Overview of Common Bone Conditions
Top Contributors - Jess Bell, Stacy Schiurring, Tarina van der Stockt and Jorge Rodríguez Palomino
Introduction
Bone is a metabolically active connective tissue that constantly remodels and repairs. However, bone tissue can be affected by many different conditions. This page introduces some clinically relevant bone conditions you may see in clinical practice. To learn more about the function and structure of bones, please see: Bone.
Osteoporosis
“Osteoporosis is a disease characterized by low bone density, deterioration of bone tissue, disrupted bone microarchitecture, compromised bone strength, and fracture.”[1]
Osteoporosis leads to fractures that contribute to morbidity and mortality, and is considered a global health issue.[2] Yet despite its significance, it is a silent disease that is underdiagnosed and undertreated.[1][3]
Pathogenesis
In healthy young adults, bone formation is balanced with bone resorption.[1] However, ageing, certain chronic conditions, and changes in hormones and biochemical exposures (e.g. glucocorticoids) can accelerate bone remodelling. This ultimately reduces bone mineral density, with cancellous (trabecular) bone affected more quickly than cortical bone.[1]
Risk Factors
As shown in Table 1, various modifiable and non-modifiable risk factors can affect bone health.[4]
| Modifiable risk factors | Non-modifiable risk factors |
|---|---|
|
|
Types of Osteoporosis

Primary: there are three types of primary osteoporosis: juvenile, postmenopausal (associated with reduced oestrogen) and senile (i.e. > 70 years).[2]
Secondary: osteoporosis that is caused by another condition, such as endocrine disorders, chronic kidney disease, rheumatoid arthritis, chronic inflammatory conditions, loss of menses, neuromuscular disease, gastrointestinal disease, nutritional conditions, glucocorticoids, certain medications, adverse lifestyle factors, malignancy, genetic conditions, etc.[2][5]
Clinical Features
As mentioned, osteoporosis can be a silent disease until a fragility fracture occurs. Some clinical features include back pain, postural changes and loss of height.[5]
Diagnosis of Osteoporosis
The gold standard diagnostic tool for osteoporosis is dual-energy x-ray absorptiometry (DEXA).[3]
Diagnostic Criteria: Osteoporosis is defined as “BMD [bone mineral density] at the hip or lumbar spine that is less than or equal to 2.5 standard deviations below the mean BMD of a young adult reference population (T-score).”[1]
The Fracture Risk Assessment Tool (FRAX®) is a screening tool with country-specific algorithms for estimating an individual’s 10-year risk of osteoporotic fracture. This calculation tool is available here.
If you are interested in learning more about screening and diagnostic recommendations, please see: Diagnostic Assessment Recommendations and Diagnostic Considerations in The clinician's guide to prevention and treatment of osteoporosis[1]
Please watch the following video if you would like a quick re-cap on the pathology, causes, symptoms, diagnosis and treatment of osteoporosis:
Osteoporosis Management
Osteoporosis management includes pharmacological and non-pharmacological treatments.
The cause of osteoporosis (i.e. primary or secondary) must be determined to ensure optimal management. In secondary osteoporosis, the underlying cause must be identified and managed.[2]
Dietary Supplements
To learn more about the link between Calcium and Vitamin D[7] in bone health, please read this optional article.
Pharmacological Treatment
Some medications used to manage osteoporosis include:[1] [7]
- bisphosphonates: inhibit bone resorption by osteoclasts (cells that break down bone) (e.g., alendronate, ibandronate, risedronate, zoledronic acid);[8][1] bisphosphonates rely on calcium to work[7]
- denosumab: inhibits RANK-ligand (RANKL), which is needed for the differentiation of osteoclasts
- strontium ranelate: increases bone formation and decreases bone resorption
- parathyroid hormone analogues (PTHrP): increase bone formation (e.g. teriparatide)
- oestrogen-related therapy
- sclerostin inhibitor (e.g. romosozumab)
Non-pharmacological Treatment
Non-pharmacological treatment focuses on the following areas.
