Sources, Effects and Risks of Ionizing Radiation

Background
Removal of teeth results in both horizontal and vertical changes of hard and soft tissue dimensions. The magnitude of these changes is important for decision-making and comprehensive treatment planning, with provisions for possible solutions to expected complications during prosthetic rehabilitation.

Objectives
To review all English dental literature to assess the magnitude of dimensional changes of both the hard and soft tissues of the alveolar ridge up to 12 months following tooth extraction in humans.

Methods
An electronic MEDLINE and CENTRAL search complemented by manual searching was conducted to identify randomized controlled clinical trials and prospective cohort studies on hard and soft tissue dimensional changes after tooth extraction. Only studies reporting on undisturbed post-extraction dimensional changes relative to a fixed reference point over a clearly stated time period were included. Assessment of the identified studies and data extraction was performed independently by two reviewers. Data collected were reported by descriptive methods. Weighted means and percentages of the dimensional changes over time were calculated where appropriate.

Results
The search provided 3954 titles and 238 abstracts. Full text analysis was performed for 104 articles resulting in 20 studies that met the inclusion criteria. In human hard tissue, horizontal dimensional reduction (3.79 ± 0.23 mm) was more than vertical reduction (1.24 ± 0.11 mm on buccal, 0.84 ± 0.62 mm on mesial and 0.80 ± 0.71 mm on distal sites) at 6 months. Percentage vertical dimensional change was 11–22% at 6 months. Percentage horizontal dimensional change was 32% at 3 months, and 29–63% at 6–7 months. Soft tissue changes demonstrated 0.4–0.5 mm gain of thickness at 6 months on the buccal and lingual aspects. Horizontal dimensional changes of hard and soft tissue (loss of 0.1–6.1 mm) was more substantial than vertical change (loss 0.9 mm to gain 0.4 mm) during observation periods of up to 12 months, when study casts were utilized as a means of documenting the changes.

Conclusions
Human re-entry studies showed horizontal bone loss of 29–63% and vertical bone loss of 11–22% after 6 months following tooth extraction. These studies demonstrated rapid reductions in the first 3–6 months that was followed by gradual reductions in dimensions thereafter.

A systematic review of post-extractional alveolar hard and soft tissue dimensional changes in humans.

Renal osteodystrophy

Depleted uranium (DU) is a by-product from the chemical enrichment of naturally occurring uranium. Natural uranium is comprised of three radioactive isotopes: (238)U, (235)U, and (234)U. This enrichment process reduces the radioactivity of DU to roughly 30% of that of natural uranium. Nonmilitary uses of DU include counterweights in airplanes, shields against radiation in medical radiotherapy units and transport of radioactive isotopes. DU has also been used during wartime in heavy tank armor, armor-piercing bullets, and missiles, due to its desirable chemical properties coupled with its decreased radioactivity. DU weapons are used unreservedly by the armed forces. Chemically and toxicologically, DU behaves similarly to natural uranium metal. Although the effects of DU on human health are not easily discerned, they may be produced by both its chemical and radiological properties. DU can be toxic to many bodily systems, as presented in this review. Most importantly, normal functioning of the kidney, brain, liver, and heart can be affected by DU exposure. Numerous other systems can also be affected by DU exposure, and these are also reviewed. Despite the prevalence of DU usage in many applications, limited data exist regarding the toxicological consequences on human health. This review focuses on the chemistry, pharmacokinetics, and toxicological effects of depleted and natural uranium on several systems in the mammalian body. A section on risk assessment concludes the review.

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Depleted and natural uranium: chemistry and toxicological effects

https://courses.washington.edu/gradorth/Ortho%20565%20Spring%20Theory/Suir%20AJODO_2004.pdf

Delayed tooth eruption: pathogenesis, diagnosis, and treatment. A literature review.

