Osteoporosis of vertebral column

International publicized data

GMCD Instructional Course Lectures

Author:

Dr. med. Guy MC Declerck MD (GMCD)

Medical FRCS-, FRCS Ed Orth-, M Ch Orth-, PhD-studies

Spinal Surgical and Research Fellow, Perth, Western Australia

Spinal Orthopaedic Surgeon and Surgical Instructor

Consultant R&D Innovative & Restorative Spinal Technologies

President International Association of Andullation Therapy (IAAT)

Copywriter / Translator:   Filip Vanhaecke PhD

Illustrative expertise:   Jasper Baele, HHP and ProVision, Waregem, Flanders, Belgium

Review scientific literature:   Medical Consulting Advice, Ostend, Flanders, Belgium

Support:   International Association of Andullation Therapy

Legal advice:   Anthony De Zutter, kornukopia.be

Dedication to Bruno Nuyttens, CEO HHP. July 2014

With a flow of eloquent raillery or good-natured sarcasm, the CEO endorsed my ambition to finalise this part of my original research. His selfless devotion to promoting it have benefited me in more  ways than I can count. He became a friend and always has been my help and  strength to continue in all difficult circumstances. 

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Introduction

Relying on the work of giants is the lifeblood of scientific research. Indeed, if I have seen further, it is by standing on the shoulders of giants. One might even say that I have always depended on the kindness of strangers in this regard (*).

The continuous support by professor BA Kakulas (Neuropathology), professor JR Taylor (Spinal Anatomy and Human Biology), and Sir George M Bedbrook (Spinal Orthopaedic and Rehabilitation Surgeon) made it possible to analyse 27539 post-mortem human spines, normal and pathological, in the Department of Neuropathology, Royal Perth Hospital/University Western Australia, Perth.

Note: in order not to disturb easy reading of the underneath scientifically based chapters, only a few authors are mentioned in the text where dr. Guy considered it essential. Their names are placed between brackets. Further information on their individual research can be read in the last chapter ‘Literature Encyclopedia’.

(*) Mirsky Steve. Copy That. Technology is making it harder for word thieves to earn outrageous fortunes.

     Scientific American, February 2014, p.64

Table of contents

1. What is bone tissue?

2. Law of Wolff (1892) and regular exercises

3. Piezoelectric phenomenon

4. Hereditary factors

5. Where do breakdown and synthesis of bone take place?

6. Different types of bone cells

7. Living apart but together

8. How much bone is broken down and resynthesized?

9. Initial maximal bone mass

10. The first thirty years of life

11. How much bone does a human skeleton lose?

12. What happens from the age of 30 years onwards?

13. Osteoporosis. What is the definition?

14. Does osteoporosis occur frequently?

15. Osteoporosis in women

16. Osteoporosis in men

17. Why should we feel concerned about osteoporosis?

18. Social and personal financial consequences

19. Main causes of osteoporosis

20. Osteoporotic fragility fractures

21. Vertebral body: the most frequent fragility fracture

22. Frequency of osteoporotic vertebral fractures

23. Women develop much more osteoporotic vertebral fractures

24. Evolution following the occurrence of the first osteoporotic vertebral fracture

25. Localization of osteoporotic vertebral fractures

26. Three types of osteoporotic vertebral fractures

27. The first osteoporotic vertebral fracture causes limited or no inconvenience

28. When do people consult a doctor?

29. The first radiographic image: mostly nothing to see

30. Immediate diagnosis by a MRI-STIR scan

31. Osteoporotic kyphotic round back formation

32. Medical consequences of the osteoporotic kyphotic evolution

33. Life quality, morbidity and mortality

34. Why does bone become osteoporotic?

35. Functional interruption between vertebral body and adjacent discs

36. Why does an osteoporotic vertebra break?

37. How could a correct diagnosis of the bone strength be made?

38. Indirectly measuring the BMD by DEXA scan

39. What exactly is the meaning of bone mineral density (BMD)?

40. Many approaches to treat osteoporosis

41. Treatment is simple: prevention!

42. Naturopathy

43. Intake of calcium and vitamin D (supplements)

44. Regular activities

45. Pharmaceutical medication

46. Biophysical therapies

47. Treatment of osteoporotic fractures

48. Osteoporotic vertebral fracture: routine approach

49. Osteoporotic vertebral fractures: cementoplasty

50. Spinal surgery is a dangerous challenge

51. Innovative treatment perspectives

52. Literature Encyclopaedia

1. What is bone tissue?

Bone tissue is a solid protein construction. This tridimensional protein network is built up for 90 % collagen type 1 fibers. This construction can be compared to the tridimensional organization of concrete support beams in the building process of a skyscraper. In such a tridimensional network - called trabecular network - different types of bone cells and calcium salts are present. Thus, bone tissue constitutes an enormous reservoir of minerals. Built from calcium (Ca) and phosphor (P), these bone minerals can be compared with the geological structure of other calcium phosphate hydroxyapatite crystals [Ca10(P04)6(OH)] occurring in nature (Fig. 1). Therefore, bone tissue is the essential provision source to fulfil the metabolic needs of all our body cells. Without calcium the heart cannot beat nor will the brain function. And when e. g. calcium blood levels are too low, osteoclasts will break down more bone in order to liberate calcium.

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Fig. 1. Bone tissue mainly consists of collagen type 1 fibers forming a solid 3-D organic network in which bone cells and CaP-crystals (white circles) are found

2. Law of Wolff (1892) and regular exercises

Bone tissue is not an inert mass. It is a very dynamic tissue which has to react quickly to the needs of the body. In 1892, Wolff already observed that bone tissue reacts to biomechanical stress. Hence the expression : 'If you don’t use it, you lose it’. Bone becomes stronger when subjected to stress but breaks down when not loaded. Therefore, everyone is recommended to regularly perform body exercises. Regular exercises not only lead to stronger muscles. Exercises stimulate the osteoblasts to produce more bone in order to resist increasing muscular strength as well.

3. Piezoelectric effect

The body not only has to adapt to different degrees of physical effort but also to the different vibrations acting upon it. Unlike astronauts and deep-sea divers, on earth’s surface we are strongly subjected to gravity and thus to numerous earth vibrations. The continuous alterations in physically loading and unloading bone tissue and the varying types of vibrations, are responsible for submitting the body to mechanical pressure phenomena. These forces lead to the generation of electric micro-potentials which are co-responsible for the synthesis of collagen fibers. This piezoelectric effect (= production of electricity due to pressure) was discovered by Pierre and Jacques Curie in the 19th century. It is one of the explanations why vibrations, as a biophysical treatment method, are researched, developed and applied for human beings.

4. Hereditary factors

Only within safe limits can the cartilaginous tissue in the intervertebral discs of the lower lumbar vertebral column be subjected to all kinds of compression, tension and torsion forces. Every individual only can load his bone tissue within his own individual healthy limits. The presence of abnormal DNA genes (a. o. the collagen COL1A1 gen and the polymorphisms of the vitamin D-receptor-gen, FokI and TaqI) is responsible for osteoporosis appearing sooner in the gen-bearing person.

