Hunter-Schreger Band patterns in human tooth enamel

Using light microscopy, we examined Hunter‐Schreger Band (HSB) patterns on the axial and occlusal/incisal surfaces of 160 human teeth, sectioned in both the buccolingual and mesiodistal planes. We found regional variations in HSB packing densities (number of HSBs per mm of amelodentinal junction length) and patterns throughout the crown of each class of tooth (maxillary and mandibular: incisor, canine, premolar, and molar) examined. HSB packing densities were greatest in areas where functional and occlusal loads are greatest, such as the occlusal surfaces of posterior teeth and the incisal regions of incisors and canines. From this it is possible to infer that the behaviour of ameloblasts forming enamel prisms during amelogenesis is guided by genetic/evolutionary controls that act to increase the fracture and wear resistance of human tooth enamel. It is suggested that HSB packing densities and patterns are important in modern clinical dental treatments, such as the bonding of adhesive restorations to enamel, and in the development of conditions, such as abfraction and cracked tooth syndrome.     

The aetiology of developmental defects of enamel: a prevalence and family study in East London, U.K

The aim of this study was to investigate genetic and environmental factors associated with hypoplastic defects of enamel in a detailed family study combined with an overall prevalence study. 68 percent of 1,518 children with a "complete" permanent dentition had enamel defects, 14.6 percent having hypoplasia. The Family Study consisted of 101 Index Cases from the Prevalence Study having 2 or more teeth with hypoplasia and their first degree relatives: they were compared with 101 matched controls and their relatives. The clinical examinations were supplemented with structured interviews to obtain social, medical and dental histories. Three Index Cases had amelogenesis imperfecta and 18 had "chronological hypoplasia". Bilateral hypoplasia of lower central incisors had a multifactorial aetiology (heritability 70 percent +/- 38 percent), while hypoplasia of pre-molars was associated with familial occurrence of defects. There was evidence suggesting a predisposition in some families to developmental defects of enamel.     

Safe Casting and Reliable Cusp Reconstruction Assisted by Micro-Computed Tomographic Scans of Fossil Teeth

Dental replicas are frequently utilized in paleoanthropological studies of perikymata and enamel hypoplasia. However, fossil teeth are often fragile and worn, causing two problems: (1) the risk of damage by removing enamel fragments when impression-making material is separated from the fossil tooth surface, and (2) the need to reconstruct worn portions of the crown to assess perikymata number, distribution, and hypoplasia timing. This study presents the advantages of μCT data of canines and lateral incisors for (1) detecting cracks along the enamel-dentine junction (EDJ) which could cause damage when casting, and (2) reliably and non-destructively reconstructing worn or broken cusps. Fragile teeth of Homo naledi, Miocene, and Pleistocene specimens were μCT-scanned: 2D virtual sections and 3D models allowed for inspecting crack pattern beyond the external surface and 2D virtual sections were used to digitally reconstruct cusp tips (only Homo naledi). Micro-CT scans allowed cracks running along the EDJ and communicating with radial cracks in the enamel to be identified prior to casting. Cusp reconstructions using μCT data were conducted as precisely as when using thin-sections or photographs, and with high intra- and inter-observer agreement, while preserving the original specimen and affording numerous planes of virtual section. When available, μCT data should be inspected prior to tooth casting to exclude teeth that show a pattern of cracks that could lead to damage. Virtual sections allow for accessible, reliable, and non-destructive cusp reconstructions that may be used for developmental (e.g., perikymata and enamel hypoplasia) or enamel thickness studies. Anat Rec, 302:1516–1535, 2019. © 2018 American Association for Anatomy     

