Most often, when visiting a doctor, people complain of discomfort in the neck and back. Without timely treatment, back disease can develop into a chronic disease and significantly complicate the patient’s life. One of these diseases of the locomotor system is fatty degeneration of the vertebral bodies, and in the article we will understand what this disease is.
Fatty degeneration of vertebral bodies
About the spine and degenerative changes
Intervertebral discs consist of several structures: the fibrous ring, the intervertebral joint, the nucleus and the plate. The fibrous ring serves as a holder for the core and its correct location, because it acts as a kind of shock absorber that helps keep the spine straight when walking, unfolding, bending and running.
A third of the spine is made up of intervertebral discs. The kernels contained in them “love” moisture - thanks to it they become soft and elastic and can absorb shock.
A degenerative disease of the locomotor system is the loss of softness of the intervertebral discs due to the harmful effects of sedentary work, extra pounds, back injuries, and crooked posture. Destroyed tissues, ligaments and joints lead to metabolic disorders and poor cell nutrition. Depleted intervertebral discs, their compaction, and growths after some time lead to the appearance of cracks, hernia, incessant pain and discomfort, numbness, limited movement, and even to a wheelchair.
Degenerative-dystrophic changes can develop due to an inactive lifestyle
The human spine is designed in such a way that it is able to independently distribute the pressure exerted on it. With an even posture and strong muscle tissue, the spine is able to withstand all “tests” without harm to it. People leading an inactive lifestyle wear out their muscles and ligaments, rendering them unusable, which results in wear and tear of the spinal discs. Excessive stress for an unprepared body also has a detrimental effect and has serious consequences.
Important! Depletion of intervertebral discs is almost always a consequence of a sedentary lifestyle. When stress is placed on the spine, weak ligaments excessively consume moisture, which is why injuries, sprains, and cracks appear. And impaired metabolism and blood supply worsen the process of tissue regeneration, delaying it for a long period.
Changes can be provoked by a variety of reasons, which will not depend at all on age, physical fitness and the presence of injuries. Main reasons:
- cells and tissues begin to age, the supply of nutrients is disrupted;
- genetic inheritance;
- abuse of bad habits (smoking, alcohol);
- inactive lifestyle;
- overweight;
- inflammatory and infectious processes in the body;
- various minor and severe injuries received due to a very large load on the spine;
- heavy loads with heavy weight, for example, when playing sports.
Dystrophic changes in ligaments occur slowly and can last for a long period of time, so it is not always possible to identify the cause in time. People who try to cure their illness using traditional medicine without turning to a specialist only make their situation worse.
Causes
So, why does fatty bone marrow occur? In fact, there are several reasons, but there are a number of conditions in which partial replacement of bone marrow with fat is considered normal.
Violation occurs for the following reasons:
- various oncological diseases, not necessarily related to the hematopoietic system;
- metabolic disorders;
- osteochondrosis;
- chronic infections;
- arsenic and benzene poisoning;
Please note: fatty degeneration may occur if you take medications from the following groups for a long time:
- Non-steroidal anti-inflammatory drugs.
- Medicines that lower blood pressure.
- Sleeping pills belonging to the barbiturate group.
- Antibiotics.
- Sulfonamides.
- Cytostatic drugs.
If a person is over 65 years old, in any case, part of his bone marrow is replaced by adipose tissue. This is not regarded as a pathology and does not require therapy.
Signs of degenerative-dystrophic changes in the lower back
Dystrophic changes in the lower back have the following characteristic signs:
- mild pain in the lumbar region, which intensifies with movement, bending and walking. May disappear in a quiet position;
- Pain in the legs and arms may occur;
- reduced activity of the cervical vertebrae is created;
- organs located in the pelvis begin to work incorrectly;
- constant fatigue;
- "unruly" limbs.
Signs of dystrophic changes in the lower back are fatigue, weakness, pain
If dystrophy is not prevented in a timely manner, paralysis and paresis may occur.
Provoking diseases
Symptoms may be accompanied by several ailments, usually occurring in parallel:
Degenerative changes in the cervical spine
Over time, every person experiences neck pain, but most often such pain does not cause a serious illness and goes away on its own. People often claim that they were just “blown away” or that they slept on an uncomfortable pillow, which in some cases can actually be the cause of pain, but you should not always attribute discomfort to such “harmless” reasons.
Very often, the cause of neck pain is pathological changes. This occurs naturally due to tissue wear, and not all disorders that occur in the spine are cured.
What does this all mean?
The first question that interests a patient who hears such a diagnosis is: “what does this mean?” Of course, any doctor knows this disease and its treatment regimen, but he cannot always recognize the cause of such changes; the reasons for the ongoing process may also remain unclear.
A healthy human neck is quite mobile - he can turn his head 180 degrees, lower it so that his chin can touch his chest, and throw it back. Such actions are possible only if there are elastic joints in the cervical region.
The cervical region consists of seven vertebrae. Their adhesion is carried out by joints, which is why they are so flexible and can perform such a large range of movements. The vertebrae are connected by three joints, which ensures their stability. But the mobility of the spine becomes less, since inside the spine there is a spinal cord, which is extremely dangerous to damage.
