• Adequate calcium and vitamin D is important for peak bone mass attainments and osteoporosis prevention in adults and postmenopausal women

Smoking

• Smoking increases osteoporotic fracture risk

Hip Protectors

• Reduce, absorb and/or shunt the impact on the hip during a fall to prevent a fracture occurring. They range from a hard shell to a dense foam padding which are worn in an undergarment to cover the trochanteric area of the hip.

Ref : https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Rheumatology/221115_MOS_CPG-Management_of_Osteoporosis-ed3_PREVIEW.pdf

Advantages

• Plaster can be tucked or pleated. Plaster requires less tension for application. Gloves are not required.

• Plaster absorbs fluids, including pus, blood, and sweat.

• If a cast saw is not available, the plaster cast may be removed by soaking and unrolling or using simple hand-cutting instruments.

  
  

Disadvantages

• Compared with fibreglass, plaster may be difficult to store in high humidity and is more difficult to keep clean.

• Plaster casts are heavier than fibreglass, exhibit more breakdown for short-leg casts, and are judged to be more restrictive and less comfortable

However in a country like India where the cost considerations come in to play POP still remains the choice of material in casting

Ref : https://pmc.ncbi.nlm.nih.gov/articles/PMC3880430/

A research had hypothesized that Proton Pump Inhibitor (PPI) are bone-specific phosphatase (PHOSPHO1) inhibitors but not for Histamine-2 Receptor Antagonist (H2RA) in animal studies. (mentioned below as 1)

Other research (mentioned below as 2) shown that PPI does not affect bone mineral density.

Vetebral and non-vetebral fracture risk (mentioned below as 3) was increased upon long term PPI usage. Possible mechanisms are visual impairment, vitamin B12 deficiency or their neurologic associated consequences such as numbness of the feet.

Reference:

1. https://link.springer.com/article/10.1007/s00223-021-00882-9#Sec1

2. https://www.gastrojournal.org/article/S0016-5085(09)02030-7/fulltext

3. https://pmc.ncbi.nlm.nih.gov/articles/PMC9504265/#sec6-ijms-23-10733

-> https://medlineplus.gov/druginfo/meds/a601011.html

-> https://www.ncbi.nlm.nih.gov/books/NBK526073/#article-17348.s7

-> https://www.mims.com/singapore/drug/info/apo-alendronate?type=full

1. Gonadal Hormone effect (Post-menopause + Smoking)

   • GH is in the post-menopause stage for a year now -> Low estrogen levels

   • Smoking further reduces free Estradiol levels

   • Low estrogen -> High IL-6 levels -> Stimulates Osteoclast activity -> Higher bone resorption.

   • GH's bone is broken down faster than it is built.

2. Calciotropic Hormone effect (Vitamin D & Calcium)

   • Smoking decreases 25-OH-D and 1,25-(OH)2-D [active Vitamin D].

   • Reduces intestinal Calcium absorption, worsened by GH's vegetarian diet (likely consisting of low Calcium intake).

   • Low Calcium -> Activates secondary Parathyroid hormone -> More bone resorption to maintain serum Calcium.

   • Bone mineralization becomes impaired.

3. Adrenocortical Hormone effect (Cortisol)

   • Smoking raises Cortisol levels.

   • Cortisol suppresses Osteoblasts -> Reduces bone formation.

   • Less bone building + More bone breakdown

   • This reduces her skeleton's ability to repair microdamage -> Chronic fractures (e.g., Height loss, Back pain)

4. Frailty & fall risk

   • Smoking contributes to muscle wasting and frailty.

   • GH is already underweight (Low BMI).

   • Increased risk of falls → Increases fracture incidence, like her recent forearm fracture.

