Analogues of Piascledine


pharmachologic effect

Manufacturer: Laboratory Expansion, France
Release form: capsules

Active ingredient: avocado and soybean oils

Piascledine is a corrector of cartilage tissue metabolism. The mechanism of action of this chondroprotector is based on the blockade of collagenase synthesis and an increase in collagen production. In addition, the plasminogenesis activator is blocked, which prevents destructive processes in cartilage.

Piascledine also promotes the synthesis of molecules in articular and other hyaline cartilage, as well as in periodontal tissue, which anchors teeth in the jaw.

Thus, Piaskledin has an analgesic and anti-inflammatory effect and restores motor activity of the joints.

Mechanism of drug action

According to the instructions for Piaskledin 300, the product belongs to herbal preparations. The main purpose is to regulate metabolism in cartilage tissues.

Taking capsules helps:

  • relieving pain and inflammation in joints;
  • inhibition of destructive processes in cartilage;
  • restoration of motor activity;
  • stimulating collagen production in joint tissue cells.

The medicinal effect occurs due to unsaponifiable compounds of avocado oil and soybeans, which:

  • increase the volume of collagen produced in cartilage tissues, due to which their firmness and elasticity increase;
  • reduce the synthesis of collagenase, an enzyme that can break down collagen;
  • regulate the activity of plasminogens, thereby preventing the destruction of cartilage tissue;
  • promote the synthesis of periodontal tissue and serve as a preventive measure for tooth loss.

The unsaponifiable part of the oil contains vitamins, carotenoids, minerals, acids, phytosterols and other biologically active substances. The presence of unsaponifiable lipids helps suppress the inflammatory process that accompanies the destruction of cartilage tissue when affected by arthrosis or arthritis.

Analogues of Piascledine

Before replacing Piaskledin cheaper or at the same price, you should first decide on the diagnosis. Since treatment will be effective only if adequately prescribed.

There are no analogues of Piascledine 300 in composition. The drug can be replaced with chondroprotectors that act similarly to Piascledine or by a different mechanism, for example, Structum, Alflutop, Arthroker, Dona and other drugs.

There are analogs that are cheaper than Piascledine, mostly these are dietary supplements that should not be confused with medications, for example, Arthrostop, Stoparthritis, Piacartil and others.

A list of analogues of the drug Piaskledin 300 with prices can be seen in the table.

AnalogueActive substanceAverage price of a package per month of treatment, rub.Country of origin
PiascledineAvocado and soybean oils1400France
TeraflexGlucosamine + Chondroitin sulfate1300USA
PiacartilDietary supplement AvoVida®800Russia
ArtraGlucosamine + Chondroitin sulfate1000USA
DonGlucosamine1200Germany
AlflutopBioactive concentrate from small marine fish1500Romania
StructumChondroitin sulfate1400France
ArthrokerDiacerein950India/Russia

Piaskledin or Piacartil - which is better

Manufacturer: Omegapharma, Russia
Release form: capsules

Active ingredient: soy protein isolate, mixture of avocado and soy unsaponifiables, silicon dioxide, mixture of tocopherols

Piacartil is a dietary supplement containing a proprietary blend of AvoVida® containing soy and avocado unsaponifiables, soy protein isolate, silicon dioxide and vitamin E.

The dietary supplement is close in composition to Piascledine, but you need to remember that this is not a medicine and is used for the prevention of joint diseases or in complex therapy together with medications - chondroprotectors and NSAIDs.

Pyacartil is used one capsule per day for at least one month. If necessary, you can take the course or repeat it regularly up to 4 times a year.

