Orangutans, enamel defects, and developmental health: A comparison of Borneo and Sumatra

Abstract

Orangutans (Pongo sp.) show among the highest occurrence of three types of developmental enamel defect. Two are attributed to nutritional factors that reduce bone growth in the infant's face early in development. Their timing and prevalence indicate that Sumatra provides a better habitat than does Borneo. The third type, repetitive linear enamel hypoplasia (rLEH) is very common but its etiology is not understood. Our objective is to draw attention to this enigmatic, episodic stressor in the lives of orangutans. We are concerned that neglect of this possible marker of ill health may be contributing, through inaction, to their alarming decline in numbers. Width and depth of an LEH are considered proxies for duration and intensity of stress. The hypothesis that Bornean orangutans would exhibit relatively wider and deeper LEH was tested on 163 independent episodes of LEH from 9 Sumatran and 26 Bornean orangutans measured with a NanoFocus AG "µsurf Mobile Plus" scanner. Non-normally distributed data (depths) were converted to natural logs. No difference was found in width of LEH among the two island taxa; nor are their differences in width or depth between the sexes. After controlling for significant differences in LEH depths between incisors and canines, defects are, contrary to prediction, significantly deeper in Sumatran than Bornean animals (median = 28, 18 µm, respectively). It is concluded that repetitive LEH records an unknown but significant stressor present in both Sumatra and Borneo, with an average periodicity of 6 months (or multiples thereof) that lasts about 6-8 weeks. It is worse in Sumatra. Given this patterning, shared with apes from a wide range of ecological and temporal sources, rLEH is more likely attributable to disease than to malnutrition.

Developmental stress in South African hominins: Comparison of recurrent enamel hypoplasias in Australopithecus africanus and Homo naledi

“…Because an object's surface is rarely level or completely flat, true depths are calculated trigonometrically from width and depth measures originally taken orthogonal to the instrument's plane. 37 'Width' is defined as an orthogonal measure from the occlusal shoulder/high point, which visually demarcates the onset of an episode of LEH, to the deepest point of the defect, assessed with reference to the cervical high point of a defect. Typically, width defined this way is about half the overall width of an LEH.…”

“…Apart from measurement error, the other major factor reducing the correlation is that LEH defects often contain more closely spaced perikymata because of reduced secretion (compression) affecting Retzius increment width. 37,49,50 Given the noted correlation, it is reasonable to calculate, for those LEH defects without observable perikymata, the likely number of constituent perikymata given their widths. As discussed elsewhere 35 , the pattern of perikymata packing can differ between taxa and tooth types; specifically, in comparison to Australopithecus, H. naledi shows more widely spaced perikymata occlusally and narrower perikymata cervically, especially in the incisors.…”

“…For this analysis, it is assumed that the steeper the angle of descent into an LEH furrow, the more intense is the felt stress. 37 The angle is calculated from the relationship between width and depth of defect (Table 6). In the overall sample, the distribution of angle of onset is uni-modal and left skewed.…”

Quantifying linear enamel hypoplasia in Virunga Mountain gorillas and other great apes

“…Previous research on LEH in great apes has primarily focused on determining defect prevalence by scoring anterior teeth using light microscopy and/or scanning electron microscopy (e.g., Guatelli‐Steinberg, Ferrell, & Spence, ; Skinner & Hopwood, ). Defect severity, defined as the depth and/or width of a defect, has been hypothesized to reflect the magnitude of the insult that caused the defect (Skinner & Hopwood, ; Skinner & Skinner, ). However, variation in the internal geometry of underlying enamel growth increments may also influence defect depth (Guatelli‐Steinberg et al, ).…”

“…However, variation in the internal geometry of underlying enamel growth increments may also influence defect depth (Guatelli‐Steinberg et al, ). While histological analysis is the only way to obtain a complete understanding of how individual defects formed (Witzel, Kierdorf, Schultz, & Kierdorf, ), nondestructive imaging‐based methods have been developed to quantitatively characterize defect morphology from the outer enamel surface (Bocaege & Hillson, ; Bocaege, Humphrey, & Hillson, ; Guatelli‐Steinberg, Larsen, & Hutchinson, ; Hassett, ; Henriquez & Oxenham, ; Hillson, ; Hillson & Jones, ; King, Hillson, & Humphrey, , Le Cabec, Tang, & Tafforeau, ; Marchewka, Skrzat, & Wróbel, ; Skinner & Pruetz, ; Skinner & Skinner, ; Temple, McGroarty, Guatelli‐Steinberg, Nakatsukasa, & Matsumura, ). These methods have the potential to reduce interobserver error in the identification and characterization of defects, but fundamental questions remain about the extent of inter‐ and intraspecific variation in defect morphology in primates.…”