Butterfly Melita Yvonne Dyason

DIAGNOSTIC HOMOEOPATHIC DOCTOR

Licence No.KZN00041D    Practice No. 0805033   Reg No: A01252

From illness to wellness

Osteoporosis

Decrease in absolute bone mass leading to skeletal weakness & fractures after minimal trauma.


Bone

There are two basic histological types of bone:

Compact Bone

Compact bone appears solid and forms the outer wall of bones.

Cancellous [or spongy] bone

Cancellous [or spongy] bone is a lattice network of trabeculae forming a complex system of interconnecting spaces. Cancellous bone forms the inner portion of bone walls and epiphyses [the ends of long bones.]

The periosteum is the connective tissue layer covering the eternal surfaces of bone except where the epiphyses are covered by articular cartilage and sesamoid bones [bones formed within tendons e.g. patella] which do not have periosteum.

The periosteum has two layers of :

  1. Outer fibrous periosteum, which contains Sharpey's fibres, Dense bundles of collagen fibres that penetrate the compact bone and firmly anchor the periosteum to the bone, and the
  2. Inner osteogenic layer which plays a role in bone nutrition, growth and repair of the bone. The osteogenic layer contains osteoblasts which become active in times of bone growth.

Blood vessels, nerves and lymphatics pass through the periosteum on their way into the bone. The endosteum, which lines the haversian cnals and bone marrow cavities, is also capable of producing new bone.

Bone itself is composed of a tough organic matrix that is strengthened by calcium salt deposits. The specialized structure of collage fibres and calcium salts similar to reinforced concrete and provides bone with the tensile and compressional strengths needed for it to carry out its functions effectively. the organic matrix is made of mostly collagen fibres, which provide bone with it tensile strength, and a ground substance composed of extracellular fluid and proteoglycans, such as chrondroitin sulphate and hyaluronic acid, thought to control the deposition of calcium salts.

Osteoporosis

Osteoporosis is a progressive bone disease that is characterized by a decrease in bone mass and density which can lead to an increased risk of fracture. In osteoporosis, the bone mineral density [BMD] is reduced, bone microarchitecture deteriorates, and the amount and variety of proteins in bone are altered.

Causes

Risk Factors

Female sex, nulliparity, early menopause, race [common in whites and orientals than in blacks], thin body, sedentary life-style and family history.

The disease may be classified as:

Primary type 1 Osteoporosis.

The form of osteoporosis most common between the ages of 51-75 and more common in women - menopausal or postmenopausal osteoporosis. This is responsible for vertebral rush factures and distal radius fractures and probably results from postmenopausal endocrinologic changes.

Primary type 2 or Secondary Osteoporosis.

Primary type 2 osteoporosis or senile osteoporosis occurs after age 75 and is seen in both females and males at a ratio of 2:1. This is more gradual, also affecting more woman. This results in fractures of the femoral neck, vertebrae, proximal humerus, proximal tibia and pelvis. This can be related to age-related reduction in Vitamin D synthesis or resistance to Vitamin D activity. Secondary osteoporosis may arise at any age and affect men and women equally. This form results from chronic predisposing medical problems or disease, or prolonged use of medications such as glucocorticoids, when the disease is called steroid-induced or glucocorticoid-induced osteoporosis.

The risk of osteoporosis fractures can be reduced with lifestyle changes and in those with previous osteoporosis related fractures - homoeopathic medications. Lifestyle change includes diet, exercise, and preventing falls.

Signs and symptoms

Clinically, osteoporosis itself has no symptoms; its main consequence is the increased risk of bone fractures. Osteoporotic fractures occur in situations where healthy people would not normally break a bone; they are therefore regarded as fragility fractures. Typical fragility fractures occur in the vertebral column, rib, hip and wrist.
Acute bone pain can be common especially backache because of pathological fractures cause collapse of vertebral bodies. Pain with local tenderness is aggravated by weight-bearing. It usually subsides in a couple of days. Fractures occur in weight-bearing vertebra [T8 and below] after minimal trauma and in other bones after a fall.