When the skeleton is loaded 'normally’, loading only has a small influence on the genetic expression of bone cells. If subjected to too few forces, certain genes on the DNA of bone cells are informed in a negative way. Typically, the bone cells of astronauts and deep-sea divers present a catabolic genetic expression. The genes on the DNA of their bone cells receive 'bad’ information because the pressure effects of gravity and daily loading activities remain absent. This results in a disturbed communication between bone cells (*), which leads to increased bone breakdown, decreased bone synthesis and … osteoporosis. Conversely, when other individuals are subjected to heavy physical training they will present an anabolic genetic expression. The genes of these bone cells are stimulated, forcing the different cells to consult each other even better. This leads to an increased production of bone tissue.

(*) cells communicate with each other through long cytoplasmic extensions called tight junctions

5. Breakdown and synthesis of bone: where?

The uninterrupted interactions between osseous cells to break down and resynthesize bone primarily occur in the more porous and spongious bone tissues. This trabecular or cancellous tissue is located within the bones and is especially found inside the vertebral bodies (Fig. 5). The cooperation between the different bone cells takes place in more or less 1 million working places scattered all over our bone system.

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Fig. 5. Illustration of vertical bone trabeculae in an L1 osteoporotic vertebra

(Declerck/Kakulas, Neuropathology, Perth, Western Australia - X90-1437, M, 63 years)

6. Different types of bone cells

The relationships between the different types of bone cells are excellent. They understand each other very well and respect each other’s abilities. They simply need each other to fulfill their functions. The osteoclasts destroy old and broken bone by digging holes. The osteoblasts fill the empty spots with some kind of cement made up by collagen type 1 fibers and other proteins. By adding CaP and other mineral crystals, the same osteoblasts gradually solidify the immature bone matrix (Fig. 6). It remains unknown which cells are in charge. Is the initiative to create new bone first taken by the osteoclasts? Or do osteoblasts first have to send signals to their colleagues for cleaning up old or broken bone fragments? However, it is already known that older osteoblasts are promoted to 'yard supervisors', called osteocytes. The receptors on their cell membranes act as signal-receiving stations. The cells are able to catch very complex chemical and mechanical signals which are processed into clear orders. Because osteoclasts, osteoblasts and osteocytes communicate with each other, they perfectly understand their chemical and molecular lingo and fully cooperate to adapt bone tissue to the required circumstances.

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Fig. 6. Bone cells in a breakdown/buildup zone

7. Living apart and together

In normal circumstances the communication between the different types of bone cells remains excellent. By the age of 30 years, bone cells get older and their degree of activity decreases. They continue to support each other even when a specific group of bone cells is endangered by external factors. Indeed, they can be manipulated for some time but will continue to 'help’ each other due to their intense life-long cooperation. These observations become very clear each time when cellular reactions are analyzed during a 6 months to 2 years follow-up testing period of new drugs in the treatment of osteoporosis. When medication is administered with the only aim of silencing the osteoclasts (= inhibition) or even killing them (= apoptosis), the osteoblasts stop their bone synthesizing activities within one year. If only pills are taken which urge osteoblasts to work harder, after 6 months already the osteoclasts refuse to do all further essential preparatory bone removing work. And even when both osteoporotic treating medications are taken simultaneously, cellular cooperation cannot be stopped. When osteoclasts are induced to halt their activities while osteoblasts are stimulated, the osteoblasts will respect the work done by their colleagues. They will take an extra year to fill up the existing bone holes, but finally will cease fulfilling their job. And what about the role of the osteocytes who supervise and coordinate the different cellular functions? Well, in osteoporotic circumstances the osteocytes either do retire (fatigue damage), either burn out (apoptosis), or die (cell necrosis).

Note. Indeed, it is easier to develop modern communication media than to map the more complicated communication systems between bone cells. Nevertheless, it remains one of the major medical challenges to develop efficient medication to prevent and treat osteoporotic diseases.

8. How much bone breaks down and is resynthesized?

In one year’s time, a healthy individual breaks down and resynthesizes up to 10 % of his existing bone mass. The adult human body renews its own skeleton every 10 years. Unfortunately these processes do not always result in identical mechanical osseous integrity and strength. Breaking down and resynthesizing bone tissue never occurs entirely along the normal physiological laws. At a certain moment and around the age of 30 years, Mother Nature decides that the equilibrium she installed between osseous breakdown and synthesis must come to an end. Osteocytes will quit their jobs one after another. Some are worn out (senescence), cannot function anymore and retire prematurely (fatigue damage). Many osteocytes feel completely useless and eliminate themselves (apoptosis or programmed cell death). Others die having fulfilled heavy duties (cell necrosis). The osteoblasts get lazier as well. They get older and transdifferentiate to fat cells. Indeed, aging and osteoporotic bone contains an increasing percentage of fat. Osteoclasts seem to survive better as they have a haematopoietic origin.

9. Initial maximal bone mass

It is essential that growth and development of the skeleton occur as normally as possible from birth on. The maintenance of a well-coordinated balance between both processes of breaking down and resynthesizing bone is extremely important. It not only maintains the integrity and strength of bone tissue at a constant level. The skeleton stays in a healthy condition as well. In normal circumstances the maximal bone mass which an individual ever will be able to accumulate during lifetime is reached around the age of 30 years. The quantity of this mass probably is determined by our genes. Hence, every person can reach its own and individually determined maximal bone mass. And the larger this initial maximal bone mass, the better she will be able to protect herself against the normally occurring aging processes which invariably are accompanied by a progressive decalcification of the skeleton.

10. The first thirty years of life

A balanced diet with sufficient calcium (Ca) and phosphor (P) minerals is necessary during the first 30 years of life. It is even more important to load the skeleton efficiently. Otherwise, the essential maximal bone mass will never be reached. Nowadays young people no longer will reach this maximal bone mass: passively surfing on the internet has become more important than physically fooling around. Importantly, an outstanding interaction between different hormones (parathormone PTH, calcitrol, calcitonin and estrogens) is a fundamental requirement to lay down calcium (Ca) and phosphor (P) in bones under the form of CaP-crystals. Consequently, major premature problems arise when hormonal disparities exist.

11. How much bone will we lose?

More bone tissue is broken down than synthesized from the age of 30 years onwards. During an average lifetime, every individual will lose 40 % of his maximal bone mass. Women lose more bone tissue than men (0,5 % versus 0,3 % per year). Once the osteoporotic processes have started, bone breakdown progresses more intensively. At a certain moment complete bone structures, called bone trabeculae, will resorb and disappear (Fig. 11a and 11b).

