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Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
Acid-Base Balance01:25

Acid-Base Balance

The human body maintains a narrow pH range regulated through acid-base balance. This balance is crucial as changes in the hydrogen ion concentration can disrupt cell membrane stability, alter protein structures, and change enzyme activities. The normal pH of arterial blood is 7.4, venous blood and interstitial fluid is 7.35, and intracellular fluid averages 7.0.
When the pH of arterial blood rises above 7.45, it results in a condition called alkalosis. Conversely, a drop below 7.35 leads to...
Renal Regulation of Acid-Base Balance01:29

Renal Regulation of Acid-Base Balance

Metabolic reactions in the body produce nonvolatile acids, such as sulfuric acid, which generate an acid load of approximately 1 mEq of H+ per kilogram of body weight daily. Excreting H+ in the urine is essential to balance this acid load.
In the kidneys, cells within the proximal convoluted tubules (PCT) and the collecting ducts secrete hydrogen ions (H+) into the tubular fluid. Specifically, in the PCT, Na+/H+ antiporters secrete H+ while reabsorbing Na+.
However, the intercalated cells in...
Disorders of Acid-Base Balance01:29

Disorders of Acid-Base Balance

The human body maintains a precise pH range of arterial blood between 7.35 and 7.45. Deviations result in either acidosis (pH < 7.35) or alkalosis (pH > 7.45). These conditions are further classified as respiratory or metabolic disorders based on their underlying cause.
Respiratory Acidosis and Alkalosis
Respiratory acidosis occurs due to an increase in the partial pressure of carbon dioxide PCO2 in the blood. It often arises from shallow breathing or impaired gas exchange caused by...
Diagnosing Acidosis and Alkalosis01:24

Diagnosing Acidosis and Alkalosis

Diagnosing acid-base imbalances involves systematically analyzing arterial blood samples, focusing on three key measurements: pH, bicarbonate (HCO3−) concentration, and carbon dioxide partial pressure (PCO2). This analysis follows a four-step process that helps identify the imbalance's underlying cause and nature.
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2  and HCO3−  values are examined to...

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Effect of bolus and divided feeding on urine ions and supersaturation in genetic hypercalciuric stone-forming rats.

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Effect of cinacalcet on urine calcium excretion and supersaturation in genetic hypercalciuric stone-forming rats.

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Metabolic, but not respiratory, acidosis increases bone PGE(2) levels and calcium release.

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Dysregulation of the calcium, phosphorus, parathyroid hormone, and vitamin D axis: what are the causes and risks?

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Effect of acidosis on urine supersaturation and stone formation in genetic hypercalciuric stone-forming rats.

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Related Experiment Video

Updated: Jun 27, 2026

Scanning Skeletal Remains for Bone Mineral Density in Forensic Contexts
07:56

Scanning Skeletal Remains for Bone Mineral Density in Forensic Contexts

Published on: January 29, 2018

Acid-base imbalance and the skeleton.

D A Bushinsky1

  • 1University of Rochester School of Medicine and Dentistry, Nephrology Unit, Strong Memorial Hospital, New York 14642, USA. David_Bushinsky@URMC.Rochester.edu

European Journal of Nutrition
|February 15, 2002
PubMed
Summary
This summary is machine-generated.

Diet-induced metabolic acidosis in humans can lead to bone mineral loss and increased fracture risk. This occurs as the body attempts to buffer acids, impacting bone health over time, especially with aging.

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Area of Science:

  • Bone metabolism
  • Acid-base balance
  • Skeletal health

Background:

  • Dietary habits commonly induce metabolic acidosis, lowering systemic bicarbonate and pH.
  • Metabolic acidosis affects bone by causing mineral dissolution and altering bone cell function, increasing resorption and decreasing formation.
  • Aging impairs renal acid excretion, exacerbating metabolic acidosis and its skeletal consequences.

Purpose of the Study:

  • To investigate the impact of metabolic acidosis on bone mineral loss and fracture potential.
  • To compare the skeletal effects of metabolic acidosis versus respiratory acidosis.

Main Methods:

  • In vitro experiments examining calcium release from bone due to metabolic acidosis.
  • Analysis of bone cell function, including osteoclastic and osteoblastic activity.
  • Consideration of age-related decline in renal function.

Main Results:

  • Metabolic acidosis causes initial physicochemical dissolution of bone mineral.
  • Chronic metabolic acidosis increases osteoclastic bone resorption and decreases osteoblastic bone formation.
  • Bone buffers protons, restoring systemic pH, but at the cost of mineral loss.

Conclusions:

  • A slight, significant metabolic acidosis is hypothesized to increase bone mineral loss.
  • This bone mineral loss is associated with an increased potential for fractures.
  • Understanding these mechanisms is crucial for skeletal health, particularly in aging populations.