Subperiosteal gain and endosteal loss in protein‐calorie malnutrition

Abstract

3- ABSTRACTSubperiosteal and medullary cavity diameters of 91 Guatemalan boys hospitalized with a diagnosis of protein-calorie malnutrition show a slight but significant increase in total width but a marked reduction at the endosteal surface, and in cortical area and percent cortical area, indicative of continuing subperiosteal apposition and a dramatic excess of endosteal resorption.m In previous studies we were able to demonstrate tubular bone loss during the course of protein-calorie malnutrition in infants and children, as apart from simple failure to grow (Garn et al., '64a,b; Garn, Rohmann and Guzmann, '66; Garn, Rohmann and Silverman, '67). Our work closely confirmed the bone-mineral determinations of Fletcher and Garrow ('64) and indicated a magnitude of tissue bone loss as great as 40%. We did not analyze the two bone surfaces, nor did we have access to the data from the Guatemalan Nutritional Survey. Recently, however, we have extended our analysis, using such national norms, and can document the surface-specific nature of bone loss in proteincalorie malnutrition in Central America.Comparing radiogrammetric data on metacarpal widths of boys hospitalized with an admission diagnosis of Kwashiorkor, with our recent national survey data (Garn and Rohmann, '66) no systematic reduction in outer bone width is evident. Rather, subperiosteal diameters of the affected boys are slightly but significantly larger than expectancy, using a chi-squared test (x2 = 4.05, p = 0.05). These data are shown in the first figure, and indicate that outer bone widths are not necessarily diminished, despite other growth failures.However, there is a marked reduction of cortical bone at the endosteal surface, compared to the sex-specific Guatemalan venile protein-calorie malnutrition is surface specific, and, as in adult bone loss, bone is lost at the endosteal surface and not at the subperiosteal. The subperiosteal surface may even continue to gain, in both juvenile and adult bone loss. 153

Recent origin of low trabecular bone density in modern humans

“…The lack of a significant difference in trabecular density between the (presumably) more active Puye and the industrial-era Terry samples also may argue for longer-term evolutionary as well as direct environmental effects. Moreover, other nonmechanical systemic factors that may influence skeletal morphology, including nutrition and disease prevalence (48,49), also were affected by the transition to food production and increased sedentism in the Holocene (50,51).…”

Dedicated to Dr. Guido Fanconi on the occasion of his 80th birthday Catch-up Growth in Malnutrition, Studied in Celiac Disease After Institution of Gluten-free Diet

“…In human malnutrition, marked deficiencies in compact and trabecular bone have been reported [2,19] as well as the cortical bone deficiency attributed to excessive endosteal resorption [18]. Very rapid and large gains in cortical bone with rehabilitation have been described [15].…”

Insights on the paleoepidemiology of ancient tuberculosis from the structural analysis of postcranial remains from the Ligurian Neolithic (northwestern Italy)

“…Metabolic insults such as malnutrition significantly alter bone development by slowing down subperiosteal apposition and accelerating medullary expansion (Garn et al, 1964(Garn et al, , 1969Himes et al, 1975). The concomitant effect of altered metabolism and activity pattern in AC5 during a crucial time for bone development is expected to result in extremely low 'robusticity' (bone mechanical rigidity scaled by body size: Ruff et al, 2006) of long bones (humerus, femur, and tibia) when compared to the rest of the Neolithic sample.…”

“…In addition, metabolic disturbances due to malnutrition disturb cross-sectional development, and there is evidence from both human and animal studies of a differential effect based on the timing, duration, and intensity of the metabolic insult. It appears that long-term chronic malnutrition results in smaller cross-sectional periosteal properties, with little effect on the medullary size (Himes et al, 1975;Glick and Rowe, 1981;Bozzini et al, 2013), while more severe insults lead to increased total area and especially medullary area, resulting in thinner cortices (Garn et al, 1969;DiVasta et al, 2007).…”

“…Following the completion of development, cortical thinning due to malnutrition, chronic disease, and inactivity (Garn et al, 1969;Himes et al, 1975;Hummert, 1983;Bass et al, 2002) is due to medullary area expansion, with little or no change in total area (e.g. Modlesky et al, 2005).…”