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Fig. 11a. Left (L3 vertebral body in a physically very active man aged 79 years - A90-149): moderately osteopenic bone structure with accentuation of vertical bone trabeculae, less horizontal bone trabeculae, more space between trabeculae and diminished intertrabecular connectivity

(Declerck/Kakulas, Neuropathology, Perth, Western Australia)

Fig. 11b. Right (L1 vertebral body in a sedentary man aged 63 years - X90-1437): severe degree of osteoporosis with a diminished amount of bone trabeculae, diminished trabecular diameter, more space between the trabeculae and diminished interconnectivity

(Declerck/Kakulas, Neuropathology, Perth, Western Australia)

12. What happens from the age of 30 years onwards?

From the age of about 30 years, not only the amount of bone trabeculae but their diameter as well start decreasing. Consequently the space between the remaining trabeculae increases (Fig. 11a and 11b). Bone becomes more and more porous and fragile.

The probability for developing osteoporosis decreases when the quantity of the initial maximal bone mass is significant. The higher the quantity, the more trabeculae, the larger their diameters but the more time is needed to break down the trabeculae. The loading intensity of bone tissue during the initial years of bone growth remains an important factor for the time osteoporosis will appear. Both the external shape of bone and the internal structure of bone tissue are determined by mechanical stress exerted on bone (law of Wolff). Finally, keeping up numerous daily (intense) activities remains accountable for the magnitude of the mechanical stress.

13. What is osteoporosis?

Osteoporosis (or 'porous’ bone) is a skeletal disease. The condition is characterized by diminishing quality and quantity of bone tissue as a result of a severely disturbed balance between bone breakdown and bone synthesis. Because of the progressing collapse of the trabecular bone architecture and the decreasing bone mass (= decreasing bone mineral density BMD), the porosity of all bones in the skeleton increases (Fig. 13a and 13b). Bones becomes more fragile and can fracture easier.

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Fig. 13a. Left (X90-1420, L2) and Fig. 13b. Right (X90-464, T11).

Along the process of becoming porous, the number of trabecular struts decreases. As the horizontal trabeculae break down easier the vertical ones become more prominent

(Declerck / Kakulas, Neuropathology, Perth, Western Australia)

14. Does osteoporosis frequently occur?

Although everybody will develop osteoporosis, the occurrence of this disease is highly underestimated. Everybody 'knows’ about it but, of course, everybody is convinced she or he never will develop it. Nobody can feel it is happening but when you 'have’ it, it is too late to prevent this relentlessly progressing disabling condition. So, be aware as osteoporosis becomes a gigantic health problem taking huge proportions worldwide. Most people develop this disease once the age of 65 is reached (senile osteoporosis). Especially women develop osteoporosis, unfortunately at younger age and when menopause starts around 50 years (postmenopausal osteoporosis) (Fig. 15). Because of the diminished production of estrogens, less Ca and P is deposited in bone tissue and bone breakdown becomes more important than bone synthesis.

15. Osteoporosis in women

From the start of the menopause and during the ensuing 8 to 10 postmenopausal years women lose bone mass at a rate of 2 % to 5 % per year. Afterwards it is reduced to 0,5 % a year. One out of three women aged between 60 to 70 years and two out of three women older than 80 years are struck by this disease.

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Fig. 15. Osteoporosis especially affects female population

16. Osteoporosis in men

In men, testosterone is biochemically converted into estrogen. The aging processes reduce the production of male hormone. This lowering concentration of testosterone results into the development of osteoporosis but the disease evolves at a slower rate and much later in life. Consequently, the quite different prevalences of osteoporosis (= those who have the disease) in women and men are rather logical. In general, 7 women are affected by osteoporosis compared to 3 men. In the USA 50 % of women aged more than 50 years have osteoporosis, but only 1 man out of 8. In the EU 1 out of 8 citizens older than 50 years suffers this irreversible disease.

17. Why worry about osteoporosis?

Bone decalcification starts when the aging processes are initiated around the age of 30. This decalcification develops unnoticed and evolves without any apparent complaints or symptoms. Without noticing or feeling the disease, bones become more porous and more fragile. At a certain moment in life, and generally when the age of 50 years is reached, a bone will break if osteoporosis already developed (= fragility fracture). It usually happens 'suddenly’. Without alarming signals, a bone fractures spontaneously during normal daily routine activities or as a result of a rather trivial incident (e. g. turning around suddenly, picking up an object, ...). When by that time other medical problems are present (e. g. vascular and/or pulmonary diseases, diabetes, etc ...) osteoporosis very quickly leads to an irreversible evolution. The disease results in chronic pain, decreased life quality and increased risk of death.

18. Social and personal financial consequences

It is important to realise that society as a whole will have to bear the direct and indirect financial costs related to osteoporosis. It has been calculated that in 2030 the disease will cost 164.000.000 $ per day ! This means that every aging patient will have to contribute more and more to finance his treatment.

19. The main causes of osteoporosis

1. From the age of 30 years onwards, aging processes are responsible for losing the built-up maximal bone mass. Every woman will lose 0,5 % of her bone mass each year during the premenopausal phase. Every man loses 0,3 % of his bone mass. This means that each individual will lose up to 40 % of maximal bone mass during an average lifetime.

2. Lack of estrogens. Especially women fall victim to this worldwide disease. Not only the normal aging processes play an important role but especially the decreased production of estrogens when the menopause begins. During the first 8 to 10 menopausal years women lose about 2 % to 5 % bone per year. Thereafter, loss is normalized again to 0,5 %. In men, bone resorption is less dramatic because they produce testosterone their whole life long.

3. Physical inactivity and immobility. In 1892 Wolff already observed that bone tissue reacts to mechanical loading of the skeleton. In other words: bone tissue is generated where and when it is loaded and removed where and when it is not loaded. A regular and healthy physical activity, which shouldn’t take more than a daily walk or bike ride, helps to maintain the level of bone mass. It can even increase bone mineral density (BMD) with 1 % to 2 %. Simply, just a little bit more physical effort will make the difference between normal and excellent. Bone loss increases dramatically in bedridden patients following accidents and operations, during immobilization, and in paralyzed or wheelchair patients. The increasingly sedentary lifestyle in our modern digitalized world is by no means a bone synthesizing factor. Indeed, if you rest you rust. On the other hand, women who perform very intense and extreme physical activities at whatever age produce less estrogens causing more bone decalcification.

4. Smoking and alcohol. Smoking leads to an increased catabolism of estrogens, to an earlier start of the menopause, and results in a loss of body weight preventing bone formation. Chronic heavy drinking has long been proven to increase the risk of bone loss.

5. Dietary habits, lack of vitamin D, malnutrition. Excess of caffeine, salt (Na), saturated animal fat and soft drinks (containing phosphor acid) influence the intestinal absorption of calcium. Lack of sun leads to lack of vitamin D. Limiting the intake of calcium, proteins, vitamin B6, B12, C, D, K during adolescence will lower the essential initial maximal bone mass. These facts all result in reduced bone mineral density (BMD) values.

6. Medications such as corticosteroids, thyroid hormones, certain antibiotics, anticoagulants, anticonvulsants, anti-cancer drugs etc. lead to bone mass reduction.