Effect of Down syndrome on the dimensions of dental crowns and tissues

Abnormal growth in Down syndrome (DS) is reflected by variable reduction in size and simplification in form of many physical traits. This study aimed to compare the thickness of enamel and dentine in deciduous and permanent mandibular incisor teeth between DS and non‐DS individuals and to clarify how these tissues contribute to altered tooth size in DS. Sample groups comprised 61 mandibular incisors (29 permanent and 32 deciduous) from DS individuals and 55 mandibular incisors (29 permanent and 26 deciduous) from non‐DS individuals. Maximum mesiodistal and labiolingual crown dimensions were measured initially, then the crowns were sectioned midsagittally and photographed using a stereomicroscope. Linear measurements of enamel and dentine thickness were obtained on the labial and lingual surfaces of the crowns, together with enamel and dentine–pulp areas and lengths of the dentino‐enamel junction. Reduced permanent crown size in DS was associated with a reduction in both enamel and dentine thickness. After adjustments were made for tooth size, DS permanent incisors had significantly thinner enamel than non‐DS permanent teeth. The DS permanent teeth also exhibited significant differences in shape and greater variability in dimensions than the non‐DS permanent teeth. Crown dimensions of deciduous incisors were similar in size or larger in DS compared with non‐DS deciduous teeth. Enamel and dentine thicknesses of the deciduous teeth were similar in DS and non‐DS individuals. The findings indicate that growth retardation in DS reduces both enamel and dentine deposition in the permanent incisors but not in the earlier‐forming deciduous predecessors. The results are also consistent with the concept of amplified developmental instability for dental traits in DS. Am. J. Hum. Biol. 13:690–698, 2001. © 2001 Wiley‐Liss, Inc.     

Assessment of enamel hypoplasia in a high status burial site

Social differentiation is a characteristic of all societies, and higher social status is often associated with better nutrition and good health. Traditional archeologically inferred social status has been linked with biological evidence such as skeletal robusticity and the incidence of disease. In this regard, linear enamel hypoplasia (LEH) is considered a good indicator of health, and individuals with a high status should, at least in theory, not suffer from severe defects. In order to test this hypothesis, the prevalence and occurrence of LEH were assessed in a skeletal sample at the Fort Center, Florida, site. Located near Lake Okeechobee, this site was occupied from about A.D. 200–800, and was considered a mortuary ceremonial center. These archeological findings suggested that individuals buried there belonged to a high class and merited special mortuary rituals. Although 1,835 teeth were found, only 679 maxillary and 393 mandibular teeth were analyzed. The upper I1 and lower C are reported to be most representative for LEH, and were thus selected for further analysis. There were 45 left incisors and 48 left canines. Results indicated that about 95% of incisors and 98% of canines were affected. The occurrence of severe hypoplastic lines was much lower (between 30% and 40%). The minimum number of defects affecting the canine surpassed three, thus showing evidence of repeated stress during childhood. Hypoplasia was first observed between the ages of 1.0 and 1.5 years for incisors and between 2.0 and 2.5 years for canines. Severe defects were first noted to occur at 2.5–3.0 years of age for incisors and 3.0–3.5 years for canines. In conclusion, the high frequency of LEH in this socially elite population seems to prove that in prehistory even privileged classes were severely subjected to stress and the social stratification alone was not sufficient to buffer them from rigorous environments. Am. J. Hum. Biol. 9:213–222, 1997. © 1997 Wiley-Liss, Inc.     

Deposition of cellular cementum onto hypoplastic enamel of fluorotic teeth in wild boars (Sus scrofa L.)

The nature of deposits present in hypoplastic defects of fluorotic enamel of wild boar teeth was studied by light microscopy and scanning electron microscopy. The fluorotic enamel showed different developmental abnormalities, denoting a severe disturbance of ameloblast function during the secretory stage of amelogenesis. These abnormalities included the occurrence of grossly accentuated incremental lines with associated zones of aprismatic enamel and the presence of different forms of hypoplastic defects. Two types of deposits were present on the hypoplastic enamel: cellular cementum and posteruptively acquired, presumably partially mineralized dental plaque. Coronal cementum is not normally formed in pig teeth. Presence of this tissue in fluorotic teeth of wild boars is seen as indicative of a premature disintegration of the enamel epithelium prior to the completion of amelogenesis. This was supposed to have resulted in a contact of mesenchymal cells of the dental follicle with the surface of the immature enamel and, in consequence, in a differentiation of these cells into cementoblasts. To our knowledge, this is the first study reporting the formation of coronal cementum as part of the spectrum of pathological changes in fluorotic teeth in a species whose tooth crowns are normally free of cementum.     

Natal teeth: a review

The incidence of natal teeth is approximately 1:2,000 to 1:3,000 live births. The most commonly affected teeth are the lower primary central incisors. Natal teeth usually occur in pairs. The eruption of more than two natal teeth is rare. The majority of natal teeth represent the early eruption of normal primary deciduous dentition. Less than 10% of natal teeth are supernumerary. Natal teeth might resemble normal primary dentition in size and shape; however, the teeth are often smaller, conical and yellowish, and have hypoplastic enamel and dentin with poor or absent root formation. Complications include discomfort during suckling, sublingual ulceration, laceration of the mother's breasts and aspiration of the teeth. A dental roentgenogram is indicated to differentiate the premature eruption of a primary tooth from a supernumerary tooth. Tooth extraction is indicated if the tooth is supernumerary or excessively mobile. If the tooth does not interfere with breastfeeding and is otherwise asymptomatic, no treatment is necessary.     