This can happen because of multiple reasons:

1. Weak muscles & poor posture

2. Changes in the bone structure

   • Osteoporosis

   • Growth problems

3. Degeneration

4. Others

   • Trauma

   • Congenital (Birth) deformities

   • Conditions affecting connective tissues

     • Ehlers-Danlos syndrome

     • Rheumatoid Arthritis

     • Sarcomas

There are multiple different types of Kyphosis:

1. Postural Kyphosis: Most common type, which happens during your teen years, and affects girls more than boys. This is due to slouching or poor posture that stretches the ligaments and muscles holding your vertebrae in place -> Pulls the vertebrae out of their normal position -> Causes a rounded shape in the spine.

2. Scheuermann's Disease: When the vertebrae has a different shape than normal. The wedge-shaped bones curve forward, making the spine look rounded.

3. Congenital Kyphosis: Kyphosis present at birth. When the spine doesn't develop completely when the baby is in the uterus.

4. Cervical Kyphosis (Military Neck): This type occurs when the cervical spine (the part of the spine at the bottom of the head to the upper back) curves toward the front instead of the natural curve to the back.

5. Hyperkyphosis: A severe forward curvature of the spine, which is more than 50 degrees. This type is more common after the age of 40.

Treatment/Management:

1. Physical therapy

2. Medications (To ease pain and increase ROM)

3. Bracing (To control the progress of the spinal curve while a child is still growing)

   • Applies corrective force to the spine, helping to hold the spine in a more upright and aligned position -> Improves overall posture and function.

4. Spinal Fusion surgery

   • A surgery where the surgeons will join 2 or more vertebrae (spinal bones) together so they heal into a single, solid bone.

   • By attaching metal rods, screws, and wires to the spine, that will hold the bones in a corrected position.

   • Over time, these bones grow together and fuse the vertebrae into one solid piece.

Ref : https://www.radiologyinfo.org/en/info/dexa

In a sample of Chinese adults aged 40–75, those in the highest diet of fruit + vegetable (FV) intake had higher bone mineral density (BMD) at multiple skeletal sites (whole body, lumbar spine, total hip, femur neck) compared to those who ate less vegetables and fruits

FUN FACT :When they looked separately, fruit intake showed somewhat stronger or more consistent beneficial associations with BMD and osteoporosis risk than total vegetables or vegetable subgroups.

Why Vegetables & Fruits Might Help Bone Health

1. Minerals and Alkaline Load

• Vegetables and fruits are rich in minerals such as potassium and magnesium. These contribute to an alkaline environment (less acid load) which may reduce bone resorption (i.e. less leaching of calcium from bone). 

• In contrast, diets high in acid-producing foods (e.g. large quantities of meat, processed foods) may lead to low-level chronic acidosis, prompting bone to release alkaline minerals (calcium, magnesium) to buffer the acid, which could worsen bone loss.

2. Vitamins, Antioxidants & Phytochemicals

• Fruits and vegetables supply vitamins (C, K, E), B-complex vitamins, carotenoids, and other antioxidants or bioactive compounds. These may help by neutralizing oxidative stress, reducing inflammation, and supporting collagen formation and bone remodeling. 

• Some of the phytochemicals may inhibit osteoclast activity (cells that break down bone) and/or stimulate osteoblast activity (cells that build bone).

3. Inflammation & Oxidative Stress Reduction

• Chronic inflammation and oxidative stress are implicated in bone loss. Because vegetables and fruits are anti-inflammatory and antioxidant, they may help mitigate these processes, thus protecting bone. 

4. Synergy with Other Nutrients

• Vegetables and fruits may enhance absorption of nutrients beneficial for bone (e.g. vitamin C helps with collagen cross-linking, which is part of bone matrix).

• They may also improve gut health (microbiome) which can affect mineral absorption.

• The review suggests that vegetarian diets (particularly strict vegan diets) may be associated with a modestly increased risk of lower bone mass / osteoporosis / fractures, primarily when key nutrients are not adequately provided.

• But it also highlights that risk is not uniform: lacto-ovo vegetarians may fare better, and plant diets that are carefully planned (with fortification / supplementation) can mitigate much of the risk.

  *Lacto → includes dairy products (milk, cheese, yogurt, butter).

  Ovo → includes eggs.