7. Hormonal diseases such as diabetes, hypogonadism, hyperparathyroidism, hyper- and hypothyroidism, delayed menarche, premature menopause, pregnancy and breast-feeding may be accompanied by bone loss.

8. Various diseases like rheumatoid arthritis, liver cirrhosis, anorexia, bulimia, etc. ; gastro-intestinal diseases like Crohn’s disease, lactose intolerance, gastrectomy, bowel resection, intestinal bypass, etc.; and tumors like myeloma, lymphoma, leukemia, metastases are accompanied by loss of bone mass.

9. Intoxications with heavy metals such as cadmium and led lead to bone loss.

10. Genetic diseases like osteogenesis imperfecta, homocystinuria, ... and the presence of abnormal genes in the DNA (a. o. the collagen COL1A1 and the polymorphisms of vitamin D receptor gene FokI and TaqI) lead to premature osteoporosis.

11. Note : a high body mass index (BMI) and consequently overweight protect against osteoporosis. This is explained by the increased load on the skeleton and the production of leptin hormone.

20. Osteoporotic fragility fractures

Osteoporosis is a progressive and irreversible disease affecting all bones simultaneously (Fig. 20). However, most 'fragility fractures’ occur at the level of the wrist, hip and vertebrae. Especially women aged over 50 years easily break their wrist and / or hip. And far too many patients die prematurely or get severely handicapped due to an osteoporotic hip fracture.

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Fig. 20. Bone scan. In this individual, the zones of high tracer uptake indicate osteoporotic fractures

21. Vertebral body: most frequent fragility fracture

The most frequently occurring osteoporotic fracture is the compressive fracture of a vertebral body (Fig. 21a and 21b). Despite the fact that at the same time aging processes have developed into the intervertebral discs (IVD), initially the height of the IVDs mostly remains preserved (Fig. 11b, 21a, 21b). This is due to bone loss at the level of the endplates (= upper and lower surfaces of the vertebral bodies) which allow the aging intervertebral discs (IVD) to penetrate into the porous and fragile bone of the vertebra. Then, a routine X-ray always gives the false impression that the IVD is 'normal’. However and when the IVD height starts decreasing, which is a typical sign of evolving degenerative processes and lesions of the disc, the IVD will be co-responsible for the occurrence of compressive fractures when the bone becomes osteoporotic.

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Fig. 21a. X-ray and post-mortem sagittal section of an osteoporotic compression fracture at the level of the 1st lumbar vertebra. Notice the accentuation of vertical trabeculae, central compressions of the endplates and oval protrusions of aging disc tissue into the vertebral body.

Note: the intervertebral discs show aging signs but their height has not decreased

(Declerck / Kakulas, Neuropathology, Perth, Western Australia)

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Fig. 21b. Very common illustration of the osteoporotic spine when aging. The T5 vertebra has collapsed Intravertebral fractures are developing in the T7, T8, T11 and L1 vertebral bodies. The intervertebral discs (IVD) are aging but their heights remain normal. The IVDs rather penetrate into the porous and fragile bone of the vertebra. Once the IVD starts degenerating, their height will decrease

(Declerck / Kakulas, Neuropathology, Perth, Western Australia)

22. Frequency of osteoporotic vertebral fractures

About 85 % of all compressive vertebral fractures are due to osteoporosis. The remaining 15 % are caused by road traffic accidents and cancer. More than 440,000 and 750,000 osteoporotic compressive vertebral fractures are diagnosed each year respectively in Europe and in the USA. In comparison, 250000 wrist fractures and 250,000 hip fractures are registered in the USA each year, 230000 new cases of brain haemorrhage in women over 30 years of age, and 185,000 new cases of breast cancer in all age categories.

23. More osteoporotic vertebral fractures in women

Compressive osteoporotic vertebral fractures start occurring in about one out of five or even one out of four women older than 50 years. Then, the general risk for breaking an osteoporotic vertebra varies between 20 and 25 %. In terms of age groups, the risk counts for 1 % between the age of 50 and 59 years, 8 % between 60 and 69 years, 15 % between 70 and 79 years, 30 % between 80 and 89, and 50 % from 90 years on. The incidence (= fracture may occur) for men is lower, because men suffer less falls and lose less bone tissue at the level of cortical bone (which is stronger).

24. First osteoporotic vertebral fracture: evolution?

The occurrence of a first osteoporotic vertebral fracture is a major problem and the start of an irreversible progressing cascade of new fractures. A first osteoporotic fracture increases the risk of spontaneously breaking another vertebra within one year. The postmenopausal woman presents a 4 to 5 times higher risk for breaking another vertebra when one vertebra already fractured and a 12 times greater risk if already two or more compressive vertebral fractures did arise. Each time a vertebral body breaks, the back complaints and back pain get worse and physical disabilities increase. Hence, fragility fractures are accompanied by significant morbidity even if 'nothing’ is felt when the first vertebra spontaneously broke.

25. Localization of osteoporotic vertebral fractures

Osteoporosis is a disease which develops in all bones at the same time and consequently also in all vertebrae. But most of the spontaneous fractures occur at the mid-thoracic (T7-T9) and thoracolumbar (T12-L2) regions (Fig. 25).

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Fig. 25. Most osteoporotic vertebral fractures occur at the level of vertebrae T7, T8, T9, T12, L1 and L2

26. Three types of osteoporotic vertebral structures

Osteoporotic vertebrae can break in three ways. This not only depends on the presence and location of still well-functioning bone trabeculae in the vertebral bodies but on the loading patterns on the spine as well. Three types of vertebral fractures need to be differentiated: anterior vertebral collapse or 'wedge’ fracture (Fig. 26a), central collapse or 'biconcave’ fracture (Fig. 26b) or a total vertebral collapse or 'crush’ fracture (Fig. 26c).

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       Fig. 26a. Radiological image and illustration of an osteoporotic 'wedge’ fracture

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       Fig. 26b. Radiological image and illustration of an osteoporotic 'biconcave’ fracture

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       Fig. 26c. Radiological image and illustration of an osteoporotic 'crush’ fracture

27. First vertebral fracture: limited inconvenience

Fractures of the hip and wrist are accompanied by pain, swelling and important functional limitation. Although the presence of numerous sensory nerve fibers in bone tissue, strangely enough most of the first osteoporotic compressive vertebral fractures cause very few or only vague complaints and discomfort. Therefore, they are called 'benign’ fractures. In contrast, accidental spinal fractures cause a lot of pain. Consequently, most osteoporotic individuals who sustained a vertebral compression fracture are able to return to normal activities following a period of 6 to 8 weeks. Only 30 % of these individuals experience intense pain for which sometimes hospitalization is required.

