Zometa and Bonviva (bisphosphonates) are often prescribed for the treatment of osteoporosis and the fight against metastases in oncology. Like all medications, they have some side effects that patients who have dental problems or are planning dental treatment in the future should be aware of. The chief physician of Dial-Dent, Sergei Vladimirovich Tsukor, gives several recommendations to such patients. In this article, he will talk about the tactics of behavior of patients planning an appointment, taking or taking the drugs Zometa and Bonviva.
What are bisphosphonates?
Bisphosphonates are a large group of drugs that stop bone loss. This group includes many different drugs with different names from different manufacturers, including Zometa and Bonviva.
In a healthy bone, from birth to death, two processes occur in parallel: the construction of new bone by osteoblasts (special bone tissue-building cells) and the thinning of bone by osteoclasts (bone killer cells). These two processes are related to each other like day and night. The processes of building new bone and thinning old bone must be in complete balance. Any imbalance, dominance or shutdown of one of the processes indicates illness. In a healthy person, due to the renewal of bone tissue, the entire skeleton is replaced in six months! Bone is a tissue that regenerates 100% precisely due to metabolic processes.
Bisphosphonates interfere with the balance of normal processes of bone renewal (thinning of old and building new). Bisphosphonates kill bone-destroying cells (osteoclasts). The bone loss process stops. But along with it, the ability of the bone to regenerate is also turned off! The bone seems to be there, and it seems to be stronger, because osteoclasts do not act. But in any situation where the restoration potential of the bone is needed, for example, a fracture or tooth extraction, bone restoration does not occur, since bisphosphonates “turned off” the renewal. A number of very unpleasant complications can occur, including suppuration of the bone - osteomyelitis.
You need to understand that bisphosphonates are a great discovery of medicine that have saved many people’s lives! Bisphosphonates are very effective in killing the growth of bone metastases, for example, in breast cancer. Therefore, for oncological diseases that cannot be treated surgically, taking bisphosphonates is justified. But the problem is that bisphosphonates are not always prescribed in extreme cases! Taking bisphosphonates for osteoporosis seems questionable, since in this case they do more harm than good. With osteoporosis, there is no question of life and death; there are many ways to prevent this condition. And taking bisphosphonates will make any surgical dental treatment affecting the bone impossible in the future, since the bone simply will not heal!
Even a single dose of bisphosphonates is a lifelong contraindication to dental implantation! There may be problems with bone healing even after banal tooth extractions. If, nevertheless, the benefits of taking bisphosphonates are more important than the harm, then you need to carefully prepare for their use.
BONVIVA (tablets)
Russian drug, the active substance is ibandronic acid, which is effective in the treatment of osteoporosis.
In fact, even with my secondary specialized medical education, I can easily name the differences between arthrosis and osteoporosis, as well as what they have in common.
I am, of course, not a doctor, but with arthrosis, deformation of the bone articulation begins, which is accompanied by severe pain, swelling and inflammatory processes. It develops almost unnoticed over the years. It is these signs, all of them, that my mother has.
Osteoporosis is also a chronically progressive process, but it is accompanied by other problems, such as bone fragility and fractures of the musculoskeletal system.
As you can see, the differences between the two diseases are not so dramatic, but not small either.
On the cardboard box containing the blister with the tablet, all the information is printed in medium font, everything is easy to read.
There is a specially designated place on the box where you can write the date of administration, and all this because it is recommended to take the pill on the same day, once a month. And this is such a kind of reminder.
There is a production date and expiration date.
The cost of Bonviva ranges from 1,300 to 2,000 rubles, depending on the status of the pharmacy. I bought a pill for my mother at the nearest small private pharmacy.
Country of origin: Switzerland.
The instructions are designed very conveniently, there is no “sheet” here, a small book with good binding, volume 50 pages)
The manufacturer has done a great job of taking care of those who take this medicine. For maximum effect, Bonviva is taken strictly on the same day. By the way, the doctor recommended that my mother take it in the first half of the day, between meals. And the instructions say that 1 hour before the first meal.
I hope that these photos are NOT INSTRUCTIONS, but only its contents, will not bother anyone. Using the contents, it is very convenient to quickly find the information you are interested in.
