Ozone Therapy Hypertonic Musculature
Trigger points are one of the most frequent causes musculoskeletal pains. However, in the last few years has appropriate attention been given to this trigger points, except for the earlier work by a few pioneers in this field.
Myofascial pain syndromes (MPS) as percentage of all forms of chronic pain affecting the locomotor system
Skootsky 1989 30%
Fishbain 1989 85%
Fricton 1990 55%
Gervin 1995 93%
Since the practical significance of trigger points was discovered, there has been a veritable boom both in basic research and in the therapeutic possibilities. As jet, the diagnosis myofascial trigger point can be made only clinically, but not based on laboratory-chemical or radiological findings.
Tissular pO2 measurements of the chronically hypertonic M. erector spinae in 20 patients, compared with 10 healthy controls were carried out by Brückle.
Interestingly, the pO2 levels in the hypertonic musculature rose proportionately to the degree of hypertonia musculature. The mean tissular pO2 level was 38.5 mmHg, which was 9 mmHg more than that of the healthy controls, with a standardised mean reference value of 29.5 mmHg.
The objection, that the pain is caused by small, scattered islands of hypoxia in the hypertonic musculature, could be refuted by the measurement technology used.
Various authors have found significantly low levels of adenophosphate in the
hypertonic musculature, with high pO2 level. It can therefore be resumed that the raised pO2 levels result from deficient oxygen utilisation due to an inadequate supply of high-energy phosphates.
Myogeloses are olive- to plum-sized areas of hardening in the muscles.
The histological pictures show a degeration of the myofibrils, or necroses with a “moth-eaten” appearance (ragged red fibres), as well as large amounts of glycogen and mitochondrial material.
The tissular pO2 measurements showed raised pO2 levels at the margin of the myogeloses, which towards the centre fell to hypoxic levels of under 5 mmHg*.
Text Box: pO2 = 5 mm Hg
Gradual lowering of the pO2 level from the margin towards the centre of the myogelosis.
The explanation for this is the occlusion of the microcirculation at the margin of the myogeloses. This is possibly triggered by compression due to spasm of muscle fibres surrounding the blood vessels within the muscle. Compression of the microcirculation causes local hypoxia, with subsequent acidosis due to the formation of lactate. The lowering of the pH value leads to loss of flexibility of the erythrocytes and occlusion of the already stenosed vessels. Also vasoneuroactive substances histamine, bradykinin, substance P (SP) and calcitonin gene-related peptides (CGRP) are released. As a result, an oedema is formed which further compresses the vessels and exacerbates the hypoxia. The oxygen can then pass from the margin into the interior of the myogelosis only by diffusion, because of which there is a gradual lowering of the pO2 level towards the centre.
The deficiency of high-energy phosphates causes a disturbance of the function of the calcium-ion-pump both in the chronically hypertonic musculature and in the myogelosis. There is a partly exhaustive autonomous contraction which in turn leads to a further reduktion of the alkali reserve, with further disturbance of the muscle metabolism.
As already mentioned, mediators of inflammation and vasoactive substances are formed, which sensitises the nociceptors in the sense of hyperalgesia. On the other hand, the inflammatory metabolism leads to the creation of oxygen radicals, the formation of which is promoted by the raised pO2 level in the hypertonic muscle. The excess of oxygen radicals causes a dekompensation of the enzymatic scavenger system. The obvious assumption is that the free radicals can lead to further destruction of muscle tissue and nerve tissue – with an increase in the hyperalgesia.
Working Hypothesis on Ozone Therapy Hypertonic Musculature
The following factors, among others, are important for the physiological development of muscular contraction:
Ø A supply of oxygen sufficient for an aerobic contraction.
Ø An amount of glycogen, which as an energy carrier with an adequate supply of oxygen provides the necessary energy.
Ø High-energy phosphates, which facilitate utilisation of the oxygen.
Ø Adequate amount and composition of electrolytes that are important for the muscular contraction.
Ø Elimination of iron, folic acid and vitamins B1, B6, B12, c deficiency, hypothyroidism and hypoglycaemia.
Ø Elimination of any excess of free radicals.