Deposition of cellular cementum onto hypoplastic enamel of fluorotic teeth in wild boars (<Emphasis Type="Italic">Sus scrofa</Emphasis> L.)

The nature of deposits present in hypoplastic defects of fluorotic enamel of wild boar teeth was studied by light microscopy and scanning electron microscopy. The fluorotic enamel showed different developmental abnormalities, denoting a severe disturbance of ameloblast function during the secretory stage of amelogenesis. These abnormalities included the occurrence of grossly accentuated incremental lines with associated zones of aprismatic enamel and the presence of different forms of hypoplastic defects. Two types of deposits were present on the hypoplastic enamel: cellular cementum and posteruptively acquired, presumably partially mineralized dental plaque. Coronal cementum is not normally formed in pig teeth. Presence of this tissue in fluorotic teeth of wild boars is seen as indicative of a premature disintegration of the enamel epithelium prior to the completion of amelogenesis. This was supposed to have resulted in a contact of mesenchymal cells of the dental follicle with the surface of the immature enamel and, in consequence, in a differentiation of these cells into cementoblasts. To our knowledge, this is the first study reporting the formation of coronal cementum as part of the spectrum of pathological changes in fluorotic teeth in a species whose tooth crowns are normally free of cementum.     

Enamel hypoplasia in molars of sheep and goats, and its relationship to the pattern of tooth crown growth

Enamel is the most highly mineralized and durable tissue of the mammalian body. As enamel does not undergo remodeling or repair, disturbances of enamel formation leave a permanent record in the tissue that can be used for life history reconstruction. This study reports light and scanning electron microscope findings on hypoplastic enamel defects, and on the chronology of crown growth in the molars of sheep and goats. A marked reduction of enamel extension rates in cervical compared with more cuspal crown portions of sheep and goat molars was recorded, with formation of the cervical 25% of the crown taking about the same time as that of the upper 75% of the crown. This explains the more frequent occurrence of enamel hypoplasia in cervical compared with upper and middle crown portions. Regarding the identification of hypoplastic enamel defects by external inspection, our results suggest a dependence on the type of defect and the associated presence of smaller or larger amounts of coronal cementum. Defects considered to reflect a slight to moderate impairment of secretory ameloblast function can normally be correctly diagnosed as they are not occluded by thick layers of cementum. In contrast, defects denoting a severe impairment of enamel matrix secretion can typically not be correctly identified because they are occluded by large amounts of cementum, so that neither depth nor extension of the defects can be assessed on external inspection. In these cases, microscopic analysis of tooth sections is required for a correct diagnosis of the hypoplastic enamel defects.     

激光扫描并三维重建对重庆地区正常牙合数字化模型的测量

背景：研究采用三维测量仪和计算机辅助系统分别对中国人正常牙合牙齿颊侧和舌侧表面形态进行了三维测量,证实了中国人牙齿各数据与国外数据相比,有明显差异。 目的：旨在获得重庆地区正常牙合数字化模型牙体形态的矫正学数据资料,结合Andrews、国人测量结果及Ormco舌侧托槽数据,比较不同人种,不同地区牙体在唇(颊)侧,舌侧的形态差异,为个性化矫正系统提供测量依据。 方法：激光扫描并三维重建45副重庆地区未经矫正治疗的正常牙合数字化模型,通过计算机辅助系统精密测量唇(颊)侧及舌侧各4项测量指标：牙冠轴倾角、转矩角,凸距和磨牙补偿角。 结果与结论：重庆地区正常牙合牙体的矫正学测量结果特点：①牙冠轴倾度角：上前牙,尖牙较白种人直立;双尖牙,磨牙近中倾斜明显。②牙冠转矩角：上前牙较唇倾,磨牙舌倾较白种人明显,但倾斜度均小于国人。③牙冠凸距：上下牙合磨牙凸距比白种人大,同时,尖牙凸距比国人大。④磨牙补偿角：上颌磨牙补偿角较白种人偏小,与国人大致相似。结果表明,重庆地区正常牙合的牙齿形态与白种人,国人有较大的差别,统计显示有其自身特征。测量方法可为直丝弓矫治技术,舌侧矫治技术提供准确的牙体矫正学所需数据,有助于制订个性化的矫正方案,帮助正畸医生更全面和客观地评估不同地区、不同人种的牙牙合畸形特征。关键词：正常牙合;数字化模型;模型测量;牙冠轴倾度;牙冠转矩;牙冠凸距 doi:10.3969/j.issn.1673-8225.2012.17.030     

