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Can Multiple Myeloma Survivors Heal Bone Damage?

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Myeloma Bone Damage (MBD) needs a multidisciplinary approach including anti myeloma treatment and the use of other supportive modalities like BPs, radiotherapy, pain control, vertebro-kyphoplasty, and surgical interventions…

Very keen on understanding bone health.  How do I connect with you? I have just gone into a 2nd relapse with bone damage and need to address the situation immediately. I am based in Mumbai, India

Hi Vanya-
I am sorry to read of your relapse with bone damage. Bone damage aka lytic lesions, are both a MM symptom and MM side effect. While bone damage is the most common symptom/side effect for MM patients and survivors, it can be managed. 
You won’t be able to fully understand bone health in one email but I will outline the basic issues for you below. 
My main point is that conventional MM oncology is limited when treating bone damage for MM patients. According to the study linked below-

“It is well documented that lytic lesions in MM never heal.

I experienced extensive bone damage to my spine and iliac crest when I was first diagnosed. While it takes time and effort, my lesions have healed according to my imaging studies. 

There are several issues for you to consider. 
The 2 different type of bone damage for you to look for are:
  • thinning bones- osteopenia, osteoporosis
  • lytic lesions- plasmacytoma-
The 2 diagnostic tests shown to identify bone damage:
  • blood chemistry- serum calcium
  • imaging studies- imaging studies such as MRI, PET even “hot spots” on x-rays-
The five types or categories of therapies for you to undergo to treat bone damage are:
  • bisphosphonates, denosumab-
  • radiotherapy-
  • vertebroplasty/kyphoplasty
  • surgery
  • non-toxic nutrition, supplementation, lifestyle (green leafy veggies, vitamin D3, magnesium, exercise, WBH, others)
To put the above information into a possible therapy plan for you, 
  • you might begin bisphophonate therapy to reduce your risk of bone fracture,
  • you might then undergo kyphoplasty/vertebroplasty to stabilize your spine,
  • you might undergo radiation therapy specifically to a lesion to kill the MM activity IN the lesion and
  • finally, you would undergo evidence-based, non-toxic therapies such as nutrition, supplementation and lifestyle therapies
in order to increase your bone mineral density aka make your bones healthier and stronger. 
If you would like to learn more about managing your bone damage (as well as your MM) with both conventional and non-conventional therapies please consider the Multiple Myeloma Cancer Coaching Program.
In the meantime, good luck and hang in there, 
David Emerson
  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

Recommended Reading:

Bone Disease in Multiple Myeloma: Pathophysiology and Management

“Myeloma bone disease (MBD) is a devastating complication of multiple myeloma (MM). More than 80% of MM patients suffer from destructive bony lesions, leading to pain, fractures, mobility issues, and neurological deficits.
MBD is not only a main cause of disability and morbidity in MM patients but also increases the cost of management. Bone destruction and lack of bone formation are main factors in the development of MBD. Some novel factors are found to be involved in the pathogenesis of MBD, eg, receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG) system (RANKL/OPG), Wingless (Wnt), dickkopf-1 (Wnt/DKK1) pathway. 
The addition of novel agents in the treatment of MM, use of bisphosphonates and other 
supportive modalities such as 
  • radiotherapy, 
  • vertebroplasty/kyphoplasty, and 
  • surgical interventions
all have significant roles in the treatment of MBD. This review provides an overview on the pathophysiology and management of MBD…
MM. In myeloma bone disease (MBD), lesions could be in the form of 
  • a classic discrete lytic lesion (radiolucent, plasmacytoma), 
  • widespread osteopenia, or
  •  multiple lytic lesions affecting any part of skeleton, preferably spine, skull, and long bones.
The higher the number of lesions, the poorer the prognosis. Increased osteoclastogenesis with suppressed osteoblastic activity is the main mechanism of MBD.

Management of Myeloma Bone Disease

About 80–90% of myeloma patients suffer from osteolytic lesions during the course of disease affecting axial and appendicular skeleton. 
As a result of MBD, patients may suffer from bone pain (70–80%),
  • fractures (50–60%), 
  • hypercalcemia (15%), 
  • spinal cord compression (2–3%), 
  • decreased quality of life, and poor mobility.
Management of MBD needs a multidisciplinary approach including antimyeloma treatment and the use of other supportive modalities like BPs, radiotherapy, pain control, vertebro-kyphoplasty, and surgical interventions…

Systemic antimyeloma treatment

Disease control is a major element in treatment of MBD…

Bisphosphonates (BPs)

Bisphosphonate therapy (BPT) is standard of care in treatment of MBD…
Pamidronate and zoledronic acid are widely used nitrogen-containing BPs. They reduce pain and other skeletal related events (SREs), eg, vertebral fractures, hypercalcemia, and are equally effective in this regard. They are recommended in symptomatic MM, with or without evidence of bone disease...
Patients on long-term BPT should be monitored for adverse effects like renal toxicity and osteonecrosis of jaw (ONJ). Pamidronate-associated renal damage may present as proteinuria or nephrotic syndrome, and zoledronic acid may cause acute tubular necrosis, resulting in renal impairment. Serum creatinine and urinary protein should be monitored regularly in these patients. Another serious adverse outcome with BPT is ONJ with incidence of 1–10% in long-term users of these agents. Incidence is higher with zoledronic acid as compared to pamidronate (10% vs. 4%). ..
  • Pain control
  • Radiotherapy
  • Vertebroplasty/kyphoplasty
  • Surgical intervention
It is well documented that lytic lesions in MM never heal; however, novel therapeutic agents like bortezomib not only have antimyeloma effect but also increases osteoblastic activity resulting in the recovery of lytic lesions.”

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