Introduction

Osteoarthritis (OA) is a disease that develops as a result of the interaction of various mechanical and biological factors that disrupt the normally existing balance between the processes of degradation and synthesis of all matrix components, primarily in articular cartilage [1].
Currently, OA is considered as an organ pathology, since all tissues of the joint are involved in the process: subchondral bone, synovial membrane, capsule, ligaments and periarticular muscles. OA is the most common form of joint damage. The prevalence of the disease in the population correlates with age, reaching maximum values ​​in people over 65 years of age. Women suffer from OA almost 2 times more often than men. The most commonly affected joints are weight-bearing joints (knees, hips), small joints of the hands (distal and proximal interphalangeal joints, first metacarpal joint), and spinal joints. The development of the disease leads to a deterioration in the quality of life of patients, limits their physical capabilities, and often social functions, causing disability. Thus, OA of the knee joints ranks 4th among the causes of disability in women and 8th in men [2–4]. Currently, increasing attention is being paid to the problem of OA of the joints of the hands. The prevalence of this type of OA in European populations increases from 10% at the age of 40–49 years to 92% at the age of over 70 years. Despite the great social significance of the disease, the pathogenesis of OA has not been sufficiently studied. According to modern concepts, OA is a multifactorial disease with a large number of recognized risk factors, which include age, gender, hereditary predisposition, excess weight, etc. The main clinical signs of OA are pain and impaired functional ability of the joints. Radiologically, OA is characterized by joint space narrowing, osteophytosis, subchondral sclerosis, and cyst formation.

It has been established that the pathogenesis of OA is based on the degradation of cartilage tissue, inflammation of the synovial membrane and the restructuring of subchondral bone. The process of cartilage degradation is not characterized by a strictly progressive course: from time to time attempts are made to restore lost cartilage, which suggests the ability of chondrocytes to synthesize even at the final stage of the disease [5–7].

It is assumed that one of the pathogenetic mechanisms of OA is an imbalance between matrix degradation and its synthesis by chondrocytes. During cartilage degradation, there is an overproduction of metalloproteinases, including collagenases (MMP-1, 8, 13) [8–10], aggrecanases (ADAM-TS4 and TS5) [11], stromelysin-1 (MMP-3) [12, 13] and gelatinase (MMP-2, 9) [14, 15], by chondrocytes. The production of metalloproteinases is increased by interleukin 1β (IL-1β), which is a cytokine found in increased amounts in OA-affected cartilage tissue [16–18]. IL-1β makes a significant contribution to cartilage degradation by inhibiting the synthesis of matrix components (aggrecan and type II collagen) [19, 20]. It also stimulates the synthesis of cytokines IL-6, IL-8, macrophage inflammatory protein, which enhance the inflammatory process [21–23].

Currently, therapy for OA is aimed at relieving pain and reducing functional impairment. Medicines used in the treatment of OA are divided into two main groups: symptom-modifying drugs (analgesics and non-steroidal anti-inflammatory drugs - NSAIDs), which relieve pain and inflammation in the joints, and structure-modifying drugs, which can modify the structure of cartilage. This group of drugs not only slows down the progression of the disease, but also actively affects the main symptoms of OA – inflammation and pain, i.e., it also has a symptom-modifying effect [4]. This group of drugs is also called SYSADOA (symptomatic slow acting drugs for osteoarthritis), and one of its representatives is Piascledine (PS), which has proven clinical effectiveness and potential chondroprotective properties.

PS is avocado and soybean unsaponifiable compounds (NSACs) obtained by hydrolysis in a 1:2 ratio (Piascledine, A1S2, Laboratoires Pharmascience, Courbevoie, France). The combined use of avocado and soybean extracts has been shown to cause greater cytokine inhibition compared to their isolated use, and the degree of inhibition depends on the ratio of these ingredients [30]. Incubation of drugs with different ratios of these components - 1: 2 (A1S2), 2: 1 (A2S1) and 2: 2 (A2S2) with a culture of human chondrocytes for 72 hours in the absence or presence of IL-1β showed that NSAS in proportions 1 : 2 and 2: 2 caused a significant decrease in stromelysin activity in cell culture (p < 0.5) with a decrease in the expression of IL-6 and IL-8. A significant decrease in collagenase activity was noted only with the use of these NSAS (at a concentration of 10 μg/ml), while the decrease in the level of prostaglandin E2, stimulated by IL-1β, was the same with the use of all mixtures. It was found that a mixture containing two parts of soybean extract and one part of avocado (A1S2) is the most effective substance, which began to be used as a medicine.