Exercise: it is important to engage in appropriate levels of exercise throughout the lifespan.[3][9] Exercise should include (1) regular weight-bearing exercises (e.g. walking, jogging, tai chi, stair climbing, dancing, tennis), (2) strengthening / resistance exercises (e.g. weight training and resistive exercises, such as yoga, Pilates, etc.) and (3) balance and fall prevention exercises.[1]
Fall prevention: helps to reduce the risk of fracture. Fall prevention interventions focus on identifying and addressing modifiable fall risk factors (e.g. polypharmacy, hypotension, gait or vision issues).[1] Fall prevention exercises include balance exercises and functional training.[10]
Proper nutrition: ensure adequate calcium intake across the lifespan[3] (e.g. low-fat dairy products, fish with bone, fruits, vegetables, and fortified foods[1]) and adequate vitamin D intake (e.g. fortified milk, breakfast cereals, saltwater fish, such as salmon, mackerel and tuna, and cod liver oil; some calcium supplements and many multivitamin tablets contain vitamin D).[1]
Reducing modifiable risk factors: individuals should be encouraged to stop smoking and avoid alcohol misuse.[3]
High-risk groups should also be screened.[1][5]
These interventions are discussed in more detail here: Universal Bone Health Recommendations in The clinician's guide to prevention and treatment of osteoporosis.[1]
Exercise Options
The Royal Osteoporosis Society recommend the “Strong, Steady, Straight” approach to exercise. Table 2 summarises this approach, focusing on information relevant to all individuals with osteoporosis. This table does not include information for individuals with osteoporosis and vertebral fractures or individuals who are frail and have osteoporosis. You can find this information here. Remember that every exercise programme must be tailored to the individual, depending on their presentation, risk profile and abilities.
| Strong: physical activity / exercise that promotes bone strength and prevents fractures | Steady: exercise and physical activity to reduce falls | Straight: modify physical activity and exercise to reduce vertebral fracture risk, improve posture and manage symptoms after vertebral fracture |
|---|---|---|
Recommendations relevant to everyone with osteoporosis:
|
Recommendations for everyone with osteoporosis (particularly those aged 65 years or more or who have balance deficits):
|
Recommendations for all people with osteoporosis:
|
Recommendations for people with osteoporosis but NO vertebral fractures / multiple low-trauma fractures:
|
Recommendations for people with osteoporosis who are already having falls:
|
For further information for individuals with osteoporosis and vertebral fractures, please see: Strong, steady and straight: UK consensus statement on physical activity and exercise for osteoporosis and the Royal Osteoporosis Society: Strong, Steady, Straight: Quick Guide Summary. This guide also includes exercise ideas.
For a general exercise guide for individuals with osteoporosis, please see: Healthy Bones Australia: Exercise and Bone Health.
The following videos also include useful information on exercise for individuals with osteoporosis:
Osteomalacia

Osteomalacia is a "metabolic bone disorder characterized by the inadequate mineralization of bone tissue"[14] that causes softening of bone (known as Rickets in children).
Four mechanisms lead to osteomalacia:[15]
- vitamin D deficiency or resistance: has both extrinsic and intrinsic causes
- calcium deficiency rickets (independent of vitamin D nutritional status)
- phosphate depletion
- inhibition of bone mineralisation caused by various drugs
Most cases are associated with nutritional or lifestyle factors, but there can be genetic, renal, malignant and iatrogenic causes.[16]
Extrinsic causes of vitamin D deficiency include inadequate intake of vitamin D in diet, with vitamin D being the most common nutritional deficiency in both adults and children. Other external factors are decreased exposure to sunlight, wearing sunscreens with high SPF, wearing clothes that fully cover the body, and dark skin pigmentation.[15]
Intrinsic causes of vitamin D deficiency include decreased cutaneous production of vitamin D, which is associated with ageing, and vitamin D malabsorption. Malabsorption can occur due to conditions such as gluten enteropathy, gastrectomy, small intestinal disease, resection, bypass, etc.[15]
Individuals with osteomalacia may present with diffuse aching, bone pain and tenderness. They may have fragility fractures, fatigue, weight loss and proximal muscle weakness and wasting. They may also develop postural deformities and bowing of the tibia and femur. Other clinical manifestations include osteopenia, neuropathies, increased falls and altered gait (e.g. waddling gait).[5][14][15]
The following optional video describes osteomalacia in more detail:
Vertebral Hemangioma

Vertebral hemangiomas are the most common benign tumour of the spine. They are vascular in origin and while they can affect anyone, they are more common in adults aged 40-50 years and in women.[18]
They can appear at all levels of the spine and in all parts of the vertebral body,[19] but the most commonly affected vertebrae are L1, L4, and T12.[20]
Only a minority of cases of vertebral hemangiomas cause symptoms - around 89-99% are asymptomatic.[20] In 55% of symptomatic cases, individuals will experience pain alone. However, in around 45% of symptomatic cases, a vertebral hemangioma can cause neurological deficits.[21]
Avascular Necrosis of the Hip
Avascular necrosis of the femoral head (or osteonecrosis) “is caused by disruption of the blood supply to the proximal femur.”[22]

Avascular necrosis can be non-traumatic or traumatic, and it is most common in physically active people who are aged 20-40 years.[22] Symptoms include decreased hip range of motion and pain, which can radiate to the groin or the medial knee.