28. When do people consult a doctor?

Approximately 70 % of patients only seek medical advice when already multiple fractures have occurred. She becomes concerned about her decreasing body height and an increasing forward bended posture (= kyphosis) (Fig. 28). The loss of her body shape is associated with gradually increasing pain and more difficulties in performing the daily routine activities. They remember having experienced short periods of 'some’ back discomfort, but were told by their relatives that 'torn muscles’ were the reasons!

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Fig. 28. Several spontaneous vertebral fractures lead to a decreasing body height and a more pronounced bended forward posture, the so-called round back. The body height of the 75 years old lady decreased with 8 cm. She never experienced pain (Courtesy of the involved family members)

29. First radiological image: usually 'nothing’ to see

Another strange reality! If the patient is really concerned about sudden (minimal) back discomfort and a radiological investigation is finally performed, very often 'nothing’ special can be observed. This is not an observational error by the radiologist, nor a failure of the used technique. Following the spontaneous occurrence of the first osteoporotic vertebral fracture, radiologists in Europe and in the USA as well report that nothing can be seen in 55 % to 70 % on radiological images. Nevertheless, the 'still invisible’ fracture is not at all a stable break but shows dynamic characteristics. Indeed, the porous vertebra fails biomechanically over a period of 6 to 18 months until it collapses (Fig. 29a and 29b).

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Fig. 29a. Normal evolution of a spontaneously occurred osteoporotic vertebral fracture in a 78 years old lady. September 2000: sudden severe pain making her bedridden - October 2000: compression at the level of the superior endplate - November 2000 : 'wedge’ type osteoporotic structure

(Courtesy, professor Deramond, Amiens, France)

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Fig. 29b. A spontaneously occurring osteoporotic vertebral compression fracture shows dynamic characteristics and continues to 'collapse’ over a period of 6 to 18 months

(Courtesy, professor Deramond, Amiens, France)

30. Quick and correct diagnosis by MRI-STIR scan

It is essential to make a correct diagnosis not only in an attempt to 'halt’ the progress of vertebral osteoporosis, but also to quickly stabilize, align and/or repair the loss of vertebral height. Whatever the nature of a fracture in the body, it never will heal by just taking 'tablets’.

The MRI-STIR sequence (Short Tau Inversion Recovery) is the most sensitive method to diagnose an acute vertebral fracture and to repair or avoid its height loss in time (Fig. 30a, 30b and 30c). These MRI scans are important as well to diagnose possible avascular bone necrosis in case of persistent pains. Indeed, a non-stabilized vertebral fracture can give rise to a very painful 'false joint’ within the broken vertebra (= Kϋmmell disease).

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Fig. 30a. Clear evidence of a vertebral fracture on radiology and MRI (without STIR sequence). But is it the only problem? Can vertebral height be restored? Is it possible to stabilize this fracture? Or is some other pathology going on? It is impossible to know without MRI-STIR sequence

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Fig. 30b. An acute fracture edema (L2) appears as a 'black’ spot on the T1 sequence. The intensity of ‘brightness’ on the T2 sequence of the same edema directly depends upon the amount of liquid. Because the STIR-sequence only denotes liquid (but no fat nor bone marrow), 'fresh’ edema (with lots of water) will form a very 'bright’ signal representing a recent fracture.

Note : The other vertebral fractures at T12-, L3-, L4- and L5-levels are not acute but old 'healed’ fractures. Liquid no longer is present and the fractures are 'healed’: the bone contains bone marrow and fat deposits

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Fig. 30c. The MRI-T1 and MRI-T2 sequences show a fracture, but only the MRI-STIR sequence indicates that the fracture recently occurred (T12). Tablets will not heal this acute fracture. Respecting the orthopaedic laws of fracture treatment, an acute fracture needs to be stabilised, aligned and its height loss corrected

31. The osteoporotic round back formation (kyphosis)

The progressing kyphotic round back deviation resulting from an increasing number of vertebral fractures (Fig. 31) will evolve to more intense pains and a decrease of life quality. The inevitable catastrophic cascade of medical problems is NOT related to the occurring 'osteoporotic’ discomfort BUT to the collapse of the spontaneously broken vertebral bodies. If the normal spinal stature could be maintained, there probably would not be that amount of disability. The negative consequences on physical, social and psychological functioning become irreversible - no matter whether or not you take 'pills’.

osteoporosism_30.jpg

Fig. 31. Osteoporosis is the beginning of round back formation and numerous medical problems

32. Medical consequences of osteoporotic round back

The progressing formation of the osteoporotic round back leads to an unstoppable chain of severe medical problems such as (a) chronic back pain, (b) increasing number of spontaneously occurring vertebral fractures associated with attacks of acute pain, (c) difficult walking pattern and advancing immobility consequently leading to more bone loss, (d) decreasing daily activities, (e) less appetite, more heartburns, and gastrointestinal problems because the kyphotic evolution diminishes the space in the abdominal cavity and compresses the stomach, (f) increasing number of pulmonary ailments and respiratory difficulties (COPD and pneumonia) due to (1) the decreasing pulmonary functions as a result of less space and volume in the thorax and (2) the more limited mobility of the ribs, (g) increasing psychological depression resulting in less self-esteem and more fear, (h) increasing social isolation and dependency on others, (i) more hospitalizations (with more bed rest and thus further bone loss), (j) overall deterioration of quality of life and finally (k) an increased risk of death.

33. Quality of life, morbidity and mortality

Patients with three or more compressive osteoporotic vertebral fractures experience a decreased quality of life which can be compared to those suffering oncological conditions or had a cerebral haemorrhage. Important neurological disorders occur in 2 % of patients for whom only surgical interventions could be helpful if the vertebrae were less porous. Compared to patients of the same age and with the same medical conditions but who as yet have not developed osteoporotic vertebral fractures, those with a osteoporotic kyphotic round back show a 23 % to 34 % higher chance of succumbing earlier. When severe pulmonary complications develop, the five-year survival rate is 61 % compared to 78 % for the same age group without osteoporotic vertebral fractures. Finally, one will succumb earlier from osteoporotic vertebral fractures than from osteoporotic hip fractures (78,6 versus 80,1 years).

34. Why does bone become osteoporotic?

From the age of 30 years onwards and at the onset of the aging processes the three dimensional network structure of proteins (= collagen type I fibers) will gradually starts disintegrating (see 'What is bone tissue?’). The collagen network starts experiencing difficulties in fixing and retaining the calcium phosphate crystals. It can be compared to trying to catch the same amount of fish in a well-stocked area but with older and increasingly worn nets. Hence, the question why the average aging individual starts taking higher than normal doses of calcium! Moreover, it is dangerous (see 'Treatment by calcium intake’).

Some explanatory factors:

First of all: the two factors which determine the strength of trabecular vertebral bone are bone quantity (= bone mass) and bone quality (= microarchitecture). The quality of the supporting bone trabeculae depends upon the chemical constituents of bone tissue. On the one hand this comprises the organic trabecular matrix made up for 90 % of collagen fibers and on the other hand the mineral trabecular matrix mainly consisting of calcium phosphate crystals Ca10(PO4)x(OH)y.