The main mechanism of action of PS is its influence on the expression of cytokines. It inhibits IL-1, stimulates collagen synthesis in cultured chondrocytes and the production of proteoglycans, and blocks IL-1, suppressing its collagenolytic effect on chondrocytes and synoviocytes [29, 30]. When exposed to human chondrocytes, PS inhibits the synthesis of collagenase, stromelysin, IL-6 and IL-8, as well as prostaglandin E2, i.e. those biological substances that are actively involved in the development of the inflammatory response and, as a consequence, subsequent damage to cartilage in OA. In addition, PS increases the expression of transforming growth factors β1 and β2, as well as plasminogen activator inhibitor-1 (PAI-1). Transforming growth factors are synthesized by chondrocytes and osteoblasts and regulate the synthesis of macromolecules of the intercellular substance of articular cartilage. They have an anabolic effect, being not only powerful stimulators of the synthesis of hyaline cartilage macromolecules, but also blockers of their degradation. The action of PAI-1 is aimed at suppressing the production of plasminogen activator, which is involved in cartilage damage both due to direct effects (through the degradation of proteoglycans) and indirectly through stimulation of metalloproteinases [32].

Numerous in vivo studies have confirmed data from in vitro studies showing that NSAS increase the level of tissue production stimulants and may have a chondroprotective effect in induced OA. In an animal experiment, it was demonstrated that NSAS have a preventive effect on the development of post-traumatic OA in rabbits. Altinen et al. [34] found that the levels of transforming growth factors β1 and β2 in the synovial fluid of dog knee joints were significantly increased in groups receiving high and low doses of NSAS compared with controls. In another in vivo study conducted on dogs with induced knee OA, the first group of dogs received NSAS at a dose of 10 mg/kg for 8 weeks, the second received placebo. Dogs treated with NSAS showed a significant reduction in macroscopic cartilage damage on the surface of the tibia. Histological examination also confirmed that the severity of cartilage tissue damage in dogs receiving NSAS was significantly lower [35].

The effectiveness and safety of PS have been studied in a number of randomized clinical trials (RCTs).

The symptom-modifying effect of PS was proven in a double-blind, placebo-controlled RCT [24], which included 164 patients with OA of the knee and hip joints. For 3 months, patients with moderate or severe pain received PS 300 mg/day or placebo. The main criterion for assessing the effectiveness of the drug was the need for NSAIDs: in the interval between the 60th and 90th days of therapy, it was significantly lower in the PS group (43.4 versus 69.7% in the placebo group; p < 0.001). In addition, the cumulative dose of NSAIDs used by patients in the interval between the 45th and 90th days of treatment was significantly lower in the PS group (p < 0.01).

A year later, Maheu et al. [25] published the results of another RCT, the duration of which was 8 months (6 months for therapy, 2 months for assessing the aftereffect of the drug). For all main indicators, PS was superior to placebo. Thus, the average severity of pain by the end of treatment in the main group decreased from 56.1 ± 1.6 to 35.3 ± 2.3 mm on the visual analogue scale (VAS; p ​​= 0.003), and in the comparison group – from 56.1 ±1.8 to 45.7 ±2.6 mm. There was also a significant improvement in the functional state of the joints and a decrease in the Lequesne index (-2.1 ± 0.5; p < 0.001) compared to the placebo group. The need for NSAIDs during the treatment period was lower in the main group, amounting to 48 versus 63% in the placebo group (p = 0.054). Of particular note is the assessment of the need for NSAIDs carried out in this study 2 months after discontinuation of PS and placebo: it was 40.5 and 56.4%, respectively (p < 0.05). This study confirmed the clinically significant superiority of PS over placebo throughout the entire treatment period. The authors concluded that NSAS is a slow-acting symptomatic drug with a persistent effect and a high degree of safety, and the persistence of the symptomatic effect after discontinuation of PS indicates that the drug has a pronounced aftereffect.

In a 3-month multicenter RCT conducted by Appelboom et al. [26], the effectiveness and safety of different doses of PS (300 and 600 mg/day) were assessed in 260 patients with gonarthrosis. The results of the study showed that the effectiveness of PS at doses of 300 and 600 mg/day was significantly higher than placebo at all control points; no difference was found between the two dosages. In addition, 71% of patients taking PS were able to reduce the dose of NSAIDs by more than 2 times, while in the placebo group this effect was achieved only in 36% of patients.

