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Organohalogen concentrations and a gross and histologic ...

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Chapter 3<br />

Bone mineral density <strong>and</strong> periodontitis in<br />

East Greenl<strong>and</strong> polar bear skulls collected<br />

from 1892 to 2002<br />

Of the 283 skulls analysed for FA, all were analysed for periodontitis <strong>and</strong> 149<br />

were X-ray scanned for bone mineral density (BMD) to detect signs of osteoporosis.<br />

Information on age <strong>and</strong> gender was unfortunately missing in 10 individuals<br />

<strong>and</strong> therefore only 139 skulls could be used in the further statistical<br />

analysis. The purpose was to investigate period differences (1892-1960 vs.<br />

1961-202), a continuous time trend over the entire period (1892-2002) <strong>and</strong> the<br />

relation between individual levels of organohalogens (∑-PCBs, ∑-DDTs, dieldrin,<br />

∑-HCHs, ∑-CHLs, HCB <strong>and</strong> ∑-PBDEs) in subcutaneous adipose tissue<br />

<strong>and</strong> BMD (BMD was also analysed in 52 bacula in the present investigation).<br />

These results are described in details in paper III-a,b.<br />

Background<br />

Calcium-phosphate (hydroxyapatite) <strong>and</strong> the double-helix collagen (type 1)<br />

are the two major components of bone tissue <strong>and</strong> determines the hardness<br />

<strong>and</strong> the elasticity, respectively (e.g. Ganong 1991, Doige <strong>and</strong> Weisbrode 1995,<br />

Geneser 1996). Bone density expresses the bone mineral content determined<br />

by the activity of osteoblastic bone formation <strong>and</strong> osteoclastic bone resorption<br />

which is primarily regulated by parathyroid hormone, <strong>and</strong>rogens <strong>and</strong> estrogens<br />

through cytokines <strong>and</strong> growth factors (e.g. Ganong 1991, Doige <strong>and</strong><br />

Weisbrode 1995, Manalagas <strong>and</strong> Jilka 1995, Manalagas et al. 1995, Geneser<br />

1996). Exogenous organohalogens have the potential of disrupting this homeostasis<br />

through their agonism <strong>and</strong> antagonism to naturally endogenous<br />

hormones (sex steroids, parat hormone, calcitonin, thyroid hormones, cortisol<br />

a.o.) leading to dysosteogenesis (osteoporosis, periodontitis a.o.) (e.g. Bergman<br />

<strong>and</strong> Olsson 1985, Bergman et al. 1992a, Colborn et al. 1993, Feldman 1995,<br />

de March et al. 1998, S<strong>and</strong>au et al. 2000, Damstra et al. 2002, Letcher et al. 2002,<br />

Hakk <strong>and</strong> Letcher 2003, AMAP 2004).<br />

Specific in polar bears, recent studies of endocrine disruption on Svalbard of<br />

121 male polar bears have shown that Σ-PCB <strong>concentrations</strong> (sum of 16 congeners)<br />

made significantly contributions to the variation in plasma testosterone<br />

levels (Oskam et al. 2003). In female polar bears (n=86) progesterone was<br />

found to be positively correlated with Σ-PCBs (Haave et al. 2003) <strong>and</strong> in both<br />

sexes Σ-PCBs <strong>and</strong> chlorinated pesticides was altering the cortisol levels<br />

(Oskam et al. 2004). Regarding plasma retinol <strong>concentrations</strong> <strong>and</strong> the ratio of<br />

total T 4 to free T 4 , these decreased linearly with increasing <strong>concentrations</strong> of Σ-<br />

PCBs in Svalbard bears of varying sex <strong>and</strong> age investigated in 1991-1994<br />

(Skaare et al. 2001). These studies all indicate that organohalogens in Svalbard<br />

polar bears (<strong>and</strong> likely also East Greenl<strong>and</strong> bears, as the OHC levels are comparable)<br />

potentially affect the endocrine homeostasis, which again may lead to<br />

bone mineral disturbances (osteoporosis, periodontitis a.o.) (Ibid.). Another<br />

polar bear study from Svalbard have associated high levels of OCs with low<br />

levels of IgG suggesting possible immunotoxic effects (Bernhoft et al. 2000, Lie<br />

et al. 2004, Lie et al. Submitted). This potential effect may decrease the immune<br />

response <strong>and</strong> enhance stress-induced bone mineral changes through an activation<br />

of the hypophyseal-adrenal/thyroid axis, leading to enhanced parathy-<br />

35

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