Secondly: the tridimensional and tri-helical structure of collagen fibers (type I) is made from many thousands separate little pieces. These numerous collagen fibrils are linked to each other according to a genetically determined 'crosslink pattern’ (Fig. 34a). Thus, everyone has its own typical tridimensionally constructed collagen network. This explains why the specific biomechanical bone strength of the cancellous bone is different for each individual. It probably also explains why the spontaneous osteoporotic fractures in each individual (can) occur at different moments notwithstanding identical values of bone mineral density (BMD). The slightest interruption in these typical individual crosslinks changes the structure of the collagen fibers and consequently their function of fixing and retaining the CaP crystals. Then, it remains a mystery why so many people spend fortunes to consume the same type of collagen!

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Fig. 34a. Several collagen fibrils are linked to each other by a well-defined and genetically determined crosslink pattern. Collagen then is different in each individual

Finally: the calcium phosphate crystals are fixed in and on this trihelical structure of the collagen type I fiber. Despite decennia of intense research, scientists do not yet perfectly understand the mechanisms of how the 'fixing’ and 'retaining’ processes occur. Moreover, research work is hindered because the calcium phosphate crystals in these trabeculae, and unlike their analogous crystals in geological minerals and corals (Fig. 34b), show an inferior crystalline structure with a lot of impurities (carbonates) and a lack of Ca and OH.

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Fig. 34b. Calcium crystals found in the trabeculae of the cancellous bone in human bone (right) are analogous to calcium crystals occurring in nature in the trabeculae of e. g. minerals (left) and corals (middle)

35. Functional interruption between vertebral body and

      adjacent discs

The aging processes are responsible for breaking up the important but mutually dependent functional interaction between the healthy vertebra and the healthy intervertebral disc (IVD). Both structures need to cooperate to support and to distribute the forces and loads exerted on the entire vertebral column. A healthy IVD and a uniform trabecular structure in the vertebral body allow an equal transmission of these loads through the endplates (Fig. 35). Once degeneration processes arise in the IVD and / or the trabecular bone, a spinal axis deformation gradually develops.

osteoporosis_018.jpg

Fig. 35. In normal circumstances the trabeculae in cancellous bone of the vertebral bodies (depicted by the pink surfaces) bear 90 % of forces and loads acting upon the vertebrae. These loads are equally distributed through the endplates (blue lines)

Nevertheless both important vertebral structures, IVD and trabecular bone, do not present as universal features in every human individual. It is remarkable how African women who carry heavy loads on their heads their whole life long, can develop spinal axis deformations primarily as a result of degenerative phenomena in the intervertebral discs if they ever develop these! These ladies very rarely develop vertebral osteoporotic compression fractures. The causes very probably are multifactorial. African women may have more advantageous genetic material and do not experience the side effects of manipulated Western food. They continuously enjoy the daily influences of sun, UV, and higher levels of vitamin D synthesis. Above all African women experience the daily impact of piezoelectric phenomena and the law of Wolff’s which are the electrical and mechanical stimulators for synthesizing collagen fibers and bone tissue.

36. Why does an osteoporotic vertebra break?

The vertebral body breaks when it cannot longer resist the forces and/or loads exerted onto it. The trabecular bone structures (= struts) within the softer spongious bone of the vertebrae are responsible for carrying 90 % of the daily forces and/or loads. The remaining 10 % bearing capacity is taken care off by the stiffer cortical and endplate surroundings (Fig. 35).

The strength of bone and its resistance to break when loaded depend on the direction in which the bone is loaded. In a healthy vertebra the compressive bone strength in axial direction (= bone loading during walking, standing) is about twice as large as the bone strength in lateral or anteroposterior direction.

In an osteoporotic vertebra the trabecular micro-architecture in the vertical direction no longer is similar to that in the horizontal directions. The irreversible osteoporotic processes result in a decreasing diameter of all vertical trabeculae and a disappearance of the horizontal connecting trabeculae between them. Hence the appearance of large regional differences in the trabecular microarchitecture (Fig. 5, 11A, 11b, 21).This aging process decreases the mechanical behavior of trabecular bone in its prevention of fracturing. Osteoporosis leads to a dramatic decrease of compressive vertebral bone strength in axial direction (120 MPa in 20 years old individuals to 20 MPa at the age of 80). Because the vertebral trabecular bone becomes weaker and less resistant to gravity and to daily mechanical stresses during walking or sitting, trabeculae gradually will break to finally develop a compressive fracture (Fig. 21b, 26a, 26b, 26c).

A spontaneous osteoporotic vertebral fracture arises when the impact of the 'incident’ exceeds the compressive bone strength of vertebral trabecular bone. In other words: a vertebra will break when the compressive strength of the trabecular bone no longer is able to resist the vertical forces and loads on the vertebra (Fig. 36a).

osteoporosis_011.jpg

Fig. 36a. The upper arrow indicates an indentation in the vertebral endplate. The lower arrow shows a fracture in the vertebral body.

A preexisting osteoporotic vertebral fracture increases the risk for developing a new spontaneous break because the center of gravity (G) acting upon the vertebral column moves forward (Fig. 36b). As osteoporosis mainly develops in the anterior part of the vertebrae (Fig. 21, 29a, 29b, 30a, 30c), the anterior spinal column less easily resists the increasing axial weight bearing forces.

osteoporosis_004.jpg

Fig. 36b. The gravitational force (represented by the red line 'G’) normally acts near the center line of the vertebral column. When a first osteoporotic vertebral compression fracture has developed, the vertical impact of forces moves forward. Then an increasing larger force acts upon the more anterior parts of the vertebral bodies where as a consequence of osteoporosis much less weight bearing trabeculae remain available. As eventually a new spontaneous fracture will develop, the vertically acting gravitational force (G) in standing / sitting position again will move forward increasing the risk of new fractures. An irreversible process!

37. How could an exact diagnosis be made?

I briefly like to reiterate. Osteoporosis is a disease that causes the skeleton to become more porous and to decrease its bone strength. Through the presence of the osseous trabeculae, bones are capable of carrying weight and resisting forces acting upon them. Then, spontaneous breaks are prevented. Research (mainly performed on bone tissue in vertebral bodies) indicates that this bone strength depends upon (1) the quantity of bone (bone mass), (2) the quality of that bone (micro-architecture and connectivity of the trabeculae), and (3) the crosslinking profile of the collagen fibers (type 1) which retain the calcium phosphate crystals. But how can these data be checked in the osteoporotic patient? Simply, it can’t be done! In clinical practice it remains, for the time being, still impossible to measure directly the trabecular bone strength.

The characteristic strength of a material is a biomechanical concept. The strength is measured in MPa (megapascal) and indicates the resistance of a material against the pressure exerted on it before being damaged. It ensues that bone tissue first needs to be isolated through an operation before mechanical strength of its trabecular part can be measured. But even this procedure would by no means give a correct value (in MPa) but probably an average one. Moreover, it is not known where the bone biopsy should be performed. Bone mass, bone quality and the collagen crosslink profile vary in various zones in the bone itself.