The structure-modifying effect of NSAS was demonstrated in the work of Lequesne et al. [27]. This two-year RCT assessed the effect of PS on the progression of joint space narrowing in 163 patients with clinically and radiologically evident coxarthrosis. At the end of the study, similar joint space narrowing was detected in both groups. However, when analyzing subgroups, it turned out that the narrowing of the joint space in the most severe patients with coxarthrosis (initial width ≤ 2.45 mm) after 2 years of treatment was significantly less in the main group compared to placebo (-0.43 mm and -0.86 mm, respectively; p < 0.01), which allowed the authors to express the opinion that PS has a chondroprotective effect.

In 2009, Maheu et al. [38] presented the results of a study of the structure-modifying effect of PS in 345 patients with coxarthrosis (ERADIAS). Patients were stratified by the severity of coxarthrosis (joint space width < 2.5 mm or > 2.5 mm) and randomized into 2 groups, one of which received 300 mg PS (166 patients), and the other received placebo (179 patients) for 3 years. And although the difference in joint space narrowing over 3 years between the PS and placebo groups turned out to be statistically insignificant (-0.64 and -0.67 mm, respectively; p = 0.72), there were 20% fewer patients with OA progression in the PS group than in the placebo group (p = 0.039), which indicates that the drug has structure-modifying properties.

In a large comparative study that included 364 patients with knee OA conducted by Pavelka et al. [31], the effectiveness and safety of PS (300 mg/day) was studied in comparison with chondroitin sulfate (400 mg 3 times a day) for 6 months of treatment. The drugs showed similar results. In the middle and at the end of the study, in patients of both groups, the WOMAC and Lequesne functional indices decreased by approximately 50%, and over the next 2 months of observation, these indicators continued to decrease, demonstrating the presence of an aftereffect. Almost 80% of patients in the compared groups rated the effectiveness of therapy as “significant improvement” and “improvement,” and almost all patients were able to reduce the daily dose of NSAIDs. Tolerability of PS, as well as chondroitin sulfate, was good. It should be noted that a single dose of PS is most convenient for patients and can significantly increase compliance with therapy.

A meta-analysis of 4 controlled clinical trials of NSAS included 664 patients with OA of the hip (41.4%) and knee joints (58.6%), of which 336 patients received PS 300 mg/day and 328 received placebo for 6 months [ 37]. PS was superior to placebo in its effect on pain (average pain reduction according to VAS was 10.7% for gonarthrosis and 11.3% for coxarthrosis; p = 0.04) and Lequesne functional index (p = 0.0003).

However, a relatively recent systematic review indicated the need for further study of PS, since 3 of 4 RCTs recommended PS for use as a symptom-modifying drug, but one study did not confirm its effectiveness with long-term (over a year) use [36]. However, in this study, the primary endpoint was the assessment of the structure-modifying effect, which may partly explain the lack of symptom-modifying effect of PS with long-term use. Indeed, the weak correlation between symptoms and structural changes in OA is well known, and in most patients with a structure-modifying effect, a symptom-modifying effect is absent. This phenomenon has also been described with long-term use of other so-called. chondroprotective drugs.

The high safety of PS was noted in all clinical studies, in which no significant side effects or cases of drug overdose were recorded during long-term use. An important aspect of safety is the absence of significant drug interactions between PS and known drugs, this is especially important for elderly patients with OA who take a fairly wide range of drugs to treat concomitant diseases.

