Localized hypoplasia of the primary canine in bonobos, orangutans, and gibbons.
Localized hypoplasia of the primary canine in bonobos, orangutans, and gibbons.
复制标题
倭黑猩猩、猩猩和长臂猿的初级犬齿局部发育不全。
DOI：
10.1002/ajpa.10149
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发表时间：
2003
影响因子：
2.8
通讯作者：
E. Newell
中科院分区：
文献类型：
--
作者：
M. Skinner;E. Newell
本文扩展了卢卡奇（[1999]）的观察。期刊。Anthropol 110:351 - 363;[2001]。期刊。在大型猿、长臂猿、倭黑猩猩和猩猩中，初级犬科动物（LHPC）的局部发育不全。LHPC是犬牙唇面牙釉质缺失的一个大致圆形区域，根据目前来自人类的证据，由于营养不良导致颅面骨质减少，在出生几个月后形成，导致隐窝开窗，使牙泡和更深层的成釉细胞暴露在正常运动婴儿发育过程中轻微的物理创伤中。我们的目标是确定LHPC在各种不同体重和社会生态的类人猿中的患病率，以阐明这种缺陷的病因。研究了3个分类群122只动物的幼年牙列：婆罗洲和苏门答腊岛8只Hylobates lar，婆罗洲和苏门答腊岛75只Pongo pygmaeus，中部非洲39只Pan paniscus。报告的变量包括分类单元，性别，拱廊，侧面和牙齿大小。通过描述、显微摄影和扫描电镜记录缺陷表达的存在/不存在和顺序严重程度。模具采用高分辨率牙印模材料，并用环氧树脂浇铸。有明显的分类差异，但没有性别差异。长臂猿的患病率为0.0%，倭黑猩猩为61.5%，猩猩为85.3%。猩猩的结果与Lukacs ([1999] Am。期刊。人类学家，110:351-363)，而倭黑猩猩比普通黑猩猩（22%）更容易受到影响，Lukacs ([1999] Am。期刊。Anthropol 110:351 - 363)。抗聚类差异不显著，但下犬齿受LHPC的影响明显大于上犬齿。我们发现，较大的牙齿受LHPC的影响更大，并且有更严重的缺陷。此外，我们还遇到了几例未愈合或正在愈合的犬隐窝开窗，偶尔与LHPC直接相关。缺陷的位置表明LHPC可能发生在围产期，但更常见的是在出生后几个月。组织学检查显示新生儿线和LHPC是解决时间问题的必要条件。我们同意卢卡奇（[1999]）的观点。期刊。人类学杂志。110:351-363)，认为分类学、解剖学和环境变量共同决定了LHPC的发生和出现。然而，我们得出结论，LHPC可能反映了婴儿猿和人类的拱廊发育不足。
This paper extends observations by Lukacs ([1999] Am. J. Phys. Anthropol. 110:351-363; [2001] Am. J. Phys. Anthropol. 116:199-208) of localized hypoplasia of the primary canine (LHPC) among large apes to gibbons, bonobos, and orangutans. LHPC is a roughly circular area of deficient enamel on the labial surface of primary canine teeth which, on current evidence from humans, forms several months after birth due to malnutrition-induced craniofacial osteopenia, leading to crypt fenestration that exposes the dental follicle and more deep-sited ameloblasts to minor physical traumata during normal motor infant development. Our goal was to determine the prevalence of LHPC among a variety of apes which differ in body mass and socioecology, with a view to elucidating the etiology of the defect. We examined juvenile dentitions from 122 animals from three taxa: 8 Hylobates lar, 75 Pongo pygmaeus from Borneo and Sumatra, and 39 Pan paniscus from central Africa. Reported variables include taxon, sex, arcade, side, and tooth size. Presence/absence and ordinal severity of defect expression were recorded by description, microphotography, and scanning electron microscopy. Molds were taken in high-resolution dental impression materials and cast in epoxy resin. There are clear taxonomic, but no sex, differences. Prevalence ranged from 0.0% in gibbons to 61.5% in bonobos and 85.3% in orangutans. The result for orangutans is similar to that reported by Lukacs ([1999] Am. J. Phys. Anthropol. 110:351-363), while bonobos are much more affected than were the common chimpanzees (22%) described by Lukacs ([1999] Am. J. Phys. Anthropol. 110:351-363). There are no significant antimeric differences, but the lower canine is much more affected than the upper by LHPC. We show that larger teeth are more affected by LHPC and have more severe defects. Also, we encountered several instances of patent or healing canine crypt fenestrations, occasionally in direct association with LHPC. Location of the defect indicates that LHPC may occur perinatally but more usually several months postnatally. Histological examination showing the neonatal line and LHPC is required to resolve the issue of timing. We concur with Lukacs ([1999] Am. J. Phys. Anthropol. 110:351-363) that taxonomic, anatomical, and environmental variables combine to determine the occurrence and appearance of LHPC. Nevertheless, we conclude that LHPC probably reflects deficient growth of the arcades in infant apes and humans.