• The evidence is not definitive, and many studies have methodological limitations, so the relationship is best viewed as potential risk if not well managed, rather than a guarantee of harm.

Calcium

• Daily Requirement: 700 mg for adults.

• Sources:

  
  

  • Dairy products (milk, cheese, yogurt)

  • Green leafy vegetables (broccoli, cabbage, okra)

  • Soya beans and tofu

  • Fortified plant-based drinks (e.g., soya drink)

  • Nuts and seeds

  • Fortified bread and cereals

  • Fish with edible bones (e.g., sardines, pilchards)

  
  

• Note: Spinach contains calcium but also oxalates, which reduce calcium absorption.

  
  

  Vitamin D

  
  

  • Daily Requirement: 10 micrograms (400 IU) for adults.

  • Sources:

    
    

    • Oily fish (salmon, sardines, mackerel)

    • Egg yolks

    • Fortified foods (e.g., some fat spreads, breakfast cereals)

    
    

  • Sunlight: The body produces vitamin D from sunlight exposure.

  
  

( breakdown bone)

Osteoblast - Bone formation

2. Serum Ca2+ levels

   controlled by Parathyroid hormone

   ( PTH), calcitonin, calcitriol ( Vitamin D)

   
   

   Low Ca = PTH released by PTH gland

   -> Increases bon resorption -> releases calcium into the blood

   
   

   High Ca= Thyroid gland releases Calcitonin -> Promotes bone formation and decrease bone resorption

   
   

   Vitamin D = Promotes Ca absorption in the gut -> Increase serum Ca -> Promotes Bone formation

*Osteomalacia bones that are soft due to insufficient mineralization (bone softening) vs Osteoporosis which is low bone density and weakened, porous bones (bone loss), which increases fracture risk

Vitamin K2 → directs calcium into bones and teeth (activates osteocalcin) and prevents calcium from depositing in arteries/soft tissues.

References:

https://www.mdpi.com/2673-396X/6/2/19?utm (MDPI) Cholesterol and Bone Resorption

https://pmc.ncbi.nlm.nih.gov/articles/PMC4617053/ (NCBI) High Cholesterol Deteriorates Bone Health

• Provide empathetic counseling and active listening.

• Educate patient on the link between smoking, nicotine withdrawal, and anxiety.

• Use motivational interviewing to encourage behavior change.

• Teach simple stress-management techniques (breathing, mindfulness, lifestyle tips).

• Offer smoking cessation therapy (nicotine replacement, medications, behavioral support).

• Help set realistic quit goals and monitor progress.

• Refer to psychologists or doctors if anxiety is severe.

- High caffeine intake (>330 mg caffeine/day) has been associated with increased risk of fragility fracture.

*330mg is equivalent to 2 medium Zus coffee cup ( 16 oz = 180 mg )

- However, the effect of caffeine appears to be mitigated by increasing calcium intake (40 mg calcium for every 177.5 ml cup of coffee).

- Patients that regularly consume caffeinated drinks should be advised to increase their calcium intake accordingly.

-Vertebral and hip fractures are reduced by 50% in women wih or without prior fracture.

-Wrist fracture is reduced by 50% in patients with prior vertebral fracture.

-Fracture reduction is seen after one year of treatment.

-Pooled analysis found an overall reduction in risk of hip fracture of 45% to 55% in patients receiving alendronate therapy.

DOSE: Alendronate 70 mg weekly has similar efficacy to alendronate 10 mg daily in the treatment of postmenopausal osteoporosis.

-Continuous use of alendronate, for up to 10 years, if clinically indicated, produces a sustained increase in BMD and a 55% significant reduction in spine fracture with a good safety profile.

*stress type fractures originating in the lateral shaft of the femur

The risk of AFFs increases with duration of bisphosphonate use.

STATISTIC: The age-adjusted incidence rate of AFFs has been estimated to be 1.78 per 100,000 person- years in patients on bisphosphonate use <2 years and the incident rate increases to 113.1 per 100,000 person-years with >8 years’ duration.

