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Childhood stunting is a major public health concern in both developed and developing countries. It is the consequence of malnutrition during the first years of life and the preconception period. It represents a socio-medical problem, it can present the first sign of a pathology and which can jeopardize a vital and functional prognosis of the child, also it can even become complicated with a small height in adulthood. This study focuses on the impact of eating behaviors, habits, and lifestyle on the stunting of 219 children aged 7 to 12 in the peri-urban area of Casablanca, Morocco. The sampling involved 219 children aged 7 to 12 from the region of Tit mellil “peri-urban area of Casablanca, Morocco. All participants completed a CAP Scoring Assessment Questionnaire. The questionnaire was divided into three sections: food groups, eating behaviour and lifestyle. The height measurement was carried out by a vertical measuring rod, the weight and the BMI using an impedence meter (krada scan). Body status was assessed by comparing BMI to WHO 2008 reference standards. The study involved 219 children (including 125 girls and 94 boys), the mean age was 9.53 ± 1.48, The prevalence of different height per age classes according to sex showed that the prevalence of growth normal and stunting is respectively 96% and 4% according to WHO (2008). The prevalence of stunting is very high in girls than boys, representing 3% and 1% respectively (Table 3). While the distribution according to age shows a high prevalence of stunting with percentages of 0.9% and in children aged 9 and 12 years. Several characteristics differentiate children with a stunting and normal growth children). Children with a stunting are less likely than normal growth children to eat breakfast often (1.83% versus 37.9% without reaching significance). 0.91% never take it, also 1.83% of children with stunting drink 6 to 8 glasses of water per day (p=0.009). In Morocco stunting prevalence is variable, with prevalence of 16.02% according to WHO standards in children aged less than 5 years (Sellam et al., 2015). The stunting estimated at 4% according to the 2008 WHO references, hence the interest of implementing a preventive strategy in order to slow the progression of this problem is necessary. Accordingly, the promotion of a healthy diet.

Prenatal and early life exposure of chlorpyrifos (CPF), a widely used pesticide, is known to cause neuronal deficits and Parkinson's disease (PD). However, data about the effect of its exposure at adult stages on PD-like symptoms and associated bone loss is scanty. In the present study, we investigated the impact of CPF on the behavioral alterations seen in PD using adult Swiss albino mice. PD is often associated with bone loss. Hence, skeletal changes were also evaluated using micro-computed tomography and histology. MPTP was used as a positive control. Cell culture studies using MC3T3E-1, SHSY5Y, and primary osteoclast cultures were done to understand the cellular mechanism for the behavioral and skeletal changes. Our results showed that CPF treatment leads to PD-like symptoms due to the loss of dopaminergic neurons. Moreover, CPF has a deleterious effect on the trabecular bone through both indirect changes in circulating factors and direct stimulation of multinucleate osteoclast cell formation. The impact on the bone mass was even stronger than MPTP. In conclusion, this is the first report demonstrating that CPF induces parkinsonian features in adult Swiss albino mice and it is accompanied by loss of trabecular bone.

Till now monocrotophos (MCP) has been addressed as a neurotoxic stressor. Limited studies investigate its aftermath on bone pathologies. Given the fact that MCP is a propensely used insecticide in developing countries, this study investigates its potential to mirror osteoporotic features and bone loss incurred in a rodent model. Briefly, Swiss albino mice were orally gavaged daily with varying doses of MCP for 8 weeks. Musculoskeletal changes were analyzed through micro-computed tomography and histology. A series of in vitro and ex vivo cell culture experiments were performed on MC3T3E-1 and primary osteoclast cultures. Results highlight that oral gavaging with MCP causes bone loss from the cortico-trabecular interface by decreasing the osteoblast and increasing the osteoclast number. Results from in vitro studies establish that MCP treatment increases the TRAP-positive multinucleated cell number during osteoclast differentiation. Ex-vivo experiments with MCP-treated animal sera further substantiate the in vivo claims with significant decreases seen in cell viability, proliferation, mineralization and differentiation studies. In conclusion MCP induces osteoclastogenesis (bone loss) on direct stimulation and alters the circulating factors in MCP-treated serum. Holistically, this work would be of potential significance to patients suffering from pesticide induced osteoporosis.

Bone loss is a non-motor symptom of Parkinson's disease (PD). It is unclear whether a patient's immobility or the endocrine changes in the body causes bone deterioration. To address this issue, we used an animal model of the disease where Swiss albino mice were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on day 1 and were left untreated for eight weeks. Behavioral phenotypes of PD, and striatal acetylcholinesterase and dopamine levels were measured. Cortical and trabecular bones were assessed by μ-CT and histology. Gene expression studies were done through quantitative real-time PCR. Effect of MPP+ and MPTP-treated mice serum on MC3T3E-1, SH-SY5Y, and primary osteoclast cells were also studied. Our results demonstrated that MPTP treatment leads to PD like symptoms. It shows a loss of trabecular bone mass and quality by decreasing osteoblast and increased osteoclast number and activity. This effect was accompanied by reduced osteogenic and elevated osteoclastogenic genes expression. While MPP+ had a cytotoxic effect on dopaminergic neurons, it did not affect bone cells. However, ex-vivo treatment of the serum from MPTP-treated mice decreased osteoblastogenesis and increased osteoclastogenesis in cell culture. In conclusion, our study suggests that MPTP-induced parkinsonian features in mice leads to trabecular bone loss by decreased bone formation and increased bone resorption due to changes in the serum circulating factors. This study characterizes the microarchitectural and cellular changes in the skeleton of a mouse model of PD that can be further utilized to investigate therapeutic avenues to treat bone loss in PD patients.