Degenerative-dystrophic changes can also develop in the neck
The spinal cord is tissue made up of nerves located inside the spinal “tube”. Nerves branch from it that control the functionality of different parts of the body. The spinal cord transmits signals that ensure the functioning of various areas of the body. The spine protects the spinal cord from injury.
Note! Joints are bone surfaces that are located opposite each other. Some of them are covered with cartilage, allowing the vertebrae to “slide” freely.
But the most important and basic connecting element of the vertebrae remains the gel-like intervertebral disc. It consists of tissue that connects the surface of the vertebrae, while providing them with mobility. Intervertebral discs are extremely important for the movement of the entire spinal column. But, unfortunately, they are most susceptible to deformation and injury.
Over time, the intervertebral disc depletes and loses its softness and elasticity, thereby losing its ability to perform its main function. The vertebrae become so close to each other that friction occurs; the discs between the vertebrae can no longer support the entire load and “shift” it to the joints. The main load in this case is on the facet joints, but since they are not at all designed for such pressure, the cartilage begins to disintegrate, in the process the bones underneath them protrude. An inflammatory process occurs, leading to irritation and pain. Each time, falling apart more and more, the facet joints become unable to cope with the loads on the spine.
Complications of degeneration of the vertebrae in the neck
Spinal stenosis
Disturbances in the functioning of the intervertebral discs also affect the vertebrae, the connection between them becomes weaker, the affected segment is now unstable, and this leads to an incorrect relationship of the vertebrae relative to each other.
Development of the disease
In the case when the nutrition of the spine is disturbed, the loss of height of the intervertebral disc and its impaired movement begin. Over time, the pathology affects adjacent muscles, joints, and nerves. One of the reasons for this is fatty degeneration of the vertebrae, or more precisely, the yellow ligaments that help hold the spine. The spinal canal narrows, causing back pain.
Important! The vertebrae are not equipped with a blood supply, so degeneration progresses much faster here than in the joints.
With age, one can also note a violation of the blood vessels; the supply of necessary substances to the internal structure of the spine becomes worse. Compression of the vertebrae leads to the “squeezing out” of the nucleus pulposus, the nucleus will lose moisture and elasticity, and the disc will “fall out” into the spinal canal. Thus, destruction of the vertebral tissues occurs, the joints will lose their flexibility and now any incorrect movement will cause severe pain.
Symptoms
Degenerative processes that begin in the vertebrae have certain symptoms:
- pain in the chest and back, radiating to the neck;
- impaired coordination, fatigue, migraine, vascular dysfunction and asthenia;
- aching in the back of the head, which becomes more intense when lying down;
- frequent “goose bumps” in the legs, numbness, chills;
- impaired motor system. This pathology leads to high energy consumption to maintain the spine in an even position.
Symptoms may vary for each patient.
The appearance of bone pathologies is a serious disease, because it is inside the bones that many stem cells are located.
Stem cells become blood cells and, due to oxygen saturation, provide increased immunity and good blood clotting. However, when the bone marrow malfunctions, fatty degeneration develops.
The clinical picture of this pathology does not differ in certain features.
As a result of this process, healthy tissue becomes less and less, their condition worsens, and fatty degeneration continues to progress. The composition of the blood sharply becomes worse, therefore, all functions performed by the blood are disrupted. The disease is progressing.
What you shouldn't do
Spinal diseases are a common problem that requires special attention. It often occurs during abnormal physical activity, injury, or as a consequence of a sedentary lifestyle. What actions are not recommended for fatty degeneration of the spine?
The answer is simple:
- First of all, physical activity is contraindicated for patients, as this can aggravate the condition of already displaced discs.
- It is worth protecting yourself from injuries, since degenerative changes in the vertebrae change the condition of the blood and worsen its movement.
- It is not recommended to take medications that can affect processes in bone marrow tissue.
Features of the pathology
During circulatory and metabolic disorders in the spine, osteochondrosis is not the only worrying problem. In addition, fatty degeneration of the cells and ligaments that support the spinal column may occur. As a result of this process, stenosis is formed. Therefore, it is so important not to have any impact on the spine during this period, otherwise problems with the nervous system, as well as partial or complete paralysis, will increase.
The process of fat deposits is also accelerated by the fact that the vertebrae do not have nerve endings and blood vessels, and they also receive nutrition through the end plate. The arteries also undergo changes, and nutrition to the vertebrae is delivered intermittently.
The degeneration process is often accelerated because the vertebrae do not receive nutrition directly
Reduced space between the vertebrae is always a consequence of the presence of fatty degeneration or osteochondrosis. To calm spasms, the body gets rid of calcium, and calcium deficiency already leads to osteoporosis.
Symptoms of pathology
For quite a long time, degenerative changes in the bone marrow are asymptomatic. The patient may complain of increased weakness and fatigue, and may have difficulty stopping bleeding even from small wounds. Susceptibility to infections is a fairly common symptom of such pathological changes in the bone marrow. This is explained by the fact that the organ, including the one that produces those blood cells that are responsible for immunity, partially ceases to function normally.