Ozone acts on the metabolism in the following ways, among others:
Ø Amounts of ozone stimulate the formation of glutathione peroxidase, which activates glycolysis.
Ø Glycolysis leads to the formation of 2,3-DPG and ATP.
Ø 2,3-DPG facilitates the release of oxygen to the tissue.
Ø Low ozone concentration activate the enzymatic scavenger system, mainly the glutathione peroxidase, catalase and superoxide dismutase. They break down the oxygen radicals that are formed by degenerative and inflammatory processes.
Ø The rheological properties of the blood are increased.
This mode of action of ozone aims at the above-mentioned pathological processes in the hypertonic musculature and in the myogeloses, and forms the therapeutic basis for extensive normalisation of the pathological states in the hypertonic musculature and the myogeloses.
Method Used Ozone Therapy Hypertonic Musculature
From the point of view of clinical practice, the following main criteria, in decreasing order of specificity, may be used for the diagnosis of trigger points:
Main clinical criteria for the diagnosis of myofascial trigger points, in decreasing order of specificity Local pain on pressure within a hard, hypertonic muscle strand
A hard, hypertonic muscle strand, palpable from its origin to its point of insertion
Local twitch response with twitching of the muscle fibres within a taut band as a reaction of mechanical stimulation of the MTrP
Radiating of a characteristic referred pain as a reaction of mechanical simulation
Renewed recognition of the pain by the patient
The frequency of the treatment is determined by the number and the mass of the affected muscles. It can be between once and five times a week.
Two types of injections can be used: Precisely targeted injections into the trigger points respectively myogeloses and multiple or fan-shaped infiltrations into large muscles.
Whenever possible, fine calibre cannulas should be used corresponded to the intended depth of the injection.
At first is lidocaine or procaine injected. The amount of lidocaine ½ percentage: 1 to 20 cc and lidocaine 1%: 1 to 10 cc. Procaine 1%: 1 to 10 cc. After injection of local anaesthetic, an ozone/oxygen mixture will be injected through the same cannula. Depending on the size of the muscle and the mode of application (injection in the hypertonic mass or at a given point), the amount of ozone injected should be 1 to 10 or eve 20 cc of a 15 to 20 µg/ml solution per muscle. The ozone should be insufflated slowly in order to avoid pain as far as possible.
During the injection the muscle should be massaged in order to obtain better distribution of the ozone.
Whenever possible, passive stretching of the shortened muscles should be carried out at the end of the tonanalgesic therapy and the patient should be given appropriate instructions for daily active muscle stretching exercises. Muscle-stabilizing exercises should also be performed during and after the end of the treatment.
Reactive muscle pain may happen, as an occasional, insignificant side effect.
It is interpreted as being a result of insufficient distribution of the ozone/oxygen mixture in the muscle or due to the injection of a relatively too large amount of ozone. The results are some times markedly better than after painless injections.
* This pO2 value corresponds to the oxygen tension observed in peripheral occlusive arterial disease POAD), in the painful phase.
Ozone Therapy Diabetes Mellitus
Ozone Therapy Effects in the Oxidative Stress Associated to Diabetes Mellitus
Saied M. Al-Dalien1, Silvia Menéndez2, Gregorio Martínez1, José I. Fernández-Montequín3,
Eduardo J. Candelario1 and Olga S. León1*
1Center for Research and Biological Evaluation, University of Havana, Institute of Pharmacy
and Food Sciences. Apartado Postal 6079, Havana City 10600, Cuba
2 Ozone Research Center, National Center for Scientific Research. Apartado Postal 6880,
Havana City, Cuba
3 Institute of Angiology and Vascular Surgery. Calzada del Cerro 1551 Cerro. Havana City,
It is well recognized the presence of oxidative stress in diabetes mellitus. Ozone can exert its protective effects by means of an oxidative preconditioning, stimulating and/or preserving the endogenous antioxidant systems. The aim of this paper is to evaluate the ozone effects, in a preclinical and preliminary clinical studies, in the oxidative stress associated to diabetes. Rats were divided in: 1-negative control group; 2- positive, using streptozotocin (STZ) as a diabetes inductor; 3- ozone, 10 treatments (1 mg kg-1), after STZ-induced diabetes and 4-oxygen (26 mg kg-1), as group 3 but using oxygen. Patients with diabetic foot were divided in 2 groups: ozone (using rectal and local ozone) and antibiotic (systemic and locally). Ozone treatment improved glycemic control and prevented oxidative stress associated to diabetes mellitus and its complications, in both studies, in agreement with the excellent results obtained clinically.