Risk factors include trauma, fracture or dislocation, long-term steroid use, alcohol misuse, chemotherapy and immunosuppressant medication, kidney disease with dialysis and sickle cell anaemia.[5][23]
Avascular necrosis can occur in other parts of the body. It usually affects the epiphysis of long bones at weight-bearing joints. Common sites aside from the femoral head are the knee, talus and humeral head.[24] Avascular necrosis can lead to subchondral collapse, so early detection and appropriate management are essential.[24]
If you are interested in learning more, the following video provides a detailed discussion of the pathophysiology and stages of avascular necrosis of the hip:
Osteomyelitis
“Osteomyelitis is an inflammatory condition of bone secondary to an infectious process.”[26]

It is caused by infection from pyogenic organisms (e.g. bacteria, fungi, mycobacteria), most commonly Staphylococcus aureus, and it can be an acute or chronic condition.[27]
Causes include:[5]
- open fracture
- haematogenous spread (bacteraemia, sepsis): "a bone infection that has been seeded through the bloodstream"[28]
- open wound or soft tissue infection[5]
Risk factors include diabetes, smoking, peripheral vascular disease, poorly healing wounds, a history of recent trauma, a history of implanted orthopaedic hardware, haemodialysis, immunosuppression, sickle cell disease, intravenous drug use and older age.[5][26]
Individuals with osteomyelitis can present with symptoms include pain and / or tenderness in the infected area, swelling and warmth in the infected area, fever and purulent drainage ("pus") from infected area.[5][26]
Please watch the following video for a detailed discussion of the causes, symptoms, diagnosis and management of osteomyelitis:
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 LeBoff MS, Greenspan SL, Insogna KL, Lewiecki EM, Saag KG, Singer AJ, Siris ES. The clinician's guide to prevention and treatment of osteoporosis. Osteoporos Int. 2022 Oct;33(10):2049-2102. Epub 2022 Apr 28. Erratum in: Osteoporos Int. 2022 Oct;33(10):2243.
- ↑ 2.0 2.1 2.2 2.3 Ebeling PR, Nguyen HH, Aleksova J, Vincent AJ, Wong P, Milat F. Secondary osteoporosis. Endocr Rev. 2022 Mar 9;43(2):240-313.
- ↑ 3.0 3.1 3.2 3.3 3.4 Rinonapoli G, Ruggiero C, Meccariello L, Bisaccia M, Ceccarini P, Caraffa A. Osteoporosis in men: a review of an underestimated bone condition. Int J Mol Sci. 2021 Feb 20;22(4):2105.
- ↑ 4.0 4.1 Hereford T, Kellish A, Balch Samora J, Reid Nichols L, Understanding the importance of peak bone mass. Journal of the Pediatric Orthopaedic Society of North America. 2024:7.
- ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 Cunningham S. Clinical Overview of Bone Health and Dysfunction Course. Physiopedia, 2024.
- ↑ Osmosis from Elsevier. Osteoporosis - causes, symptoms, diagnosis, treatment, pathology. Available from: http://www.youtube.com/watch?v=6fMkX1J9gWw [last accessed 20/08/2024]
- ↑ 7.0 7.1 7.2 Buxton S. Osteoporosis Course. Plus, 2021.
- ↑ Ganesan K, Goyal A, Roane D. Bisphosphonate. [Updated 2023 Jul 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470248/
- ↑ Sipilä S, Törmäkangas T, Sillanpää E, Aukee P, Kujala UM, Kovanen V, Laakkonen EK. Muscle and bone mass in middle-aged women: role of menopausal status and physical activity. J Cachexia Sarcopenia Muscle. 2020 Jun;11(3):698-709.