Most of the symptoms are experienced by many completely healthy people, in addition, these manifestations can be attributed to other diseases. All this is the reason why the true diagnosis - fatty degeneration of the bone marrow - may not be made immediately. That is why most often such a diagnosis is made only when various complications occur.
Possible complications
With the formation of fatty degeneration of the vertebrae, the production of blood cells becomes impaired, anemia and immunodeficiency are observed, the tone in the blood vessels decreases, and the whole body as a whole becomes worse. The tissues inside the body “suffocate” without receiving oxygen in full.
Fatty degeneration of the vertebrae can cause the following pathologies:
- Simmonds-Sheehan disease. Most often, this disease is diagnosed in middle-aged women. A change in hormonal levels appears, and most tissues begin their destruction;
Simmonds-Schien disease
- anemia. The process of insufficient creation of blood cells leads to irreparable consequences;
- osteoporosis – excess fat deposits in the bones do not allow the body to produce collagen, so the body begins to process calcium incorrectly, the bones become fragile;
- Blood clotting becomes worse and any injury can be fatal. Poor coagulation is especially dangerous when there is degeneration of bone tissue. Bones are very fragile, so getting a fracture is not that difficult, and internal bleeding often occurs at the fracture site.
Without treatment for fatty degeneration, complications may arise in the form of various diseases.
Why is it dangerous?
Bone marrow is the main organ of the human body responsible for hematopoiesis. In fact, any of its pathologies automatically means problems in hematology, which, as a rule, develop quite rapidly. Ailments caused by improper functioning of the hematopoietic system affect the general condition of the body.
In more detail, the following arises:
- Anemia, caused by a drop in the level of red blood cells.
- Deterioration of immunity, as the quality of leukocytes and, in general, the process of their formation deteriorates.
- A low number of platelets causes bleeding disorders. As a result, even a small wound can provoke prolonged bleeding, which, of course, becomes dangerous.
Impaired functioning of the hematopoietic system can cause hypoxia of various organs, which means disruption of their function.
Weakening of blood flow can lead to pathological changes in blood vessels.
Localization and varieties
The degenerative process has both post-traumatic and natural occurrence. The natural process is the aging process of tissues and bones; in old age, up to 70% of healthy tissue is replaced by adipose tissue.
But in the event of injury or an infectious process, degeneration progresses very quickly without the possibility of tissue restoration.
Cervical region
Neck pain can pose a much greater threat than just an uncomfortable position or fatigue after a day at work. Degeneration of the cervical vertebrae is the most common occurrence due to the vulnerability of the vertebrae of the neck.
A pinched nerve and compressed blood vessels are often provoked by a slight bruise or intense stress. The danger is due to the fact that there are many blood vessels and arteries in the neck, and damage to them can lead to serious health problems.
Important! The growth of bone tissue increases the friction of the vertebrae against each other, and a feeling of tightness and discomfort appears in the neck.
Causes of early fatty degeneration of the vertebrae in the neck:
- injury;
- long fixation in one position;
- heredity;
- nervousness;
- uncomfortable pillow;
- hypothermia of the cervical spine.
If you experience persistent neck pain, numbness or discomfort, you should immediately consult a specialist, since these pains may not always only indicate fatigue.
Thoracic region
Fatty degeneration of the vertebrae in the chest can be called a pathology that appears due to insufficient supply of nutrients to the cells. Subsequently, the structure of the cartilage changes, and the synovial fluid runs out.
The constant appearance of new cracks can attract inflammation in the plates of the spine, causing pain and pinching.
Fatty degeneration of the vertebrae in the chest and neck differs in the causes of development
Causes:
- uneven posture, which increases the load on the spine. As a result, osteochondrosis and scoliosis appear;
- spinal defects present since birth;
- insufficient amount of incoming useful elements to nourish tissues;
- heredity;
- trauma in the thoracic region;
- constant stress;
- lack of sleep.
Treatment
To get rid of or stop the development of fatty degeneration of the vertebrae, two methods are used: conservative and surgical. Moreover, the latter is resorted to only in extreme cases - for example, if the patient’s condition is getting worse every day, and medications and physiotherapy do not give any result.
Doctors recommend maintaining bed rest for such disorders, but staying in bed for a long time will significantly increase the recovery process.