In Russia, the effectiveness and safety of PS were studied in an open multicenter 6-month study that included 92 patients with OA of the knee and hip joints. The first group of patients (46 people) received PS 300 mg/day and NSAIDs, the second (also 46 people) received only NSAIDs. The effect of the therapy was assessed by the intensity of pain in the affected joint during exercise and at rest, morning stiffness, Lequesne functional index, as well as the daily need for NSAIDs. Already by the 3rd month of treatment, a statistically significant reduction in pain was observed in patients of the main group. By the end of the course of therapy, the intensity of pain at rest in the main group decreased by 3.5 times, and in the control group - only by 1.9 times. The intensity of pain during movement in group 1 decreased from 63.7 to 23.4 mm according to VAS, and in group 2 – from 57.3 to 35.8 mm. The Lequesne index in patients receiving PS decreased by more than 2 times by the 3rd month of observation compared to the initial level, and by the end of the 6th month - by almost 3 times. Less clear positive dynamics were observed in the control group, where it turned out to be statistically unreliable. A decrease in the severity of the main symptoms of OA made it possible to gradually reduce the dose of NSAIDs in patients treated with PS: after 3 months, the daily need for NSAIDs decreased by more than 2 times, and by the end of therapy - by 3 times [32].

These data are confirmed by numerous studies conducted in regions of Russia, where PS was shown to be highly effective and well tolerated in patients with OA of the knee and hip joints. To date, there is evidence of the effectiveness of PS in the treatment of OA of large joints, but there is no data on its effect on OA of the joints of the hands, which is what our study was devoted to.

The aim of the study was to evaluate the effectiveness and safety of PS compared with ibuprofen (IP) therapy in patients with OA of the hand joints.

Material and methods

The study included 40 outpatients of both sexes (37 women and 3 men; mean age - 65.3 ± 6.9 years) with OA of the hand joints, meeting the criteria of Althman et al., (1995), with pain in the hand joints more than 40 mm on VAS, who regularly took NSAIDs for at least 30 days over the past 3 months, and signed an informed consent to participate in the study. Twenty patients (main group) took PS 300 mg/day and PI 1200 mg/day, the remaining 20 patients (comparison group) took PI 1200 mg/day. The observation period was 4 months. Further, for some patients, therapy with Piascledine was continued for another 8 months to evaluate the effectiveness and safety, as well as the effect of the drug on radiological changes in OA of the joints of the hands. PI was prescribed after a washout period at a dose of 400 mg 3 times a day with the possibility of subsequent dose reduction.

Before the start of therapy, both groups of patients were comparable in age, duration of illness, and body mass index (BMI; Table 1). Of the 40 patients included in the study, 29 patients (72.5%) completed the full course of treatment. Fourteen patients continued the study for 12 months, of which 13 patients underwent repeat radiographic examination. One patient dropped out of the main group at visit 2 (after a month of treatment) due to protocol violation. The remaining 10 dropped out of the comparison group: 3 patients – a month after the start of treatment, of which 2 – due to the appearance of gastralgia and 1 – due to dizziness; 5 patients dropped out after 2 months of therapy, 3 of them due to the appearance of gastralgia and 2 due to lack of effect. Another 2 patients dropped out after 3 months due to the onset of epigastric pain.

. Comparative characteristics of patients before treatment.

The patients had the following concomitant diseases: arterial hypertension - 12 (60%) people in group 1 and 9 (45%) - group 2, coronary heart disease - 5 (25%) and 4 (20%) patients, chronic gastritis - 3 (15%) and 4 (20%), varicose veins – 1 (5%) and 2 (10%), diseases of the thyroid gland (nodular goiter) – 2 (10%) and 3 (15%). The frequency of concomitant pathology was approximately the same in both groups of patients.

The treatment effectiveness was assessed according to the following criteria:

  • Functional index AUSCAN (pain, stiffness, state of joint function).
  • Modified functional Dreiser index (FIHOA).
  • Assessment of the effect of therapy by a doctor (better, worse, no change).
  • Assessment of the effect of therapy by the patient (better, worse, no change).
  • Daily requirement for oral NSAIDs and/or analgesics.

These parameters were analyzed before the start of treatment (visit 1) and every month thereafter. Adverse events (AEs) and assessment of the effectiveness of the therapy were recorded at each visit.

Statistical analysis was carried out using generally accepted statistical techniques.