Uranium inhibits bone formation in physiologic alveolar bone modeling and remodeling

The introduction of uranium particles into subcutaneous tissue is a risk that affects workers engaged in the extraction, purification, and manufacture of uranium, as well as soldiers who are wounded with uranium shrapnel. The authors evaluated the effect of an internal source of an insoluble form of uranium on bone. Uranium dioxide powder (0.125 gm/kg body weight) was implanted subcutaneously in rats. After 30 days, animals exposed to uranium weighed less than controls. Bone formation activity in endochondral ossification and bone growth were also lower in the experimental animals, as evidenced by histomorphometric and morphometric methods. This is the first study to report bone damage resulting from continuous, nonlethal exposure to an insoluble compound of uranium dioxide over a period of 30 days.

Exposure to subcutaneously implanted uranium dioxide impairs bone formation.

Different groups have undertaken research work focusing their attention on the biological effects of uranium and have described kidney and bone to be the main target organs in uranium poisoning. In this study we used the skin as the route of entry of uranium. We carried out two sets of experiments in adult rats: in one of them topical applications with uranyl nitrate (UN) over different areas were performed; in the other topical applications with UN on a given area over different times were carried out. In the latter experiment the exposure to UN was stopped by removing it from skin with soap and water. Kidney and bone samples were removed for histological studies. This work is based on the determination of the survival rate of the exposed animals and on the effects elicited in kidney and bone. There is a relation between the area of the surface exposed to uranium and the time of exposure and the subsequent percutaneous toxicity. There were no surviving animals following topical application of UN to an 8 cm2 area nor when the time of exposure was 24 h. The survival rate of the animals increased when either the topical area or the time of exposure to UN was reduced. Although the inhibition of bone formation in metaphysical bone has been previously described by our group as a result of UN poisoning, this is the first time that such an effect is found after percutaneous exposure for such short periods of time. The general toxic effects of UN, evidenced as kidney histological alterations, increased in severity as either one of the two variables studied increased. This is a condition that could be considered as hazardous for those workers engaged in uranium processing and purification. It is noteworthy that a simple method such as washing with soap and water is an effective method to reduce the lethality of UN percutaneous intoxication.

Percutaneous toxicity of uranyl nitrate: its effect in terms of exposure area and time.

The alteration of bone formation by an acute intoxication with uranyl nitrate is demonstrated by histologic and histometric methods. When compared with the controls, intoxicated animals showed a markedly lower density in healing sockets, while bone formation was reduced in healing sockets as well as in metaphyseal bone.

Effects of acute intoxication with uranyl nitrate on bone formation

Exposure to uranium is an occupational hazard to workers who continually handle uranium and an environmental risk to the population at large. Since the cellular and molecular pathways of uranium toxicity in osteoblast cells are still unknown, the aim of the present work was to evaluate the adverse effects of uranyl nitrate (UN) on osteoblasts both in vivo and in vitro. Herein we studied the osteoblastic ultrastructural changes induced by UN in vivo and analyzed cell proliferation, generation of reactive oxygen species (ROS), apoptosis, and alkaline phosphatase (APh) activity in osteoblasts exposed to various UN concentrations (0.1, 1, 10, and 100 μM) in vitro. Cell proliferation was quantified by means of the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, ROS was determined using the nitro blue tetrazolium test, apoptosis was morphologically determined using Hoechst 3332 and APh activity was assayed spectrophotometrically. Electron microscopy revealed that the ultrastructure of active and inactive osteoblasts exposed to uranium presented cytoplasmic and nuclear alterations. In vitro, 1–100 μM UN failed to modify cell proliferation ratio and to induce apoptosis. ROS generation increased in a dose-dependent manner in all tested doses. APh activity was found to decrease in 1–100 μM UN-treated cells vs. controls. Our results show that UN modifies osteoblast cell metabolism by increasing ROS generation and reducing APh activity, suggesting that ROS may play a more complex role in cell physiology than simply causing oxidative damage.

Angela M Ubios

Papers

Uranium inhibits bone formation in physiologic alveolar bone modeling and remodeling

Exposure to subcutaneously implanted uranium dioxide impairs bone formation.

Percutaneous toxicity of uranyl nitrate: its effect in terms of exposure area and time.

Effects of acute intoxication with uranyl nitrate on bone formation

Ultrastructural and metabolic changes in osteoblasts exposed to uranyl nitrate.