Table No. 2. Medicines for the treatment of fatty degeneration
Name | Description |
Nonsteroidal anti-inflammatory drugs | |
"Diclofenac" | Diclofenac is taken to eliminate pain caused by degenerative changes in the spine. However, there is a problem with this drug: long-term use increases the risk of harmful effects on the kidneys, liver, and cardiovascular system. Statistics say that the likelihood of heart attacks increases by 40 percent. However, short-term use is not capable of causing such problems. For this reason, it is important to take the drug only under the supervision of a specialist. The drug is available in the form of tablets, suppositories, ointments and gels. Tablets: adults are recommended to take from 50 to 150 mg of the drug per day, divided into 2-3 separate doses. Suppositories: rectally. Adults: 100 mg once a day, 50 mg 2 times a day or 25 mg 3-4 times a day. Ointment, gel: in a dose of 2-4 g, apply a thin layer to the skin at the site of inflammation and lightly rub in, frequency of use - 2-3 times a day. |
"Piroxicam" | It has anti-inflammatory, analgesic and antipyretic effects. Suppresses the synthesis of prostaglandins - substances that are responsible for pain and swelling. Calms pain of moderate intensity. In case of articular syndrome, it weakens or relieves inflammation and pain at rest and during movement, reduces stiffness and “swelling” of joints, and helps increase the range and frequency of movements. The analgesic effect of the drug occurs quickly: usually 30 minutes after oral administration. Orally prescribed in a dose of 10 to 30 mg once a day. Rectally prescribed in a dose of 10-40 mg 1-2 times a day. |
"Naproxen" | It has anti-inflammatory, analgesic and antipyretic effects. The mechanism of action of the drug is to inhibit the movement of leukocytes, reduce the activity of lysosomes and inflammatory mediators, pain and spasms. After oral administration, naproxen is rapidly and almost completely absorbed from the gastrointestinal tract. The tablets should be taken whole with liquid and can be taken with meals. In the acute stage of the disease - 0.5-0.75 g 2 times a day. The maximum daily dose is 1.75 g. |
Muscle relaxants | |
"Tizanidine" | Tizanidine is most often used for spinal cord injuries caused by vertebral displacement or degenerative changes in any part of the spine. The drug in tablets is taken 2 mg once a day, subsequently the dose can be increased according to the instructions of a specialist. |
"Cyclobenzaprine" | The medicine helps to relax the back muscles and relieve discomfort in the area of fatty degeneration of the vertebral bodies. Since the drug has a sufficient number of contraindications and side effects, it is important to take it only under the supervision of a specialist. Cyclobenzaprine tablets are taken 20-40 mg per day in 2-3 doses. |
"Tolperizon" | The drug is recommended for use only in a hospital setting, since it has a central effect - in other words, it relaxes the muscles of the whole body, which can make a person feel unwell. If a specialist has prescribed the drug in the form of tablets, then they should be taken after meals, without chewing, 50 mg 2-3 times a day. This is considered the starting dose. After several days of use and in the absence of side effects, the dose is usually increased to 150 mg 2-3 times a day, depending on the severity of the disease. If the drug is administered by injection, 100 mg is administered in the morning and evening. If a solution is used for infusion, then it should be used at a dose of 100 mg once a day. |
Chondroprotectors | |
Chondroitin sulfate | Participates in the construction of the basic substance of cartilage and bone tissue. Improves phosphorus-calcium metabolism in cartilage tissue, inhibits enzymes that disrupt the structure and function of articular cartilage, and inhibits the processes of degeneration of cartilage tissue. Eliminates and, if necessary, prevents compression of nerve endings and connective tissue, increases the production of intra-articular fluid, increases the mobility of affected joints, and strengthens the bone tissue of the vertebrae. Available in the form of injections and tablets. In the form of injections - 1 ml intramuscularly 1 time per day; in the form of capsules (tablets) - 3 capsules 2 times a day during the first three weeks, later - 2 capsules 2 times a day until the end of the course of treatment. |
Glucosamine sulfate | Glucosamine sulfate is a common chondroprotector that has a positive effect on metabolism in cartilage tissue. It also stimulates increased synthesis of collagen and proteoglycans, stimulates the regeneration of cartilage tissue, and reduces the vascular destructive effect, which is necessary for fatty degeneration of the vertebral bodies. Glucosamine sulfate is stabilized with potassium or sodium chloride. Presented, as a rule, in the form of tablets, injections or powder for oral solution. Take 600 mg of the substance in tablets 2-3 times a day; in solution for intramuscular administration - 400 mg 3 times a week; in powder form - the contents of one powder are dissolved in 200 ml of warm water and taken once a day. |
"Diacerein" | Works both as a chondroprotector and as an NSAID. Stimulates the synthesis of hyaluronic acid, proteoglycans and glycosaminoglycans. Reduces inflammatory processes associated with cartilage and restores them. It is recommended to take 1 capsule orally 2 times a day. The course of treatment ranges from 3 months to 2-3 years, depending on the complexity of the pathology. The effect will not be noticeable immediately - as a rule, only a month and a half after the start of the course. |
Moderate and proper physical activity on a sore spine, applying a heating pad, and electrical stimulation can have a quick positive effect, in contrast to the incessant use of pharmacological drugs.
It is only important to correctly distribute the load on the spine and choose a special massage course. Sometimes manual therapy is effective.
If it is impossible to get rid of the disease using conservative methods, doctors recommend resorting to surgery.
What can be said about surgery? Medicine in most countries prefers to do without surgical procedures. Surgery is possible, but only for seriously ill patients.
Types of operations:
- discectomy with arthrodesis;
- implantation;
- intradiscal decompression;
- laser therapy.