- ↑ 10.0 10.1 10.2 Royal Australian College of General Practitioners and Healthy Bones Australia. Osteoporosis management and fracture prevention in postmenopausal women and men over 50 years of age, 2024.
- ↑ Brooke-Wavell K, Skelton DA, Barker KL, Clark EM, De Biase S, Arnold S, et al. Strong, steady and straight: UK consensus statement on physical activity and exercise for osteoporosis. Br J Sports Med. 2022 May 16;56(15):837–46.
- ↑ Royal Osteoporosis Society. Exercises to promote bone and muscle strength. Available from: http://www.youtube.com/watch?v=dHPklstvrKg [last accessed 20/08/2024]
- ↑ Royal Osteoporosis Society. How to exercise safely for your bones. Available from: http://www.youtube.com/watch?v=MiGP3nuReL8 [last accessed 20/08/2024]
- ↑ 14.0 14.1 Zimmerman L, McKeon B. Osteomalacia. [Updated 2023 Nov 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551616/
- ↑ 15.0 15.1 15.2 15.3 Minisola S, Colangelo L, Pepe J, Diacinti D, Cipriani C, Rao SD. Osteomalacia and vitamin D status: a clinical update 2020. JBMR Plus. 2020 Dec 21;5(1):e10447.
- ↑ Horvath C. Osteomalacia. In: Igaz P editor. Practical clinical endocrinology. Springer: Cham, 2024.
- ↑ 5MinuteSchool. Osteomalacia Explained In 2 Minutes! Vitamin D | Calcidiol | Calcitriol | Diagnosis and Treatment. Available from: http://www.youtube.com/watch?v=5M4E1lS8DE4 [last accessed 20/08/2024]
- ↑ Mariniello G, Pagano S, Meglio V, Barbato M, Russo C, Pontillo G, et al. Multiple vertebral hemangiomas of the thoracic spine with atypical radiological features and aggressive behavior causing myelopathy: A case report. Interdisciplinary Neurosurgery. 2021:23;100954.
- ↑ Slon V, Stein D, Cohen H, Sella-Tunis T, May H, Hershkovitz I. Vertebral hemangiomas: their demographical characteristics, location along the spine and position within the vertebral body. Eur Spine J. 2015 Oct;24(10):2189-95.
- ↑ 20.0 20.1 Abul-Kasim K, Persson E, Levinsson A, Strömbeck A, Selariu E, Ohlin A. Vertebral hemangiomas: prevalence, new classification and natural history. magnetic resonance imaging-based retrospective longitudinal study. Neuroradiol J. 2023 Feb;36(1):23-30.
- ↑ Jiang L, Liu XG, Yuan HS, Yang SM, Li J, Wei F, et al. Diagnosis and treatment of vertebral hemangiomas with neurologic deficit: a report of 29 cases and literature review. Spine J. 2014 Jun 1;14(6):944-54.
- ↑ 22.0 22.1 Konarski W, Poboży T, Śliwczyński A, Kotela I, Krakowiak J, Hordowicz M, Kotela A. Avascular necrosis of femoral head-overview and current state of the art. Int J Environ Res Public Health. 2022 Jun 15;19(12):7348.
- ↑ Lamb JN, Holton C, O'Connor P, Giannoudis PV. Avascular necrosis of the hip. BMJ. 2019 May 30;365:l2178.
- ↑ 24.0 24.1 Matthews AH, Davis DD, Fish MJ, et al. Avascular Necrosis. [Updated 2023 Aug 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537007/
- ↑ Armando Hasudungan. Osteonecrosis of the Hip (femoral head) - Avascular Necrosis. Available from: http://www.youtube.com/watch?v=wiybWLacp6A [last accessed 20/08/2024]
- ↑ 26.0 26.1 26.2 Bury DC, Rogers TS, Dickman MM. Osteomyelitis: diagnosis and treatment. Am Fam Physician. 2021 Oct 1;104(4):395-402.
- ↑ Momodu II, Savaliya V. Osteomyelitis. [Updated 2023 May 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532250/
- ↑ Fritz JM, McDonald JR. Osteomyelitis: approach to diagnosis and treatment. Phys Sportsmed. 2008 Dec;36(1):nihpa116823. .
- ↑ studymedical. Osteomyelitis - Causes, Symptoms, Diagnosis & Treatment (Pathology). Available from: http://www.youtube.com/watch?v=1nZfX1ZqTEM [last accessed 20/08/2024]