[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Bones, joints and soft tissue](https://durgical.com/en/general-pathology/areas/bone-soft/) › Bone in hyperparathyroidism and renal osteodystrophy

# Bone in hyperparathyroidism and renal osteodystrophy

- Lesion

Too much parathyroid hormone makes osteoclasts tunnel through bone. Kidney failure adds phosphate retention, low vitamin D and several bone patterns.

Updated Nov 12, 2026

## Key points

- PTH stimulates osteoclasts indirectly, through osteoblast RANKL.
- Osteitis fibrosa cystica: subperiosteal resorption (radial side of middle phalanges), dissecting osteitis, peritrabecular fibrosis, cysts and brown tumours.
- Brown tumour = reactive mass of osteoclast-type giant cells, fibrous tissue and old haemorrhage (haemosiderin); it regresses when PTH is corrected.
- Most primary hyperparathyroidism is now found early on routine calcium tests, before overt bone disease.
- CKD: phosphate retention, low calcitriol, high FGF23 and loss of klotho drive secondary hyperparathyroidism.
- Adynamic bone disease: low turnover from over-suppression of PTH, diabetes, aluminium; also β2-microglobulin amyloid in long-term dialysis.

On this page

- The basics Key points
- What it is
- Structure
- Step by step
- Memory aid
- Elsewhere in DurgiPedia

- Clinical Bone patterns in chronic kidney disease
- Clinical notes
- In the lab

- Study Test yourself

- Connections Connections

## What it is

Parathyroid hormone acts on osteoblasts, which signal osteoclasts through RANKL. When PTH is high for a long time, as in primary hyperparathyroidism or the secondary hyperparathyroidism of chronic kidney disease, resorption accelerates. Mild disease causes only osteopenia; long-standing severe disease produces osteitis fibrosa cystica, with dissecting resorption, marrow fibrosis, cysts and brown tumours. Renal osteodystrophy is the full set of skeletal changes of chronic kidney disease: high-turnover bone from secondary hyperparathyroidism, low-turnover adynamic bone, osteomalacia and mixed patterns, together called CKD–mineral and bone disorder.

## Structure

- Dissecting osteitis: osteoclasts tunnel along the centre of trabeculae, which look like railroad tracks.
- The marrow next to trabeculae is replaced by loose fibrovascular tissue (peritrabecular fibrosis).
- Brown tumour: multinucleated giant cells in a vascular, fibroblastic stroma with haemosiderin and red cells; gross brown colour.
- Cortical thinning and subperiosteal erosion on X-ray; 'salt and pepper' skull and loss of the lamina dura around teeth.
- Adynamic bone: thin trabeculae with few osteoblasts and osteoclasts and no osteoid excess.

## Step by step

- Primary: a parathyroid adenoma, hyperplasia or carcinoma secretes PTH autonomously.
- Secondary (kidney failure): falling nephron mass retains phosphate and lowers calcitriol; FGF23 rises and klotho falls.
- Low calcium and calcitriol and high phosphate push the parathyroids to hypertrophy and secrete more PTH.
- High PTH raises osteoblast RANKL, osteoclasts multiply and resorption outpaces formation.
- Bone is replaced by fibrous tissue, cysts and haemorrhagic giant-cell masses: osteitis fibrosa cystica.
- In kidney failure, acidosis, low vitamin D and treatment effects add osteomalacia or low-turnover adynamic bone.

## Bone patterns in chronic kidney disease

| Pattern | Turnover | Mechanism | Biopsy |
| --- | --- | --- | --- |
| [Osteitis fibrosa (hyperparathyroid bone)](https://durgical.com/en/conditions/ckd-mineral-and-bone-disorder/) | High | Secondary hyperparathyroidism | Many osteoclasts, tunnelling, marrow fibrosis |
| Adynamic bone disease | Low | Over-suppressed PTH, diabetes, aluminium | Few cells, little osteoid |
| [Osteomalacia](https://durgical.com/en/conditions/rickets-and-osteomalacia/) | Low | Low calcitriol, acidosis, aluminium in the past | Wide unmineralized osteoid seams |
| Mixed uraemic osteodystrophy | Variable | Several mechanisms together | Features of high turnover plus defective mineralization |

## Clinical notes

- Classic phrase for symptomatic primary hyperparathyroidism: bones, stones, abdominal groans and psychic moans.
- Kidney failure patients have bone pain and fractures, and the same mineral disorder calcifies vessels and soft tissue (calciphylaxis).
- A giant-cell lesion of the jaw or long bone in a patient with high calcium should prompt measurement of PTH before surgery.