38. DEXA scan: indirect measure of BMD

For the time being bone strength only can be measured indirectly. To diagnose small unknown bone fractures or 'worn out’ bone zones, all women above the age of 65 years should have their bone mineral density (BMD) determined by means of a DEXA scan (dual-energy x-ray absorptiometry) at the level of their hip or lower part of the spine. Every man should do this around the age of 70 years.

Early diagnosis of osteoporosis followed immediately by an adequate treatment may potentially lead to stabilizing an existing fragility fracture, preventing new ones, and certainly saving (very) high additional costs. Indeed, sufficient therapies have been developed to decrease the incidence of osteoporotic fractures at the level of the vertebrae, hips and wrists by 30 % to 65 %.

To simply have an idea of the degree of bone decalcification, BMD of trabecular bone can be measured through a DEXA (Fig. 38).

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Fig. 38. An idea of the degree of osteoporosis - but not of bone strength - can be provided by DEXA scan

39. Bone mineral density (BMD): meaning?

Bone mineral density (BMD) will decrease because osteoporosis increases the porosity of bone by decreasing both number and diameter of the load bearing bone trabeculae.

The measured BMD of an individual is compared to a so-called 'normal’ T-value which is a standard deviation (sd) to a reference value. This value represents the average BMD, measured with a DEXA scan, in a normal population of more than 100.000 young and healthy adults at the moment of their maximal bone mass and thus before the processes leading to osteoporosis start. Based on the obtained data the World Health Organization concluded that osteoporosis is diagnosed when the BMD equals or is less than 2,5 sd below this reference value. The BMD is expressed in a so-called T-value for everyone. The following arbitrary classification was made: (1) normal bone = BMD inferior to 1 sd of the average, (2) osteopenia (low bone mass) = BMD between 1,0 and 2,5 sd under the average, (3) osteoporosis = BMD of 2,5 sd and less under the average, and finally (4) serious osteoporosis = osteoporosis already accompanied by at least one fracture.

It is evident that T-values are nothing more than average values for a degree of bone porosity. T-values by no means represent a correct value of bone strength. Consequently, the BMD is worth nothing in predicting whether or not an individual will break a bone. The BMD only indicates a potential increased risk for developing a fragility fracture at the level of vertebrae, hips or wrists. Each reduction of 1 sd on the BDM scale means a potential increased risk of 50 % to 60 % for a fracture to occur.

The BMD is by no means an absolute value. With an identical BMD T-value and despite the fact that this value may be indicative for 'normal’ bone, 'osteopenia’ or 'osteoporosis’, some individuals eventually will develop a porous fracture, and others won’t! This means that other but still unknown physiological factors play a role in the development of an osteoporotic bone fracture. Recently and to be more accurate in prognosticating, the FRAX calculator has been developed. With this device a combined evaluation is performed of several generally known risk variables. The FRAX has a more important predicting value because it also takes into account age, sex, weight, length, previous fractures, smoking and drinking habits, rheumatoid arthritis and use of bone decalcifying medications.

40. Many treatments for osteoporosis

There still is no proof of an existing treatment which is able of restoring bone integrity and bone strength to previous normal levels. Nothing can stop the aging processes. But by respecting what Mother Nature allotted each of us, we increase our chances to avoid the catastrophic consequences of osteoporosis. Nevertheless, treatment methods for those suffering severe osteoporosis remain very limited.

41. Simple treatment: prevention

Prevention is the keyword. Prevention starts during youth because the maximal bone mass can only be reached during the first 30 years of life. An individual will lose approximately 40 % of this mass during an average lifespan. What does it mean? The answer is very simple and not at all difficult. During youth we all need a combination of (1) a balanced diet with sufficient calcium and vitamin D, (2) an active lifestyle with normal loading activities of the skeleton and regular exercises, (3) no tobacco, and (4) small amounts of alcohol. Anything simpler than that?

42. Naturopathy

Naturopathy stresses the importance of sufficient intake of vitamin C, vitamin B6 and B12, folic acid, vitamin K1, vitamin K2, and magnesium (Mg). Women may benefit from phytoestrogens (isoflavones) which allegedly do not present the side effects of estrogens.

43. Intake of calcium and vitamin D (supplements)

Once the diagnosis of osteoporosis has been established, it is evident that the remaining bone mass should be stabilised and hopefully increased to avoid the increasing incidence and prevalence of spontaneously occurring fragility fractures.

Calcium and vitamin D have long been regarded as the fundamental part of the treatment of osteoporosis. Therefore, it is advisable to take a normal daily dose of 800 IU of vitamin D but certainly to continue a normal calcium consumption of 600 to 1000 mg per day.

There exist no scientifically validated reasons why, in normal circumstances, these doses should be exceeded. It even may be dangerous to take extra dietary supplements of calcium (Michaëlsson)! When middle-aged and elderly women consume more than 1400 mg of calcium per day, they have a 40 % higher risk of dying from cardiovascular diseases. Indeed, the best is the enemy of the good!

The following question certainly needs consideration. Where and how can a surplus of calcium under the form of newly synthesized CaP crystals be deposited and fixed in the equally aging and disintegrating collagen type I fibers in the trabecular bone?

44. Regular activities

It is better to wear out than to rust out. An individual needs to move around, continue loading his skeleton and maintain a normal daily degree of activity as long as possible. Weekly performing sport activities (e. g. swimming, biking, walking, fitness) will decrease the possibilities of developing the catastrophic consequences of osteoporosis.

45. Pharmaceutical medication

Pharmacologic interventions surely can influence bone metabolism by slowing down bone breakdown (by blocking osteoclasts) and / or by stimulating bone buildup (through the osteoblasts). Till now, these tactics have proven to be insufficient. Bone cells communicate very well with each other. Osteocytes, osteoclasts and osteoblasts depend on each other for their functions (see: 'Different types of bone cells’). They do not allow external interference or otherwise go on strike.

When functions of osteoclasts are blocked by medications (amino-bisphosphonates, denosumab, alendronic, zoledronic), the osteoblasts cease work. Medicines which intend to stimulate osteoblasts (teriparatide) will neutralise the osteoclasts. The combination of both drug has no effect either.

The available pills disturb the cooperation between the different types of bone cells (see 'different types of bone cells’). By trying these means, it has never been possible to influence let alone restore bone mineral density (BMD). From time to time a temporary improvement is seen, but that’s all.

Moreover, in osteoporotic circumstances the work supervisors (osteocytes) are very few and the bone makers (osteoblasts) become much too fat. Cell necrosis and cell apoptosis decimate their numbers as well. How then can the work be organized and bone formation restored?