Results and discussion

Pain, stiffness and joint function were assessed using the AUSCAN index. Reliable indicators of pain reduction were recorded in all patients after 2 months of therapy and persisted until the end of the treatment period (Table 2). At the end of therapy a year later, 100% of patients rated the change in their condition as an improvement. Pain scores with PS + PI were much lower than with PI alone (97.6 ± 63.9 vs. 131.5 ± 89.4 mm, respectively), but no statistically significant differences were found, possibly due to the small number groups. A significant reduction in pain scores persisted in all patients after 12 months of therapy. When assessing stiffness, significant differences with the initial indicator were noted at all visits only in the main group. Since pain is often associated with morning stiffness and is a sign of secondary synovitis, these results confirm that PS has good anti-inflammatory activity. Analysis of the state of joint function showed a significant improvement in indicators in the 1st group after 2 months of therapy, while in the 2nd group an improvement was noted only in the 3rd month of treatment. At the end of the observation, significantly better results on the functional state of the joints were noted in the main group (235.5 ± 116.8 vs. 318.3 ± 131.0 mm in the comparison group; p < 0.05), which indicates the greater effectiveness of the combination PS + IP. The total AUSCAN index significantly decreased after 2 months of therapy in group 1 and only after 3 months in the comparison group. When assessing the functional state of the joints (Dreiser index), significant changes were noted in all patients after 2 months of therapy and persisted until the end of therapy. The dynamics of the AUSKAN functional index after a year of using Piascledine in some patients is presented in Fig. 1.


. Dynamics of functional indices in patients with OA of the joints of the hands while taking PS + PI and PI.

Of the 14 patients treated for 12 months, repeat X-ray examination was done in 13 patients, which showed no changes in the X-ray images. Of the 6 patients treated for only 4 months, 2 patients showed slight negative radiographic changes: in one patient, an increase in the size of osteophytes in the 2nd-3rd distal interphalangeal joints and an increase in cystic clearing; Another patient showed an increase in the size of osteophytes in the carpal bones.

Adverse events were observed in 13 patients: 3 from the main group and 10 from the comparison group (Table 3).

In the main group, gastralgia disappeared after reducing the dose of PI by 2 times, and the patients continued treatment. In the comparison group, in 7 patients, despite reducing the dose of PI, epigastric pain persisted, and therefore the drug was discontinued and the patients dropped out of the study. In addition, one patient from the group receiving PI developed persistent dizziness after 2 weeks of therapy, which also required discontinuation of the drug.

During the study, PI was discontinued in 6 patients of group 1 due to pain reduction, while in group 2 the drug was discontinued in 10 patients, including 8 due to the occurrence of AEs and 2 due to ineffectiveness of therapy ( Table 4).

Evaluations of the effectiveness of the treatment by the patient and the doctor are presented in Fig. 2 and 3. A month from the start of therapy (visit 2), an improvement in condition was noted in 50% of patients in the main group and only in 25% in the comparison group. After 2 months (visit 3), improvement was recorded in 79% of patients in group 1 and only in 47% in group 2, and no effect from the therapy was observed in 21 and 53%, respectively. At the end of the treatment period, i.e., after 4 months of therapy, improvement was noted in all patients receiving PS + PI, compared to 65% in the group taking PI alone.

Thus, PS is an effective and safe drug for the treatment of OA of the joints of the hands: it reduces pain, preserves and improves joint function, allows you to reduce the dose of NSAIDs used, and in some cases even abandon them. In addition, PS is characterized by excellent tolerability. Although from a small sample, some evidence was obtained of the effect of the drug on radiological signs of the disease, namely, the absence of radiological dynamics one year after the start of treatment. However, these interesting data require further confirmation in a larger sample of patients.

Piaskledin 300 or Teraflex – which is better?

Manufacturer: Contract Pharmacal Corporation, USA / Bayer, Russia
Release form: capsules

Active ingredient: Glucosamine + Chondroitin sulfate

Synonyms: ARTRA, Kondronova, Artrafik Pro

The Piascledine substitute Teraflex is produced in the USA, and the rights to the marketing authorization belong to the Russian branch.

The Teraflex analogue is a chondroprotector that promotes cartilage restoration and prevents destruction and chemical damage to cartilage tissue.

The Teraflex analogue is used for osteoarthritis and osteochondrosis, reducing the symptoms of the disease and reducing the need for anti-inflammatory painkillers.