Laser therapy
Recently, minimally invasive procedures have gained popularity - electrothermal plastic surgery of a fractured annulus fibrosus, laser disc decompression, and removal of a deformed disc using endoscopy. The technique of replacing the nucleus pulposus is also widely used in medicine - thanks to it, it has become possible to restore the integrity of the fibrous disc.
According to the Global Burden of Disease Study [1], low back pain currently ranks first among all diseases in terms of years lived with disability (YLD). In patients with low back pain, magnetic resonance imaging (MRI) often shows herniated discs, but until recently, reliable data on the correlation between the presence of herniations on MRI and low back pain were not available.
With the advent of high-field MRI, some patients with low back pain began to detect pathological changes in the bone marrow and vertebral end plates (VEP), which turned out to be significantly associated with the incidence and duration of the pain syndrome [2–9]. These signal changes were first reported by A. de Roos et al. in 1987 [3].
M. Modic et al. in 1988, classified these changes into three types, each of which differed from the others in signal characteristics on MRI [2, 10]. Subsequently, given the great importance of the created classification, it was called Modic changes (Mch).
Мсh is a lesion of the bone marrow and CAT without destruction of bone tissue, visualized by MRI. In the domestic literature there are only a few publications about changes in the CP and only one type of them is described, classified as aseptic spondylitis and corresponding to MSh1.
In this article we will use this classification, as it describes in more detail and reliably all types of gearbox changes.
Classification and characteristics of individual types of MSh
MCh1 MRI changes are characterized by a hypointense signal on T1-weighted images (WI), a hyperintense signal on T2-WI and images obtained in T2 fat-suppressed (T2-FS) or STIR modes (Fig. 1). Signal intensity increases after gadolinium administration, these MRI findings consistent with bone marrow edema. Results of micro-computed tomography (micro-CT) [11] and histopathological analysis [2, 12] demonstrate destruction and cracking of the PPC associated with thickening of bone trabeculae and an increase in the number of osteoblasts and osteoclasts supporting increased bone remodeling activity. It also reveals the replacement of normal bone marrow tissue with richly vascularized granulation tissue.
Rice. 1. Changes on MRI according to MCh1 type. 1 — hypointense signal on T1-weighted image; 2 — hyperintense signal on T2-WI; 3 - hyperintense signal in the mode with suppression of the signal from fat (STIR).
A. Fields et al. [12] revealed a significant increase in the density of innervation of the CP in MSh1 compared with unchanged CP and normal bone marrow.
S. Ohtori et al. [13] revealed an increase in the number of cells expressing tumor necrosis factor-α (TNF-a) in the CAT in MSch1. Other recently discovered pro-inflammatory, pro-apoptotic and pro-metabolic changes in cells from the MCh1 checkpoint are characterized by an increase in the expression of the migration inhibitory factor and its receptors CD74 [15], the number of Fas receptors [15], disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS-5) [16 ].
An association has been found between MCh1 and rapidly progressive degeneration of adjacent intervertebral discs [17, 18].
Signal changes of the MCh2 type are characterized by a hyperintense signal on T1- and T2-weighted images and are caused by fatty degeneration of the bone marrow (Fig. 2). Histopathological analysis demonstrates destruction of the CAT and formation of granulation tissue without hypervascularization, replacement of bone marrow with adipose tissue [2, 12].
Rice. 2. MCh2 type changes on MRI. 1 — hyperintense signal on T1-weighted image; 2 — hyperintense signal on T2-WI; 3 - hypointense signal in fat suppression mode (STIR).
Micro-CT images of MCh2 are characterized by a decrease in bone remodeling activity compared to MCh1 [11].
Signal changes of the MCh3 type are the least common and are characterized by a hypointense signal on T1- and T2-weighted MRI (Fig. 3) [10]. This type has not been studied histologically. Micro-CT reveals changes associated with an increase in the level of bone tissue formation and a decrease in its resorption [11]. In images obtained during radiography and multislice computed tomography (MSCT), this type is characterized by significant compaction of bone tissue - osteosclerosis [19, 20].
Rice. 3. Changes on MRI according to the MCh3 type. 1 — hypointense signal on T1-weighted image; 2 — hypointense signal on T2-WI.
In addition to the three described types of MSh, there are mixed subtypes: 1−2, 2−1, 1−3, 3−1, 2−3, 3−2 and 1−2-3, visualized as a combination of changes in the MR signal corresponding to edema , fatty degeneration of the bone marrow and CAT sclerosis. MRI signs of edema are found in 92.7% of the total number of mixed cases of MSh, especially in types 1−2 and 2−1 [19]. When performing MSCT of mixed subtypes of MSh, sclerotic changes in the CAT are detected in 36.6% of cases [19]. It is assumed that mixed MCh subtypes represent transitional stages between pure types [9, 21, 22].
In addition to the main one, the MSh classifications proposed by other authors are sometimes used.
In 1990, a classification was created that included, in addition to pathological types, the normal state of the bone marrow and CAT: type 0 - normal, no degeneration; Type 1 - equivalent to type MCh1; 2nd type - type MCh2; 3rd type - type MСh3 [23].