## In the lab

- Primary: high calcium, low or normal phosphate, high PTH.
- Secondary (CKD): low or normal calcium, high phosphate, high PTH, high FGF23; alkaline phosphatase rises with high turnover.

## Memory aid

Brown tumours are a bruise inside the bone: giant cells, blood and iron, healed by cooling down the parathyroid.

## Test yourself

Think of the answer, then tap the question to see it.

## How does PTH activate osteoclasts?

Indirectly: it acts on osteoblasts, which express RANKL and drive osteoclast formation and activity.

## What is a brown tumour?

A reactive mass of osteoclast-type giant cells, fibrous tissue and old haemorrhage in hyperparathyroidism.

## Why does chronic kidney disease cause secondary hyperparathyroidism?

Phosphate retention, low calcitriol, high FGF23 and low calcium stimulate the parathyroid glands.

## What is adynamic bone disease?

A low-turnover bone disease in CKD with few bone cells, often from over-suppression of PTH.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/general-pathology/bone-in-hyperparathyroidism-and-renal-osteodystrophy/)

[More Pathology questions →](https://durgical.com/en/practice/?f=pathology)

## Elsewhere in DurgiPedia

- [Calcium regulation: PTH, vitamin D and calcitonin](https://durgical.com/en/physiology/calcium-regulation-pth-vitamin-d-and-calcitonin/)
- [Phosphate and FGF-23](https://durgical.com/en/physiology/phosphate-and-fgf-23/)
- [Renal handling of calcium, phosphate and magnesium](https://durgical.com/en/physiology/renal-handling-of-calcium-phosphate-and-magnesium/)

## Connections

## Related 5

- [Primary hyperparathyroidism](https://durgical.com/en/general-pathology/primary-hyperparathyroidism/)
- [Secondary hyperparathyroidism and hypoparathyroidism](https://durgical.com/en/general-pathology/secondary-hyperparathyroidism-and-hypoparathyroidism/)
- [Chronic kidney disease and uremia](https://durgical.com/en/general-pathology/chronic-kidney-disease-and-uremia/)
- [Metabolic bone disease compared](https://durgical.com/en/general-pathology/metabolic-bone-disease-compared/)
- [Giant cell tumour of bone](https://durgical.com/en/general-pathology/giant-cell-tumour-of-bone/)

## Related conditions 5

- [Primary hyperparathyroidism](https://durgical.com/en/conditions/primary-hyperparathyroidism/)
- [CKD-mineral and bone disorder (renal osteodystrophy)](https://durgical.com/en/conditions/ckd-mineral-and-bone-disorder/)
- [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/)
- [Hypercalcaemia](https://durgical.com/en/conditions/hypercalcaemia/)
- [Calciphylaxis (calcific uremic arteriolopathy)](https://durgical.com/en/conditions/calciphylaxis/)

[← All of general pathology](https://durgical.com/en/general-pathology/)

Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Hyperparathyroidism: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/001215.htm) (MedlinePlus, US National Library of Medicine, 2025); [Primary Hyperparathyroidism](https://www.ncbi.nlm.nih.gov/books/NBK441895/) (StatPearls (NCBI Bookshelf), 2025); [Chronic Kidney Disease](https://www.ncbi.nlm.nih.gov/books/NBK535404/) (StatPearls (NCBI Bookshelf), 2025).

## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake

Representative model, for educational purposes only.

---
Source: https://durgical.com/en/general-pathology/bone-in-hyperparathyroidism-and-renal-osteodystrophy/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/bone-in-hyperparathyroidism-and-renal-osteodystrophy/