Theraflex should be taken more often than Piascledine: in the first three weeks, three capsules per day, then 1 capsule twice a day. The course of treatment is 3–6 months, depending on the degree of joint damage.

Artra

Manufacturer: Ameripharma Labs, USA
Release form: film-coated tablets

Active ingredient: Glucosamine + Chondroitin sulfate

Synonyms: Teraflex, Condronova, Artrafik Pro

Artra is a regenerator of cartilage tissue, promotes the restoration of cartilage, and prevents its destruction.

This American analogue of Piascledine is used for various diseases of the musculoskeletal system, accompanied by pain and decreased joint mobility.

In the first 20 days, Arthra is taken one tablet twice a day, then switched to a single dose. The most lasting effect is observed after a six-month course of treatment.

Reviews

Experts speak positively about the drug: the capsules are highly effective and have a natural composition. Easy to use, as one piece per day is enough. The drug helps reduce pain in chronic diseases of the spine and lower back pain. The disadvantages are the high cost of the course of treatment and the need for long-term therapy, since the drug has a cumulative effect.

Patients note a decrease in pain, swelling of the joints, the disappearance of crunching, the return of the ability to move without pain, and the disappearance of the dependence of the condition on weather changes.

Don

Manufacturer: Madaus, Germany
Release form: film-coated tablets

Active ingredient: Glucosamine

Synonyms: Sustagard Artro, Elbona, Chondroxide Maximum, Unium

Dona is a prescription analogue of Piascledine, containing a component with anti-inflammatory and analgesic properties.

The Don analogue shares with Piascledine the ability to restore cartilage tissue and reduce the development of degenerative changes in the joint. The drug promotes the synthesis of intra-articular fluid, which improves joint lubrication and increases their mobility.

Don's analogue is used for osteoarthrosis and osteochondrosis of the spine, knee and hip joints, one tablet twice a day. A reduction in symptoms appears after 15–20 days of treatment, but the medication must be continued for at least a month.

Then, if necessary, the doctor will prescribe a repeat course.

Benefits of Piascledine for athletes

The joints of athletes and people whose work involves heavy physical labor experience increased stress. In addition, playing sports is often accompanied by injuries, inflammation and pain.

You can take Piaskledin 300 to prevent sports injuries to joints and cartilage, to quickly relieve the inflammatory process to prevent it from becoming chronic. For sprains and injuries to the knee and hip joints, the capsules will help you recover faster.

To reduce the severity of inflammation, as well as the natural restoration of the joint and cartilage tissue, Piascledine should be taken in the postoperative period.

Alflutop

Manufacturer: Zentiva, Romania
Release form: injection solution

Active ingredient: bioactive concentrate from small marine fish

Alflutop is an analogue of Piaskledin 300 in ampoules, it is a concentrate from small sea fish of the herring, cod and anchovy families, obtained through extraction and subsequent release from proteins and fats. As a result, amino acids, trace elements, peptides and mucopolysaccharides, including chondroitin, remain in the extract.

Thanks to this unique composition, the Alflutop analogue prevents destruction and promotes the restoration of cartilage tissue.

The anti-inflammatory effect of Alflutop is due to the blockade of the enzyme hyaluronidase, which enhances the formation of hyaluronic acid.

The Alflutop analogue is used in the form of intramuscular or intra-articular injections for osteoarthritis, osteochondrosis and spondylosis.

Structum

Manufacturer: Pierre FabreMedicine Production, France
Release form: capsules

Active ingredient: Chondroitin sulfate

Synonyms: Chondrogard, Chondrolone, Mucosat, Artradol, Artrafik

The analogue of Piascledine Structum is a prescription French chondroprotector with anti-inflammatory activity.

Structum stimulates metabolism in cartilage tissue, reduces degenerative processes, promotes the synthesis of glycosaminoglycans, reduces calcium loss and promotes the restoration of bone and cartilage tissue.

The Structum analogue is used twice a day, 500 mg, for six months, the treatment effect lasts for another 3–5 months. In the future, the doctor decides whether to repeat the therapeutic course.

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