D. Weishaupt et al. [24], in accordance with the magnitude of changes in the CP on midsagittal images, divided MCh into four degrees: normal - no changes on T1- and T2-weighted images; lungs - the volume of signal intensity changes is less than or equal to 25% of the vertebral height; moderate - from 25 to 50%; heavy - equal to or more than 50%.
Prevalence and localization of MSh
Depending on the type of population studied, the prevalence of MCh varies from 1.4 to 68% [2, 21, 25–30]. In general, MCh2s are more common than MCh1s, although some studies [24, 31] suggest the opposite. The incidence of MCh increases with increasing age and body weight [4, 28, 32].
MCh are found at both the lumbar and cervical and thoracic levels of the spine. As a rule, they are localized in only one vertebral segment, but in some cases - in several at once. Types MCh1 and MCh2 are most common in the lumbar spine.
MCh of lumbar localization have several features. Firstly, they most often occur at the L4-L5 or L5-S1 levels [2, 32], in addition, the MCh value at these levels is usually larger [33]. Secondly, MCh1 and MCh2 are more often observed in the anterior 1/3 of the vertebra, the prevalence of MCh2 is greater in the upper CP than in the lower [34]. MCh are also characterized by a parallel arrangement on both sides of the disk and a depth ranging from 3 to 30 mm [33]. Thirdly, according to C. Chung et al. [34], asymptomatic MCh are characterized by a location at a higher level (upper end plates at the level of L3 and L4) and more ventrally, while in painful forms, MCh are located at a lower level (L4-5 and L5-S1) [2 , 33].
MCh and lower back pain
Clinical studies have shown that patients with MCh and low back pain have certain clinical and morphological features, which made it possible to distinguish them into a separate subgroup. The detection rate of MCh in patients with nonspecific low back pain varies from 18 to 62%, with different proportions for each type [2, 21, 26–29]. In the asymptomatic population, the prevalence of MCh is lower, 1.4–13% [34]. Chronic low back pain is present in 8.8% of patients with verified MSh, without MSh in 12% [5, 31]. It is noted [29-31, 35] that low back pain occurs more frequently in MCh1 compared to MCh2. In the clinical picture of MCh1, the pain syndrome often becomes inflammatory in nature [36]. The persistence of MCh1 over a long period of time in patients with low back pain correlates with an unfavorable clinical outcome [5], and with the transformation of MCh1 into MCh2, the intensity of pain and the level of social maladjustment decrease [6, 32]. These facts suggest that low back pain is etiologically associated with MCh1, and not MCh2.
Natural history of the disease and transformations between MCh types
As a rule, MCh develop over a long period of time, on average over 1–3 years [2, 21, 38]. Many authors suggest that they may be successive stages of the same process. This is evidenced by the results of several studies [21, 25, 39], which showed that from 7 to 37% of MCh1 are completely converted into MCh2, 9-15% are partially transformed, 1% are transformed into MCh3, from 8 to 46% remain without changes.
These studies also indicate that the dynamics of the process are not linear in time, since different types of MCh can recur, progress, or coexist. Additionally, there is no clear explanation why MCh1 may remain stable in some patients.
MCh2 and MCh3 correspond to clinical and biological stages of healing associated with a decrease in clinical symptoms.
Possible causes of MCh
CATs play an important role in the biomechanics of the spine. During degenerative processes in the intervertebral discs, an uneven distribution of loads on the gearbox is observed, which leads to the formation of microcracks in them, as well as edema and hypervascularization of the adjacent bone marrow [2, 40]. This hypothesis is supported by several clinical studies [22, 41], showing that surgical stabilization can lead to reduction of MCh1 and pain relief.
Other researchers [42–44] suggest that activation of inflammatory mediators in response to the penetration of nucleus pulposus substance into the PP can lead to local inflammation, manifested by edema and activation of bone remodeling processes. Pain symptoms may be associated with increased levels of proinflammatory cytokines such as TNF-α and the number of nerve fibers expressing gene product protein 9.5 in the CAT in patients with MCh [13].
It has been suggested that MCh may be associated with a local anaerobic infectious process [45]. Destruction of the annulus fibrosus, preceding the formation of disc herniation, leads to neovascularization around the extruded nucleus pulposus and the occurrence of an inflammatory reaction. The resulting conditions are a favorable environment for the development of anaerobic bacteria [46]. However, this hypothesis remains questionable due to the absence of other symptoms of infection, such as specific features on MRI or changes in general or biochemical blood tests.
Some researchers [47] point out the similarity of changes in the bone marrow in MSh and osteoarthritis of the joints. Indeed, in arthrosis of large joints, an increase in the concentration of pro-inflammatory factors, TNF-α, an increase in the density of nerve fibers [48], and proliferation of granulation tissue are found. In addition, there is a connection between increased intraosseous pressure and the occurrence of pain in arthrosis of large joints [49–51]. A similar relationship between intraosseous pressure and pain was found for low back pain [52–54].