However, it is more than evident that a lucrative and 'wild’ business has developed around the increasing prevalence of osteoporosis. Whatever the marketing methods, it remains highly advisable to consult a competent physician because all the pharmaceuticals present quite some side effects and contraindications. Because estrogens play part in the development of osteoporosis, a profitable anti-osteoporotic estrogen medication business has been developed as well. Meanwhile, every woman knows that the intake of estrogens should be taken under professional supervision!

46. Biophysical therapies

Adjunctive biophysical therapies using energy are applied worldwide by physiotherapists for treating various medical conditions. Experiencing vibrations not only is relaxing and enjoyable but this form of energy is intensively used as additional treatment in pulmonary and urological diseases, in the prevention of decubitus related to e.g. spinal traumata, during surgery for stimulation of the venous blood flow, age-related conditions such as loss of skeletal muscle mass and function (sarcopenia), walking difficulties, etc … . One of these technologies is andullation. Positioned in the horizontal position, the individual/patient experiences low-frequency sinusoidal vibrations which are amplitude and frequency stochastically modulated. Apart from the practical positional advantages, direct pressure and vibrations on the whole body have been shown to produce piezoelectric effects in the collagen fibers (see: 'Piezoelectric effect’). About 80 % of production and restoration of collagen depend on the deformation of these fibers (Fukada; Lievens; Minary-Jolandan). Indeed, vibrations and direct pressures induce electrical micro-potentials which not only enhance collagen synthesis but also bone growth. In the scant experimental and clinical literature, whole-body vibrations seem to slow down the decrease of the BMD.

47. Treatment of osteoporotic fractures

In order to eliminate fracture pain and to guarantee a quick and safe mobilization of the patient, an osteoporotic fracture, and just like any other bone fracture, needs to be repaired as quickly and anatomically as possible. However, orthopaedic fracture treatment of an osteoporotic wrist and / or hip fracture still is much simpler and easier than dealing with a vertebral fracture.

48. Osteoporotic vertebral fractures: routine approach

A painful osteoporotic vertebral fracture mostly reacts very well to the classical routine combination of bed rest, pain killers and wearing a spinal support. However, this initial approach is not successful in 30 % of patients and at the same time it is hard to predict who will belong to the 70 % success group. Moreover, the provided 'treatment’ does not guarantee a quick functional repair. By no means will this approach prevent the further collapse of the vertebral fracture neither will the classical routine attitude prevent the development of new spontaneous occurring fractures. Bed rest leads to a considerable supplementary loss of bone (law of Wolff) with a decrease of BMD varying from 0,25 % to 1 % per week. Analgesics have their known side effects when taken for a long time. Spinal supports induce sarcopenia, the hallmark of age-related loss of muscle mass and function. Last but at least, the certain and expected evolution to a vertebral and spinal kyphotic axis deviation and malformation is not at all eliminated.

49. Osteoporotic vertebral fractures: cementoplasty

Given the generally fragile state of health and the presence of other medical conditions in this group of patients, a minimally invasive intervention with minimal disruption of the back muscles is highly recommended. A professionally performed internal fracture stabilization (Fig. 49d) of vertebral fractures not 'older’ than three months can postpone and even avoid the catastrophic consequences of the osteoporotic disease in 90 % to 95 % of patients. Hence the importance of making a quick diagnosis by a MRI-STIR scan.

Well-known cementoplasty techniques are the vertebroplasty and kyphoplasty procedures. A percutaneous perpendicular technique is executed under local anesthesia and fluoroscopic control (Fig. 49a). A small amount of PMMA cement (polymethylmethacrylate) is injected into the broken vertebra (Fig. 49b and 49c). These (and other) cementoplasty techniques rapidly result in pain reduction in over 90 % of patients who quickly return to their former level of functioning. The cement injecting technique can easily be repeated when new osteoporotic incidents happen(Fig. 49c and 49d).

There is a low risk of significant complications in the hands of intensively trained, supervised and experienced surgical and/or radiological interventionists. For unknown reasons 5 % of patients do not respond to a perfectly performed cementoplasty technique. Serious symptomatic complications arise in up to 8 % of these procedures and comprise radiculopathies and neuropathies.

osteoporosism_7a.jpgosteoporosism_27.jpg

Fig. 49a. The reduction and stabilization of osteoporotic lumbar vertebral fractures need to be performed under fluoroscopy (left). CAT-fluoroscopic guidance is applied in treating osteoporotic cervical and thoracic vertebral fractures (right)

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Fig. 49b. Perpendicular cementoplasty technique three weeks after spontaneous occurrence of an osteoporotic vertebral fracture in a 87 years old lady

(Courtesy, Professor Deramond, CHU, Amiens, France)

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Fig. 49c. Each time a new osteoporotic vertebral fracture occurs, internal stabilization can be performed again under local anesthesia

(Courtesy, Professor Deramond, CHU, Amiens, France)

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Fig. 49d. Left: during vertebroplasty PMMA cement is mainly injected in the more anterior trabecular spaces. Right: the injection of PMMA during kyphoplasty is rather performed centrally in the vertebra

(Internal Instructional Spinal Course, Kyphon - Experimentally Laboratory Investigations)

50. Spinal surgery is a dangerous challenge

A surgical attempt to restore the abnormal osteoporotic axis of the vertebral column is a very serious and even dangerous challenge. Not only because of the risks related to anesthetizing elderly people. The bad quality of bone tissue does not allow simple fixations with plates and screws. The potential complications are life threatening.

However, technical progress and development in surgical techniques never come to a standstill. If extreme kyphotic round back formation is associated with very intense pains or if paralytic phenomena present (fortunately very rare), the vertebral height can now be restored quite well by an innovative percutaneous perpendicular intern splinting technique (Fig. 50a and 50b).

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Fig. 50a. How can the spinal axis of the vertebral column be repaired in case of heavy pains?

(Declerck / Kakulas, Neuropathology, Perth, Western Australia, file X90-1442:T6)

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Fig. 50b. Potential future of an innovative percutaneous perpendicular technique to correct serious osteoporotic kyphosis associated with paraplegia

(Experimental Laboratory Procedure)

51. Innovative treatment perspectives

Using their own stem cells bone tissue already can be cultured in mice. Ongoing laboratory research is now evaluating if similar results can be obtained in humans. Numerous tissues in the human adult contain sufficient mesenchymal stem cells (hMSCs) which are essential for maintaining the cellular functions. However, these hMSCs not only are capable of self-renewing. They are multipotent. Under laboratory circumstances these not-embryonic cells can be stimulated to transform into other type of cells. Fat cells can be differentiated into cells which are not present in fat, e. g. cells synthesizing bone (osteoblasts), cartilage (chondroblasts), muscle tissue (myoblasts), collagen (fibroblasts), etc … . On the other hand - and by transdifferentiation through genetic manipulation - it is also possible to reprogram a cell so that another type of cell is formed. Transdifferentiation is a well-known physiological phenomenon in Nature where e.g. amphibians regenerate a torn off tail or limb. Such laboratory techniques can one day lead to possibilities in the inhibition of bone forming cells (osteoblasts) spontaneously changing into fat cells.

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