Consumption of excess dietary salt also known as sodium chloride or table salt, is not widely accepted as a direct contributor to the development osteoporosis. Studies are limited and have had different outcomes relating to its affect on bone, but the majority of the studies all support the notion that high sodium chloride intake increases urinary calcium excretion11.
To better understand how this might affect bone, it's important to understand that the average adult contains from 90-130g of sodium and that roughly half it is in the bone. The remainder is in extracellular fluid11. This is important because the extracellular fluid is where osmolality is maintained in a state of equilibrium. According to Robert Heany, MD, a study in 1961 showed that sodium and calcium competed for the same reabsorption mechanisms in the proximal tubule of the kidneys. As sodium increases in the blood, bone remodeling stops while the osteoclasts break down the bone and release calcium to raise the calcium levels in the blood. If sodium levels continue to climb or remain high in the body it produces an effect called calciuria, which is an excretion of calcium in the urine. Heany, who reviewed and summarized the majority of the studies, indicates that urine calcium rises by about 1.0 m/mol or 20-60 mg for every 100 m/mol (2300mg) of sodium ingested12. When the amount of calcium excreted is greater than the amount of calcium that is absorbed it would make sense that bone mass would suffer.
However, there are two possible compensatory mechanisms that might counter the loss of calcium resulting in "bone loss" which might attribute to the conflicting results in various studies. As discussed earlier, the parathyroid gland, calcitonin, and Vitamin D3 all play a role in calcium homeostasis. The parathyroid glands secretes hormones in response to calcium levels. As calcium levels drop, parathyroid secretions will increase. This is supported by Heany who reports that a rise in the parathyroid hormone would raise Ca++ levels with a subsequent increase in the synthesis of vitamin D3 and ultimately calcium absorption efficiency and bone remodeling activity12. This compensatory action was mostly observed in pre-menopausal women and not in post menopausal women.
The second possible compensatory mechanism is the addition of potassium citrate to a high sodium diet. Deborah Sellmeyer and her team did a study with fifty-two (52) women for seven weeks. In this double-blind study, the women were placed into two groups. One group would receive a high sodium diet with a placebo and a second group would receive a high sodium diet with potassium citrate. According to Sellmeyer, et al., the results indicate that the post menopausal women who were given potassium citrate with a high salt diet had lower urine calcium output and a higher parathyroid hormone output than those who were given a placebo with a high salt diet13.