-Though it has been shown that Asians on bisphosphonate therapy may have an increased risk of AFFs compared to Caucasians

Overall, the benefit of reducing further osteoporotic fractures with bisphosphonate treatment is much greater than the small absolute risk of AFFs.

- number shows the amount of bone you have compared with a young adult of the same gender with peak bone mass

- -1.1 and -2.4 is classified as osteopenia (low bone mass)

- score of -2.5 and below is defined as osteoporosis.

- GR has -2.6 hence- osteoporosis

- It also has Z score value when compared with other people in your age group and of the same size and gender

- Other lab value are all normal

Inhibition of the secretion of RANKL and promotes the secretion of osteoclast-inhibiting factors such as growth hormone, GLP-1, and osteoprotegerin (OPG), thereby inhibiting bone resorption, estrogen promotes osteogenic differentiation of MSCs and maintains the number of osteoblasts.

Osteoporosis pathogenesis and treatment: existing and emerging avenues | Cellular & Molecular Biology Letters | Full Text

Efficacy of tibolone

For postmenopausal osteoporotic women aged 60 – 85 yrs-old. 1.25mg significantly increased lumbar and hip BMD, and greater absolute reduction among women with prior vertebral fracture.

Safety: not for older women due to increased risk of stroke. (women who have HTN, smoke, diabetes, and atrial fibrillation à risk of stroke)

Synthetic non-steroidal molecules that bind to estrogen receptors throughout the body. They act as an estrogen agonist or antagonist depending on the target organ.

Efficacy: RLX increase BMD by 2-3% at the lumbar spine and femoral neck and reduced incidence of vertebral fracture by 40-50% after 3 years. There were also 22% decrease incidence of major osteoporotic fractures in women.

Safety: Hot flushes, leg cramps, and peripheral oedema.

·       Overall risk-benefits > positive

·       Not for eGFR < 30ml/min (chronic Kidney stage 4-5)

·       Zoledronic acid is CI in patient with eGFR < 35ml/min

·       Review the efficacy after 3-5 years of treatment to decide whether continue.

·       Potent inhibitors of bone resorption.

a.      Alendronate at 10 mg daily for 3 years.

b.      Risedronate 5 mg daily for 3 years.

c.       Ibandronate 150mg/month

d.      Zoledronic acid à IV infusion 5 mg 15 mins once yearly. May cause flu like symptoms which last for 1 – 7 days. (pre-treat with PCM/Ibuprofen and increase infusion time)

Common side effects: gastrointestinal, nausea.

For patient with gastrointestinal disease use IV ZA or denosumab.

Recommended for up to 24 months.

For not responsive to other anti-osteoporosis therapy.

Subcutaneously, 20mcg daily for 21 months.

Benefits of anabolic therapy wear off within one year of discontinuation. Recommendation to initiate anti-resorptive therapies, when stopping anabolic therapy. To maintain bone density gains.

Safety: dizziness, leg cramps, and hypercalcemia. Check serum calcium.

CI for patients with open epiphyses. Bone disease other than osteoporosis or pre-existing hypercalcaemia.

Effective anti-resorptive therapy.

‘Drug holiday’ not recommended. Rebound in bone turnover may occur.

Treatment reassessment done after 5-10 yrs, severe patient continue.

Human monoclonal antibody (IgG) that inhibits the formation, function, and survival of osteoclast by inhibiting RANK (receptor activator of nuclear factor kappa-B) ligand, thus reducing bone resorption.

6 monthly denosumab 60 mg over 3 years

Low incidence for AE: serious infections, cellulitis, hypocalcaemia, eczema, and malignancy.

Anabolic agent. Preferred for Low CV risk patient.

12 months followed by anti-resorptive therapy (denosumab or bisphosphonate)

Humanized monoclonal antibody à binds to sclerostin. Change in BTM point to a dual effect on bone remodeling, with a transient increase in formation markers and reduction in resorption, resulting in an increase in bone formation and BMD.

Dose dependent increase in BMD.