Considering the facts stated above, it can be assumed that one of the causes of low back pain in MSh may be increased intraosseous pressure, which is detected with similar changes in large joints. The pathological mechanism in this case is presumably the following: disruption of the venous outflow from the vertebrae leads to the development of local blood stasis and ischemia of bone marrow tissue. This in turn leads to the occurrence of aseptic inflammation, manifested by bone marrow edema and increased activity of remodeling processes in the CAT. In addition, disruption of venous outflow leads to an increase in intraosseous pressure, which causes barostimulation of intraosseous non-encapsulated nerve endings, which contributes to the occurrence of both local and referred pain syndrome in the leg [55].
Examination of patients with MSh
MCh are detected by MRI examination, but differences in the characteristics of MR imaging scanners can lead to significant differences in the number, magnitude and type of MCh detected.
T. Bendix et al. [56] compared lumbar MCh in MRI with low (0.3 T) and high (1.5 T) magnetic field strength. They concluded that MCh were diagnosed significantly more frequently on high-field MRIs than on low-field MRIs. МCh1 predominate in the images of low-field tomographs, and МCh2 - in high-field ones.
To assess MSh in studies, in addition to standard T1-, T2-MRI modes, it is recommended to use T2-FS, TRIM or STIR - modes with fat suppression [19], which allow more clearly visualizing bone marrow edema in MSh1 and MSh mixed subtypes.
Since MRI does not clearly differentiate calcification and osteosclerosis in MCh3 and MCh mixed subtypes, in addition to MRI, it is recommended to use MSCT [19, 20].
Differential diagnosis of MCh
On MRI, several pathologies may be similar to MCh, such as infectious diseases of the spine - bacterial spondylodiscitis, Schmorl's hernia, tumors, etc. [57, 58], although, as a rule, they have distinctive features that allow a correct diagnosis.
In infectious spondylodiscitis, there is swelling of the surrounding paravertebral soft tissues or an epidural mass effect with a hyperintense signal on T2-weighted images; the signal from the intervertebral disc on T2-weighted images will be normal or hypointense. On T1-weighted images, the vertebral bodies and intervertebral disc space are characterized by a confluent hypointense signal [57, 58]. In addition, with infectious spondylodiscitis, erosion or destruction of the CAT is always observed. The most pronounced changes are observed with specific tuberculous spondylodiscitis, the least - with a nonspecific infectious process. In contrast, with MCh, changes always propagate linearly, parallel to the end plates, and do not lead to destructive changes in the vertebrae [33].
Schmorl's hernia is characterized by a localized defect (hypointense on T1-weighted images and hyperintense on T2-weighted images) in the endplates with a well-defined hernial sac and surrounding wall with hypointense signal (on T1-weighted and T2-weighted images) in the vertebral body [59].
The most common type of tumor found in the spine is metastasis. However, only rare cases of metastatic disc disease have been reported [37]. Thus, metastases are easily distinguished from MCh by the absence of disc involvement.
MCh Treatment
Most MCh1 spontaneously converts to MCh2 within 18–24 months [2, 22]. However, clinical intervention may influence the course of MCh. Thus, some authors [22, 60, 61] demonstrated an improvement in clinical symptoms and transformation of MCh1 into types 0 and 2 after stabilizing operations on the spine. This indicates stabilization of the MCh flow when mechanical conditions change.
A study was conducted [62] on the effectiveness of intradiscal injections of methylprednisolone. The group with MCh1 showed a more pronounced clinical effect than the group without MCh. A positive clinical effect from the use of bisphosphonates is also expected.
Among the promising treatment methods, the possibility of surgical decompression is being discussed, as well as the use of a prostaglandin analogue, iloprost.
Based on the concept of the occurrence of MSh and low back pain with increased intraosseous pressure, as well as taking into account the proven regression of pain after a decrease in intraosseous pressure in arthrosis of large joints [63], E.L. Sokov et al. [64] were the first to use intraosseous blockades (IOB) to treat patients with Mch1. Also, previously, in a series of clinical studies, the authors [65–75] demonstrated their high effectiveness in the treatment of various pain syndromes. It was concluded that VKB in Mch1 affect the improvement of venous outflow from the vertebrae, this leads to normalization of intraosseous pressure, reduction of edema of the bone marrow substance and intervertebral discs on MRI. Local administration of glucocorticoids as part of a blockade mixture additionally leads to a decrease in local inflammation and edema of the vertebral body, adjacent intervertebral disc and paravertebral tissues [64]. As a result, irritation of intraosseous receptors is reduced, which contributes to the regression of lower back pain for a long period of time.
Thus, there are several points of view on the pathogenesis of MCh, including biomechanical, mediator, bacterial theories and the theory of intraosseous blood flow disturbance (osteogenic). Based on this, foreign and Russian researchers are attempting to select optimal treatment methods: stabilizing operations on the spine are used, long-term antibiotic therapy, intradiscal injections of corticosteroids, etc. are carried out, but complete control over MCh and its clinical manifestations has not yet been achieved.
Further scientific and clinical research is needed to determine or confirm the true causes of MCh. Full disclosure of the pathogenesis of MCh will allow clinicians to correctly interpret MRI data and select optimal treatment methods, which will help to significantly reduce the incidence, prevalence and duration of disability in low back pain.