Fractures

Fractures are the most dangerous aspect of osteoporosis. Debilitating acute and chronic pain in the elderly is often attributed to fractures from osteoporosis and can lead to further disability and early mortality. These fractures may also be asymptomatic. The most common osteoporotic fractures are of the wrist, spine, shoulder and hip. The symptoms of a vertebral collapse ["compression fracture"] are sudden back pain, often with radicular pain [shooting pain due to nerve root compression] and rarely with spinal cord compression. Multiple vertebral fractures lead to a stooped posture, loss of height, and chronic pain with resultant reduction in mobility.

Fractures of the long bones acutely impair mobility and may require surgery. Hip fracture, in particular, usually requires prompt surgery, as serious risks are associated with it, such as deep vein thrombosis and pulmonary embolism, and increased mortality.

Pathogenesis

The underlying mechanism in all cases of osteoporosis is an imbalance between bone reabsorption and bone formation. In normal bone, matrix remodeling of bone is constant; up to 10% of all bone mass may be undergoing remodeling at any point in time. Bone is resorbed by osteoclast cells [which derive from the bone marrow], after which new bone is deposited by osteoblast cells.


The three main mechanisms by which osteoporosis develops are:

An interplay of these three mechanisms underlies the development of fragile bone tissue. Hormonal factors strongly determine the rate of bone reabsorption; lack of estrogen [e.g. as a result of menopause] increases bone reabsorption, as well as decreasing the deposition of new bone that normally takes place in weight-bearing bones. The amount of estrogen needed to suppress this process is lower than that normally needed to stimulate the uterus and breast gland. The α-form of the estrogen receptor appears to be the most important in regulating bone turnover. In addition to estrogen, calcium metabolism plays a significant role in bone turnover, and deficiency of calcium and vitamin D leads to impaired bone deposition; in addition, the parathyroid glands react to low calcium levels by secreting parathyroid hormone [parathormone, PTH], which increases bone reabsorption to ensure sufficient calcium in the blood. The role of calcitonin, a hormone generated by the thyroid that increases bone deposition, is less clear and probably not as significant as that of PTH.

Investigation and Diagnosis

The diagnosis of osteoporosis can be made using conventional radiography. -X-rays show decreased bone density only after more than 30% bone has been lost and by measuring the bone mineral density [BMD]. In addition to the detection of abnormal BMD, the diagnosis of osteoporosis requires investigations into potentially modifiable underlying causes; this may be done with blood tests. [Serum, calcium and phosphorus levels, serum protein electrophoresis and parathyroid hormone levels]. Depending on the likelihood of an underlying problem, investigations for cancer with metastasis to the bone, multiple myeloma, Cushing's disease and other above-mentioned causes may be performed.

Note

As of 2013 there is insufficient evidence to determine if supplementation with calcium and vitamin D results is of greater harm or benefit in men and premenopausal women. Low dose supplementation [less than 1 g of calcium and 400 IU of vitamin D] is not recommended in postmenopausal women as there does not appear to be a difference in fracture risk. It is unknown what effect higher doses have. There however may be some benefit for the frail elderly living in care homes.

While vitamin D supplementation alone does not prevent fractures, combined with calcium it might. BUT There however is an increased risk of myocardial infarctions and kidney stones. Vitamin K supplementation may reduce the risk of fractures in post menopausal women; however there is no evidence for men.

Treatment

This is preventive, symptomatic and inhibitory. Acute pain is assisted with orthopaedic support, heat and massage. Consistent exercise is encouraged. Homoeopathic medication is given. Women with severe disease are also given Homoeopathic menopausal medication to support the hormone levels.

I will never prescribe Calcium to my patients. Whilst taking calcium, there can be a risk of myocardial infarction and kidney stones. I normally check for serum calcium and phosphorus levels, serum protein electrophoresis and parathyroid hormone levels, and a bone density done before treating osteoporosis. Then I prescribe homoeopathic medication which can build bone density and therefore with less risk of fracture.