A spontaneous mutation: amelogenesis imperfecta with cysts in rats

Amelogenesis imperfecta (AI) is an inherited dental disease of enamel formation in humans, and there are various phenotypes due to the combination of enamel quality and quantity. We encountered four female IGS rats with spontaneous AI including odontogenic cysts in the incisor teeth. Histopathologically, in the incisors of the rats, the enamel organ was disorganized with the remaining enamel matrix residing within the enamel space. The expanding cysts derived from the enamel organ were formed in the periosteal connective tissue on the labial side. At the bottom of the tooth germs, the precursor cells of the epithelial root sheath were arranged regularly and the enamel organs were preserved to the same degree as those of normal rats. In the molar teeth of the affected rats an enamel matrix remained on the neck and crown of the erupted teeth; however, no abnormality was observed at the tooth root. Although an animal model of AI has been developed from mutants of the SHR-SP rat strain, the present cases represent another potential model of the disease because of the differences in the way the enamel matured and the odontogenic cyst formation in the incisors.     

SEM study of the development of rat incisor enamel hypoplasia under hypocalcemia induced by thyro-parathyroidectomy

Several clinical studies have reported the presence of enamel hypoplasia in congenital hypoparathyroidism or hypocalcemia. In previous studies we showed that thyroparathyroidectomy (TPTX) induced perturbations of the ameloblast morphology and secretion, of the rod pattern and of the enamel surface at late secretory stage and beginning of maturation, and limited hypoplasia in the erupted enamel of rat incisor. The aim of the present study was to evaluate by SEM, the extent and evolution of the enamel alterations of thyro-parathyroidectomized rats during the maturation stage. Wistar rats were thyro-parathyroidectomized and sacrificed 57 days later. The incisors were dissected out and processed for SEM. The surface of the incisor was observed from the end of secretion/beginning of maturation to its incisal erupted end. Transverse sections were prepared to study the structural defects and the prism pattern at different stages. The results showed that the surface of the TPTX incisors presented large hypoplastic defects at the end of secretion/beginning of maturation and only small defects in the erupted part. Transverse sections showed that, at the transition from secretion to maturation, the enamel defects extended to the mid-thickness of the tissue. At the incisal end the defects were limited to the outer enamel. As it is difficult to understand how the large apical defects could recover to appear as small hypoplasia at the incisal end, these results raise new questions concerning: (1) the effect of a long term calcium deficiency upon the cellular activity of the ameloblasts, and (2) the capacity of the enamel organ to compensate structural abnormalities.     

Postnatal changes in size, morphology and weight of developing postnatal deciduous anterior teeth

The present investigation is concerned with the postnatal changes in size, morphology and weight of anterior deciduous teeth (maxillary and mandibular central and lateral incisors and canines) in infants aged 0-46 weeks. Relating tooth weight and height to the age of the infant revealed the time at which each tooth achieves its maximum crown height and root formation begins, the rate of root elongation and, in the case of the canine teeth, the postnatal rate of crown elongation.     

Disturbed enamel formation in wild boars (Sus scrofa L.) from fluoride polluted areas in Central Europe