AE: major adverse cardiac events (MACE)

Vit D >800 IU/day, Ca2+ (1200mg/day elemental Ca2+)

2.      Activated Vitamin D

Calcitriol (0.25mcg bd) and alfacalcidol (1 mcg od)

1.

Direct Effects on Bone Cells

• Osteoblast inhibition:
  

  • Corticosteroids suppress osteoblast proliferation and differentiation.

  • Increase apoptosis of osteoblasts and osteocytes.

  • Result → ↓ bone formation.

  
  

• Osteoclast stimulation:
  

  • Initially increase osteoclast survival and activity via upregulation of RANKL and downregulation of osteoprotegerin (OPG).

  • Result → ↑ bone resorption (especially early in therapy).

  
  

2.

Effects on Calcium and Mineral Metabolism

• Intestinal absorption:
  

  • Corticosteroids reduce calcium absorption from the gut (by antagonizing vitamin D action).

  
  

• Renal excretion:
  

  • Increase urinary calcium excretion.

  
  

• Result → secondary hyperparathyroidism → enhances osteoclast activity and bone resorption.

3.

Hormonal Alterations

• Sex hormones:
  

  • Corticosteroids reduce gonadotropin secretion → hypogonadism → ↓ estrogen/testosterone → accelerates bone loss.

    
    

• Growth factors:
  

  • Decrease IGF-1 production → further impairs osteoblast activity.

  
  

4.

Muscle and Mechanical Factors

• Myopathy:
  

  • Corticosteroid-induced muscle weakness decreases mechanical loading on bone → disuse osteoporosis.

5.

Net Effect

• Early phase: Rapid bone resorption due to enhanced osteoclast activity.

• Chronic phase: Suppressed bone formation due to osteoblast inhibition + decreased sex hormones.

• Overall result: Reduced bone mineral density (BMD), deterioration of bone microarchitecture, and increased fracture risk (vertebral > non-vertebral fractures).

1.

Estrogen Deficiency After Menopause

• Ovarian estrogen production drops sharply after menopause.

• Estrogen normally protects bone by balancing osteoclast activity (resorption) and osteoblast activity (formation).

2.

Effects on Bone Remodeling

• ↑ Osteoclast activity:
  

  • Estrogen deficiency increases RANKL expression (from osteoblasts and T-cells) and decreases osteoprotegerin (OPG).

  • This shifts the balance toward osteoclastogenesis → more bone resorption.

  
  

• ↓ Osteoblast survival:
  

  • Estrogen normally promotes osteoblast lifespan and function. Its loss increases osteoblast apoptosis → reduced bone formation.

    
    

• ↑ Osteocyte apoptosis:
  

  • Weakens bone microarchitecture and reduces mechanosensing ability of bone tissue.

3.

Calcium and Hormonal Factors

• Secondary hyperparathyroidism may occur due to reduced calcium absorption (aging + low estrogen → ↓ calcitriol synthesis).

• ↑ PTH further enhances osteoclast activity and bone loss.

4.

Inflammatory Cytokines

• Estrogen deficiency increases IL-1, IL-6, TNF-α from immune cells.

• These cytokines further stimulate osteoclast differentiation and survival.

5.

Net Effect

• Accelerated bone turnover, with bone resorption >> bone formation.

• Rapid loss of trabecular bone (vertebrae, wrist) in the early postmenopausal years.

• Progressive loss of cortical bone (hip, long bones) over time.

hypercholesterolaemia can promote the development of male OP by excessively promoting both osteoclast activity and osteoblast activity, which excessively enhances the bone transformation rate in men.

hypercholesterolaemia damaged the bone microstructure, thus, increasing the risk of osteopenia or OP and reducing bone strength, resulting in a higher risk of fracture.

In vitro studies have shown that cholesterol enhances osteoclast differentiation and osteoclast activity.

In vitro, cholesterol directly upregulated the functions of osteoblasts.

higher risk of high-turnover osteoporosis and future fractures in men.

https://www.ncbi.nlm.nih.gov/books/NBK499878/