Diabetes mellitus is characterized by metabolic abnormalities, a disorder of carbohydrate metabolism, with the presence of hyperglycemia and glycosuria, resulting from inadequate production or utilization of insulin. Long-term complications, that cause morbidity and premature mortality, is characterized by microvascular disease with capillary basement membrane thickening, macrovascular disease with accelerated atherosclerosis, neuropathy involving both the somatic and autonomic nervous systems, neuromuscular dysfunction with muscle wasting, embryopathy and decrease resistance to infections. Such chronic complications involve the eyes, kidneys, heart, nerves and blood vessels. Accelerated atherosclerosis produces 80 % of all diabetic mortality, three fourths off it owing to coronary disease. A more frequent concomitant of distal anesthesia is the development of neurotropic ulceration, particularly on the plantar aspect of the foot. Anesthesia leads to a worsening of any minor injury because of the absence of protective painful stimuli. This problem in addition to pre-existing microvascular and macrovascular circulatory impairments characterizes the underlying mechanisms that may lead to rapid gangrene after foot injury (1,2).
It has been demonstrated, in diabetic patients, the role of the reactive oxygen species (ROS) with an increase oxidative damage at the level of lipid peroxidation, DNA injury and protein damage (3-5). Activation of polyol pathway, non-enzymatic glycosylation of proteins and the increase of ROS play an important role in diabetes complications (6,7). Also, a decrease in the antioxidant defense system, involving the erythrocyte superoxide dismutase and catalase (8,9), with a simultaneous decrease in vitamin C concentration in leukocytes (10) and a decrease in the scavenger capacity of radicals in plasma have been mentioned (11).
Ozone can exert its protective effects by means of an oxidative preconditioning, stimulating and/or preserving the endogenous antioxidant systems and by blocking the xanthine/xanthine oxidase pathway for ROS generation, as it has been demonstrated in the damage induced by carbon tetrachloride (CCl4) and in the hepatic and renal ischemia-reperfusion (12-15). Also, ozone oxidative preconditioning has been proven to preserve glycogen content and to reduce lactate and uric acid formation, controlling oxidative stress induced by CCl4 administration to rats (16). In addition, it has been demonstrated that endovenous ozone therapy, in patients with myocardial infarction, has a beneficial effect on blood lipid metabolism, decreasing blood cholesterol and provoking the activation of antioxidant protection system (17). Ozone has been used with good results in the treatment of patients with diabetic foot, taking into account its germicide properties and its influence in the processes of oxygen metabolization, besides other effects (18).
The socioeconomic impact of diabetes is devastating to individual patients and society as a whole. Any treatment that is capable to normalize oxygen metabolism, to modulate the oxidative stress and to have germicide properties can improve the quality of life of these patients, as well as diminish patient consumption of medicines. Taking into account the ozone therapeutical properties, the aim of this study is to evaluate the ozone effects in the oxidative stress associated to diabetes mellitus, using a preclinical and a preliminary clinical studies.
Medical Ozone And Immune System
OZONE AS A MODULATOR OF THE IMMUNE SYSTEM
Alessandra Larini, Carlo Aldinucci and Velio Bocci
Institute of General Physiology, University of Siena, 53100, Siena, Italy
In order to clarify the immunomodulating properties of ozone, we have investigated: a) the effects of stimulation on isolated peripheral human blood mononuclear cells (PBMC) from normal donors with either ozone or ozonated serum; b) the range (in terms of O3 concentrations) of the therapeutic window; c) the stimulatory and toxic effects and d) the pattern, of both proinflammatory and immunosuppressive cytokine production up to 86 hours after exposure to O3. Results show that ozone can act as a weak inducer of cytokines producing IL-6, IL-4, TNF-α, IFN-γ, IL-2 and IL-10 and, most importantly, there is a significant relationship between cytokine production and ozone concentration. Analysis of the proliferation index shows that progressively increasing O3 concentrations inhibit IP and therefore appear cytotoxic.
