I have mentioned previously that I was reading Lubenow’s Bones of Contention. In this post I would like to focus on Lubenow’s understanding of rickets and Neanderthal morphology. In order to discuss that I first need to discuss vitamin D deficiency
Rickets and osteomalacia are both manifestations of vitamin D deficiency. Vitamin D is one of three chemicals that regulate calcium metabolism (the other two being parathormone and calcitonin). There are actually two types of vitamin D (D2 and D3) both of which are similar in structure to cholesterol. Both are produced by the ultraviolet irradiation on ergosterol and 7-dehydrocholesterol (respectively). Basically, the UV breaks the ring structure and converts them to an active forms. Eventually, these two forms reach the liver and kidneys. In the liver a further conversion happens and the chemicals produced increase calcium absorption in the intestine. In the kidneys, there is a conversion into either a highly active form or an inactive form. Low serum calcium levels and elaboration of parathormone favor production of the active form which increases calcium absorption, while high calcium and the release of calcitonin favor the production of the inactive form. Vitamin D deficiency results in the decrease in the absorption of calcium in the intestine (most of it is excreted) and decreased transport into bone. Vitamin D deficiency is expressed in two different ways (basically) depending on whether or not skeletal growth has ceased. If growth is ongoing then it is expressed as rickets, otherwise it is osteomalacia.
There are several different types of rickets, including types that are vitamin D resistant and one that is genetic (these latter are outside the scope of this paper). The highest frequency of rickets occurs between 6 months and two years. Rickets primarily affects the epiphyseal plates. The epiphyseal plate is composed of 5 zones where new bone is formed and mineralized. Rickets, in its active form, primarily affects the maturation zone producing an increase in the transverse diameter of the bone as well as cupping of the surface. There is increased porosity of the cortical bone, diminished density and irregular and thin trabecular bone.
In the skull the anterior and posterior fontanels persist and the sutures become wider, the parietals often give asymmetrical contours with one becoming flattened. Frontal bossing is frequently seen. The cranium becomes porous and soft (this is called craniotabes). Eruption of the teeth is delayed and the teeth are poorly mineralized. The mandibular ramus is occasionally deformed. The ribs display cupping and the costochondral junctions and occasionally rows of nodules are seen on either side of the sternum (this is called the rachitic rosary) which may be acutely angled, there is also asymmetrical flattening of the thorax. the limbs, metacarpals and phalanges may be bowed and have enlarged ends. The neck of the femur is bent downward. Post rickets, there is bone deposition at the areas where the deformed bone is stressed the most.
We see some of these changes in osteomalacia, the bowing of the limbs for example, along with pseudofractures – areas of poor mineralization that occur perpendicular to the bone surface. The picture below should give you some idea of what this looks like.
In the next post I will look at what Lubenow says about rickets and neanderthals.