The pathological alterations of enamel structure in the teeth of wild boars from fluoride polluted areas in N-Bohemia (Czech Republic) and S-Saxony (Germany) were studied on a macroscopic and a microscopic level. Mandibular bone fluoride concentration (mg F(-)/kg, dry wt; mean +/-SD, individuals <24 months of age) in the specimens from N-Bohemia (754.3+/-149.6) and S-Saxony (490.8+/-135.1) was significantly higher than that of controls (free of dental fluorosis), originating from the western part of Germany (304.7+/-91.0). Fluoride content in bulk enamel (mg F(-)/kg, ash wt) of fluorotic permanent teeth from N-Bohemia (382.1+/-165.2) and S-Saxony (125.0+/-38.3) was likewise significantly increased over that of non-fluorotic control teeth from W-Germany (33.6+/-26.7). Macroscopically, fluorosed wild boar enamel exhibited opacity and discoloration of varying extent, accentuated perikymata as well as hypoplastic and posteruptive surface defects. Microradiographic and scanning electron microscopic analyses revealed enamel subsurface hypomineralization, accentuated Retzius lines and occurrence of broad, hypomineralized incremental bands of abnormal structure underlying hypoplastic enamel surface defects. The presence of zones of aprismatic enamel was associated with these bands. Incremental bands with altered enamel structure and enamel surface hypoplasias, both denoting a severe disturbance during the secretory stage of amelogenesis, have previously been observed in rodents following acute parenteral fluoride dosing. It is concluded that in the chronically fluoride exposed wild boars periods of especially elevated plasma fluoride levels exerted an acute toxic effect on the secretory ameloblasts. A feature not previously reported from fluorosed enamel was the occurrence of canal-like structures that originated at the broad incremental bands and extended into the external enamel. The presence of these canals presumably results from a delay in the resumption of secretory activity by groups of ameloblasts following a fluoride insult. Based on experimental evidence in domestic pigs and in sheep, the overall subsurface hypomineralization of fluorosed wild boar enamel is attributed to a disturbance of enamel maturation. The distribution of fluorotic enamel changes within the dentition of the wild boars could be related to the developmental sequence of tooth formation in the species. Teeth whose crown formation took place prenatally (deciduous teeth) or largely pre-weaning (permanent first molars) exhibited no or only moderate fluorotic enamel alterations. Based on the extension of enamel surface hypoplasias along the coronoapical axes of the tooth crowns, the timing of excess fluoride exposure that caused a marked disruption of enamel matrix secretion was estimated in specimens with a known date of death. The results indicate that the wild boars had been exposed to a particularly severe fluoride impact during autumn and winter of their first year of life.     

Ultrastructural Study of Tooth Enamel with Amelogenesis Imperfecta in Al-Nephrocalcinosis Syndrome

This paper describes the ultrastructure of the affected enamel and the clinical features in two siblings with the syndrome of nephrocalcinosis and amelogenesis imperfecta. Nephrocalcinosis was diagnosed by intravenous pyelography, and confirmed by ultrasonography and CT scan. Amelogenesis imperfecta AI was diagnosed clinically and histologically.

Light microscopy showed that the affected enamel surfaces were rough and the enamel was hypoplastic and mainly positively birefringent. Scanning electron microscopy revealed a rough and extensively cracked enamel surface covered with oval shaped blister-like protrusions. TEM snowed porous enamel consisting of loosely packed and randomly oriented thin ribbon-like crystals with little or no prismatic structure.

Observations showed that hypoplasia together with hypocalcification and/or hypomaturation defects were present in the same tooth, indicating the possibility of an abnormality in interstitial matrix, leading to dystrophic calcification in the kidney and abnormal tooth enamel formation, or alternatively an involvement of two separate but closely linked genes.     

Reduction of Pax9 gene dosage in an allelic series of mouse mutants causes hypodontia and oligodontia

Missing teeth (hypodontia and oligodontia) are a common developmental abnormality in humans and heterozygous mutations of PAX9 have recently been shown to underlie a number of familial, non-syndromic cases. Whereas PAX9 haploinsufficiency has been suggested as the underlying genetic mechanism, it is not known how this affects tooth development. Here we describe a novel, hypomorphic Pax9 mutant allele (Pax9neo) producing decreased levels of Pax9 wild-type mRNA and show that this causes oligodontia in mice. Homozygous Pax9neo mutants (Pax9neo/neo) exhibit hypoplastic or missing lower incisors and third molars, and when combined with the null allele Pax9lacZ, the compound mutants (Pax9neo/lacZ) develop severe forms of oligodontia. The missing molars are arrested at different developmental stages and posterior molars are consistently arrested at an earlier stage, suggesting that a reduction of Pax9 gene dosage affects the dental field as a whole. In addition, hypomorphic Pax9 mutants show defects in enamel formation of the continuously growing incisors, whereas molars exhibit increased attrition and reparative dentin formation. Together, we conclude that changes of Pax9 expression levels have a direct consequence for mammalian dental patterning and that a minimal Pax9 gene dosage is required for normal morphogenesis and differentiation throughout tooth development.     