Leukocytes comprise a heterogeneous cell population composed of lymphocytes (20-25%), monocytes (about 5%) and three type of granulocytes of which the neutrophils are about 70%. We have been the first to show that an appropriate ozone dose can induce a small release of interferon γ (IFN- γ) from human blood (Bocci and Paulesu, 1990). Later on the number of cytokines has expanded to IFN-β, interleukin 2 (IL-2), IL-6, IL-8, tumor necrosis factor α (TNF-α), transforming grow factor β1 (TGF-β1) and granulocyte-monocyte colony stimulating factor (GM-CSF) (Paulesu et al., 1991; Bocci et al., 1993a, b; 1994; 1998a, b). Later on several authors (Beck et al., 1994; Arsalane et al., 1995; Jaspers et al., 1997) have confirmed that ozone can induce the production of cytokines after that epithelial cells of the respiratory mucosa have been in contact with ozone.
Our results were obtained by ozoning blood directly and cytokines were detected in the plasma during the following 4-8 hours of incubations. These initial studies shed light on several aspects such as the protective effect of blood antioxidants, the dissimilar production of different cytokines and the progressive inhibitory activity of increasing ozone concentrations, particularly above 80 µg/ml per ml of blood. However they had limitations because firstly, whole blood can be incubated only for a limited time and, most importantly, we could not decide which cell type produced the cytokines.
During the last year we decided to isolate from normal blood donors either peripheral blood mononuclear cells (lymphocytes and monocytes, PBMC) in order to investigate their viability and the production and type of cytokines released after two different ozonation modalities. The first is a direct ozonation of PBMC suspended in human serum, so that cells undergo the total action of ozone due to immediate effects by hydrogen peroxide (H2O2) and other unidentified reactive oxygen species (early ROS), with very short half-life, and late effects, provided by lipid oxidative products (LOPs), with fairly long half-life. The second approach has examined the effect of ozonated serum 20 min before addition to PBMC and therefore ozone activity is expressed only by “late LOPs”.
Ozone Therapy Female Infertility
Ozone Therapy in Female Infertility
Rajani Chandra-D’Mello & Ronald D’Mello1
Institute of Obstetrics & Gynaecology, Baku, Azerbaijan.
1Institute of Surgery, Baku, Azerbaijan.
The purpose of this work was to study the effect of ozone therapy female infertility of inflammatory aetiology.
We administered ozone to 56 patients (50 out of which were infertile), who had previously unsuccessfully undergone various kinds of treatments for inflammatory diseases of the genitalia,.
Ozone therapy in the concentrations used by us has good curative effect on infections caused by bacteria, chlamydia, mycoplasma, ureaplasma, toxoplasma, herpes simplex and cytomegalovirus and eliminates inflammation thus facilitating patency of the fallopian tubes which in turn has a positive effect on female infertility of inflammatory origin.
Infertility even today remains one of the most significant medical as well as social problems of the world. Approximately 8 – 10 % couples are classified as infertile. This means, that infertility is quite a global phenomenon and affects about 50 – 80 million people around the world. Infertility might be a result of host of factors although for a majority of infertile women inflammation of the genitalia remains the most important cause.
From the very beginning of human civilisation, inflammation has been synonymous with disease, which is true to this day. Among women suffering from inflammatory diseases of the genitalia, 75 % are young and not undergone parturition. Lately, both the frequency as well as the clinical picture of inflammatory diseases of the genitalia have undergone considerable changes. In almost 80 – 82 % patients, the inflammation process is chronic. Significant rise is noted in sexually transmitted gynaecological diseases, e.g. in 1989 there were about 50 million fresh cases of chlamydiosis in the world and in 1995 there were about 89 millions. Moreover, these diseases increase the patient’s susceptibility to HIV and quite often complicate into infertility. The infections are quite often found in various combinations, such as chlamydiosis along with Herpes simplex (17%), along with gardnerella (14%), along with ureaplasmosis (33%), along with mycoplasmosis (21%) and along with candidosis (13%).