is likely to be related to some of the cytokines secreted by the lesions.