Epidemiology of enamel hypoplasia in deciduous teeth: Explaining variation in prevalence in western india

This study is based on seven samples of school children (n = 516) from rural (five groups) and urban (two groups) settings in western Maharashtra, India. Height and weight were recorded for each subject. Intra‐oral observation of the labial surface of maxillary and mandibular anterior teeth was conducted with a low power (3×) illuminated hand lens. Presence of enamel hypoplasia was recorded on a dental chart by drawing the size and location of the defect on the affected tooth. Data analysis was conducted in two stages: 1) Enamel hypoplasia (EH) prevalence was analyzed by percentage of teeth and by percentage of individuals affected for the composite sample and independently for each study group and 2) an assessment of the relationship between anthropometric variables (height and weight), socio‐economic status (SES), and localized hypoplasia of primary canines (LHPC; Skinner, 1986) was evaluated using multiple linear regression analysis. EH was observed less often in deciduous incisors (0.2% in di₂ to 2.5% in di²) than in deciduous canines (dc). Mandibular dc were affected with the greatest frequency (23.1%, tooth count). The overall individual count prevalence of dc hypoplasia (LHPC) is 26.2% (134/511) for all village samples and sexes combined. Difference in LHPC frequency by sex is non‐significant, with males (24.7%, 70/284) and females (28.2%, 64/227) exhibiting nearly equal values. Significant inter‐group variation in LHPC prevalence was documented among the seven groups, and the range of LHPC prevalence the among living groups exceeds variability in LHPC among four prehistoric Chalcolithic skeletal series of the Deccan Plateau. Multiple regression analysis revealed no significant relationship between height‐for‐age or weight‐for‐age in four school samples (two urban/two rural), but a significant association between stature and LHPC was found for three rural endogamous groups. Children with LHPC were significantly shorter by 1.5 cm than children who lacked the defect after controlling for differences in age. While the association between low birth weight and EH is strong and well documented clinically, the association between childhood stature and LHPC is more variable across groups and may reflect inter‐group variation in the duration and intensity of environmental stress. Am. J. Hum. Biol. 13:788–807, 2001. © 2001 Wiley‐Liss, Inc.     

Effect of tooth size on the ageing and chronological distribution of enamel hypoplastic defects

The location of enamel hypoplastic defects on the tooth crown has been used to determine the age of an individual at the time the defect-producing stress occurred. The assumptions made in following this methodology are examined, and one in particular, that tooth size variation has a minimal impact on ageing and subsequent chronological distributions, is tested. Teeth with no occlusal or minimal wear and with enamel hypoplasias were measured for crown height and the location of the defect on the crown. Two samples are used, one comprising a series of archaeological specimens and the other from modern clinical extractions. The chronological distributions of the defects are determined by three different methods: one is based on a tooth mineralization chart; the second method uses the same chart but incorporates individual crown heights; and the third method adjusts the chart for the sample's mean crown heights. Significant differences between the age estimates are observed in both the modern and archaeological samples. Tooth size does affect the ageing of hypoplastic defects and the chronological distributions. By adjusting the mineralization chart for the sample's mean crown heights, the significant differences in age estimates can be corrected.     

Enamel Hypoplasia in a Pliocene Hominid from Chad

Abel is the first Australopithecine known west of the East African Rift Valley. The fossil finds include a perisymphyseal fragment of an adult mandible with well-preserved crowns of the right I 2 -P 4 and the left C-P 4 . Abel's dentition displays many enamel defects, which are described in detail for each tooth. Pitting affected every tooth, while larger, shallow depressions were observed on the canines alone. From two to four pit bands occurred on the different teeth, each resulting from a separate hypoplastic episode. In modern humans, a large number of causes, both environmental and genetic, have been suggested for such enamel defects. It seems probable that Abel's pathology was systemic. However, the occurrence of a number of bands and the variable intensity of the attacks make it difficult to say whether there was a single, repetitive cause or different etiologies. Possible causes discussed here include recurrent fevers and seasonal nutritional deficiencies.     

Enamel hypoplasia in a pliocene hominid from Chad

Abel is the first Australopithecine known west of the East African Rift Valley. The fossil finds include a perisymphyseal fragment of an adult mandible with well-preserved crowns of the right I2-P4 and the left C-P4. Abel's dentition displays many enamel defects, which are described in detail for each tooth. Pitting affected every tooth, while larger, shallow depressions were observed on the canines alone. From two to four pit bands occurred on the different teeth, each resulting from a separate hypoplastic episode. In modern humans, a large number of causes, both environmental and genetic, have been suggested for such enamel defects. It seems probable that Abel's pathology was systemic. However, the occurrence of a number of bands and the variable intensity of the attacks make it difficult to say whether there was a single, repetitive cause or different etiologies. Possible causes discussed here include recurrent fevers and seasonal nutritional deficiencies.