Evidence of amelogenesis imperfecta in an early African Homo erectus

Zilberman, Uri; Smith, Patricia; Piperno, Marcello; Condémi, Silvana

doi:10.1016/j.jhevol.2004.02.005

Cited by 27 publications

(13 citation statements)

References 31 publications

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“…From the Early Pleistocene these unusual cases include the massive perimortem periostitis of KNM-ER 1808 [54], the amelogenesis imperfecta of Garba 4 [55], and the diffuse craniofacial lesions of Dmanisi D3444/D3900 [56]. In the Middle Pleistocene, such abnormalities include the unilateral lambdoid synostosis of Atapuerca-SH cranium 14 [57], the probable torticollis of Salé 1 [58], the unilateral labyrinthine ossification and parietal enlargement of Singa 1 [59], and the lumbar kyphotic deformity, spondylolisthesis, and Baastrup disease in the Atapuerca-SH pelvis 1 [60].…”

Section: Discussionmentioning

confidence: 99%

An Enlarged Parietal Foramen in the Late Archaic Xujiayao 11 Neurocranium from Northern China, and Rare Anomalies among Pleistocene Homo

Xing

Trinkaus

2013

PLoS ONE

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We report here a neurocranial abnormality previously undescribed in Pleistocene human fossils, an enlarged parietal foramen (EPF) in the early Late Pleistocene Xujiayao 11 parietal bones from the Xujiayao (Houjiayao) site, northern China. Xujiayao 11 is a pair of partial posteromedial parietal bones from an adult. It exhibits thick cranial vault bones, arachnoid granulations, a deviated posterior sagittal suture, and a unilateral (right) parietal lacuna with a posteriorly-directed and enlarged endocranial vascular sulcus. Differential diagnosis indicates that the perforation is a congenital defect, an enlarged parietal foramen, commonly associated with cerebral venous and cranial vault anomalies. It was not lethal given the individual’s age-at-death, but it may have been associated with secondary neurological deficiencies. The fossil constitutes the oldest evidence in human evolution of this very rare condition (a single enlarged parietal foramen). In combination with developmental and degenerative abnormalities in other Pleistocene human remains, it suggests demographic and survival patterns among Pleistocene Homo that led to an elevated frequency of conditions unknown or rare among recent humans.

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Section: Discussionmentioning

confidence: 99%

An Enlarged Parietal Foramen in the Late Archaic Xujiayao 11 Neurocranium from Northern China, and Rare Anomalies among Pleistocene Homo

Xing

Trinkaus

2013

PLoS ONE

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“…Dental enamel hypoplasia defects represent an interruption in the growth process of teeth and can be attributed to genetics (Brook, 2009; Hart et al, 2002; Zilberman et al, 2004), trauma (Brook, 2009), and insult (Goodman, 1988; Sarnat & Schour, 1942; Sarnat & Schour, 1941). Those linked to external biological insult (e.g., foreign disease pathogen, injury) develop when resources normally directed to growth and development are rerouted to defending the body or are only insufficient to sustain maintenance activities (e.g., malnourishment, diarrhea) (Sarnat & Schour, 1942; Sarnat & Schour, 1941).…”

Section: Introductionmentioning

confidence: 99%

Frequency and developmental timing of linear enamel hypoplasia defects in Early Archaic Texan hunter-gatherers

Berbesque

Hoover

2018

PeerJ

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Digital photographs taken under controlled conditions were used to examine the incidence of linear enamel hypoplasia defects (LEHs) in burials from the Buckeye Knoll archaeological site (41VT98 Victoria county, Texas), which spans the Early to Late Archaic Period (ca. 2,500–6,500 BP uncorrected radiocarbon). The majority (68 of 74 burials) date to the Texas Early Archaic, including one extremely early burial dated to 8,500 BP. The photogrammetric data collection method also results in an archive for Buckeye Knoll, a significant rare Archaic period collection that has been repatriated and reinterred. We analyzed the incidence and developmental timing of LEHs in permanent canines. Fifty-nine percent of permanent canines (n = 54) had at least one defect. There were no significant differences in LEH frequency between the maxillary and mandibular canines (U = 640.5, n1 = 37, n2 = 43, p = .110). The sample studied (n = 92 permanent canines) had an overall mean of 0.93 LEH defect per tooth, with a median of one defect, and a mode of zero defects. Average age at first insult was 3.92 (median = 4.00, range = 2.5–5.4) and the mean age of all insults per individual was 4.18 years old (range = 2.5–5.67). Age at first insult is consistent with onset of weaning stress—the weaning age range for hunter-gatherer societies is 1–4.5. Having an earlier age of first insult was associated with having more LEHs (n = 54, rho = −0.381, p = 0.005).

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“…In addition to susceptibility to caries, mutations in the ENAM gene have been described to cause enamel defects such as hypoplasia (thinner and more irregular enamel) and hypomineralization linked to Amelogenesis imperfecta (AI) disorders [ 37 ]. Local hypoplastic enamel defect occurs from <1% to >56% of living humans depending on populations, and was rare in Neanderthals [ 37 ] and earlier human groups [ 56 , 57 ].…”

Section: Resultsmentioning

confidence: 99%

Neanderthal and Denisova tooth protein variants in present-day humans

et al. 2017

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Environment parameters, diet and genetic factors interact to shape tooth morphostructure. In the human lineage, archaic and modern hominins show differences in dental traits, including enamel thickness, but variability also exists among living populations. Several polymorphisms, in particular in the non-collagenous extracellular matrix proteins of the tooth hard tissues, like enamelin, are involved in dental structure variation and defects and may be associated with dental disorders or susceptibility to caries. To gain insights into the relationships between tooth protein polymorphisms and dental structural morphology and defects, we searched for non-synonymous polymorphisms in tooth proteins from Neanderthal and Denisova hominins. The objective was to identify archaic-specific missense variants that may explain the dental morphostructural variability between extinct and modern humans, and to explore their putative impact on present-day dental phenotypes. Thirteen non-collagenous extracellular matrix proteins specific to hard dental tissues have been selected, searched in the publicly available sequence databases of Neanderthal and Denisova individuals and compared with modern human genome data. A total of 16 non-synonymous polymorphisms were identified in 6 proteins (ameloblastin, amelotin, cementum protein 1, dentin matrix acidic phosphoprotein 1, enamelin and matrix Gla protein). Most of them are encoded by dentin and enamel genes located on chromosome 4, previously reported to show signs of archaic introgression within Africa. Among the variants shared with modern humans, two are ancestral (common with apes) and one is the derived enamelin major variant, T648I (rs7671281), associated with a thinner enamel and specific to the Homo lineage. All the others are specific to Neanderthals and Denisova, and are found at a very low frequency in modern Africans or East and South Asians, suggesting that they may be related to particular dental traits or disease susceptibility in these populations. This modern regional distribution of archaic dental polymorphisms may reflect persistence of archaic variants in some populations and may contribute in part to the geographic dental variations described in modern humans.

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Evidence of amelogenesis imperfecta in an early African Homo erectus

Cited by 27 publications

References 31 publications

An Enlarged Parietal Foramen in the Late Archaic Xujiayao 11 Neurocranium from Northern China, and Rare Anomalies among Pleistocene Homo

An Enlarged Parietal Foramen in the Late Archaic Xujiayao 11 Neurocranium from Northern China, and Rare Anomalies among Pleistocene Homo

Frequency and developmental timing of linear enamel hypoplasia defects in Early Archaic Texan hunter-gatherers

Neanderthal and Denisova tooth protein variants in present-day humans

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