The authors declare no conflict of interest.
Measures for prevention and prevention of pathology
In the field of medicine, unfortunately, they have not learned how to completely treat such diseases, but they can successfully maintain the patient’s condition, restoring his ability to work and his usual way of life. However, it is best to prevent this disease than to endlessly treat it in the future.
Unfortunately, the aging process of bones and deformation of intervertebral tissue cannot be stopped. But every person is able to slow down this process, delaying it for many years. The spine experiences daily stress - sometimes it can be very strong - so it is important not to forget about prevention, which can slow down the process of tissue wear, keeping the musculoskeletal system in perfect order. Simple exercises will strengthen your back muscles, give elasticity to your ligaments, keeping your back healthy and strong for a long time.
Preventive measures.
- Strengthening your back muscles through physical exercise: even 15 minutes of exercise after waking up will make your back stronger and more resilient.
- You should always try to get out of bed on both legs - this allows you to evenly distribute the load on your back.
- It is important to always try to keep your back straight, and under no circumstances allow your posture to bend. Walk, sit, read a book, keeping your back straight. This will prevent spinal deformation.
- The right mattress is the key to not only good sleep, but also good health. The mattress should provide complete relaxation to the spine, giving it the opportunity to rest after a working day. An overly hard or very soft mattress will not be able to provide the necessary conditions for resting your back.
In order not to encounter such a pathology, it is worth paying attention to prevention
Degenerative-dystrophic changes in the spine are a serious pathological disorder of the locomotor system, which is almost impossible to correct. The violation leads to constant pain, discomfort during movement, and loss of ability to work. Therefore, it is more correct to prevent such disorders in your body, so as not to have to deal with them for the rest of your life. But if, nevertheless, back pain makes itself felt, there is no need to delay the moment of going to the doctor - this can only aggravate the condition of the body, adding new ones to the existing problems.
Bone marrow degeneration
Bone marrow is a tissue mass that fills the cavity of the bones of the spine. The bone marrow is responsible for hematopoiesis, and it constantly replaces dead cells with new ones, and also maintains and builds immunity.
When any pathologies develop in the bone marrow, they are immediately reflected in hematopoiesis, blood clotting, the functioning of blood vessels and the body as a whole. The altered composition of the blood causes poor passage through the vessels, which also has a detrimental effect on the functioning of the body.
In case of any pathology of the bone marrow, the whole body suffers greatly
The degenerative process begins to set in for everyone with age. If degeneration occurs at the appropriate age, then there are not as many problems from it as, for example, if it began earlier than the physiologically prescribed time. When the pathological process begins, the myeloid tissue in the bone marrow changes to adipose tissue.
With age, degenerative processes become more active, which is why by the age of 70 most of the tissues in the spine are replaced by fat, and at an even older age they completely occupy all the space.
The replacement of myeloid tissue with adipose tissue occurs due to impaired metabolism, the presence of metastases in the bone marrow, and chronic infection.
What diseases cause degenerative fatty process in the bone marrow?
- Hypoplastic and aplastic anemia.
- Osteoporosis.
Some diseases that arise in parallel with fatty degeneration of the vertebral bodies often become the “trigger” of bone marrow pathologies
Hypoplastic and aplastic anemia
Hypoplastic and aplastic anemia
Osteoporosis
Not long ago, scientists believed that adipose tissue could protect the spine from osteoporosis. However, over time it became clear that this was not the case. The presence of fat cells impairs collagen production and proper calcium absorption. As a result, bone tissue weakens and degenerative processes begin, which leads to osteoporosis.
Conservative treatment
If fatty degeneration of the bone marrow develops in old age, then this pathology cannot be completely cured. Such changes are irreversible. You can only stop the progression of dystrophy.
If pathological changes are caused by intoxication, infections, tumors and endocrine diseases, then it is necessary to treat the underlying disease.
As we have already mentioned, most often foci of fatty degeneration form in the vertebral bodies. Such pathological changes are accompanied by pain and discomfort in the back. In this case, treatment should be aimed at relieving pain and improving the condition of cartilage and ligaments. The following groups of drugs are prescribed:
- Nonsteroidal anti-inflammatory drugs: Diclofenac, Ibuprofen. They help eliminate discomfort in the back.
- Blockades with Novocaine. This treatment method is used for severe pain.
- Muscle relaxants: “Sirdalud”, “Mydocalm”. The drugs help relieve muscle spasms.
- Chondroprotectors: “Chondrolon”, “Hondrex”, “Teraflex”. These medications help restore damaged cartilage.
- Calcium preparations. Prescribed to patients with severe osteoporosis.
- Medicines that stimulate the process of hematopoiesis: “Maltofer”, “Sorbifer Durules”, “Folacin”, “Ferretab comp”. They are prescribed for signs of anemia.
The doctor selects an individual diet for the patient. It is recommended to consume foods rich in gelatin, iron and vitamin B12.
After pain relief, therapeutic exercises are prescribed. Treatment is complemented by physiotherapy: massage, electrophoresis, acupuncture, magnetotherapy.