There is only one indication for use in Bonviva - postmenopausal osteoporosis to prevent fractures! Excuse me, what does my mother have to do with pain in the small joints of her hands?
Now about contraindications. Reduced levels of total calcium in the blood plasma, that is, with hypocalcemia, Bonviva is contraindicated.
Side effects. There are some real horrors here, so many things can happen, so if you are a suspicious person, then after studying all the possible adventures, you will probably refuse to take Bonviva. Nausea, vomiting, diarrhea, dizziness, rash, gastritis - these are the smallest and most harmless things that can happen to you))
Pah-pah, mom didn’t have any side effects at all, although she was worried, she was ready for them.
Well, let's take the pill already. The name and dosage are written on the blister.
Here it is, the only pill, I even want to call it a miracle pill, if I took it once a month and forgot about some of my ailments. But miracles don't happen(
The tablet must be taken while standing or sitting with a glass of water. After taking it for an hour, you need to stay awake and not lie down. There is no need to chew it, if it is difficult for you to swallow it whole, you can break it, but there are no notches here.
Mom has already taken 2 tablets, one in August, the other in September, all the rules for taking Bonviva are strictly observed. She has been taking glucosamine-chondroitin complex and calcium D3 for a month and a half now, and has undergone a course of magnetic therapy (10 sessions).
And my hands still hurt and still hurt...
I made an appointment with the doctor next week.
How can I rate this drug? I do not exclude its positive effect in other patients, perhaps with other diagnoses.
Someone will say that the course of treatment has not yet been completed, yes, only 2 tablets have been taken, but shouldn’t you already feel an improvement? But even simple meloxicam for 200 rubles was more beneficial.
I will give 3 points and advise you not to trust the opinion of only one doctor when prescribing treatment, one head is good, but two are better.
Be healthy!
Recommendations for patients taking Zometa or Bonviva:
- If the patient comes to the dentist with a history of taking bisphosphonates, then it is necessary to notify the doctor about the fact of taking them (drugs of the group: Zometa, Bonviva, Zoledronate, Bondronat, Boniva, etc. ). There is NO statute of limitations on these medications. Even if you only took bisphosphonates once five years ago, you should tell your dentist.
- The dentist you notify about taking bisphosphonates should try to avoid any surgical dental treatment that requires bone healing (tooth extraction, dental implants, etc.). If treatment is still necessary, for example, tooth extraction, then you should be prepared for complications in order to cope with them more easily.
For all questions regarding dental treatment while taking bisphosphonates, please contact the relevant government medical institutions.
Bonviva is a powerful anti-osteoporotic bisphosphonate.
The article discusses the pathogenesis of osteoporosis, non-drug and drug methods of its treatment, and methods for assessing the effectiveness of the latter. The results of clinical studies of the effectiveness and tolerability of the third generation nitrogen-containing bisphosphonate, Bonviva, in patients with osteoporosis are presented.
Rice. 1. Bone mineralization during Bonviva therapy
Rice. 2. Microarchitecture of developing bone
Osteoporosis (OP) is a systemic metabolic disease of the skeleton, characterized by a decrease in bone mass and a violation of its quality (microarchitecture), which leads to a decrease in bone strength and an increased risk of fractures. Primary AP, predominantly postmenopausal, accounts for 85% of cases.
In AP, there are no characteristic early pathognomonic symptoms, except for previous fractures [1]. Epidemiological studies show a lower incidence of hip and forearm fractures in men compared to women [2]. At the same time, the prevalence of vertebral fractures is the same in patients of both sexes. Mortality rates due to osteoporotic fractures are higher in men.
The state of bone mass is reflected by the indicator “bone mineral density” (BMD). Low BMD in old age may be a consequence of both insufficient accumulation of peak bone mass in youth and accelerated loss of bone mass in later life.
On average, peak bone mass (maximum bone density values) is reached between 25 and 30 years of age, followed by a plateau period. According to G.P. Kotelnikov and S.V. Bulgakova (2010), the rate of bone turnover of the skeleton per year is 8–10%. Moreover, the rate of bone turnover in cortical bone is seven times lower than in trabecular bone (4 and 28%, respectively) [3]. From 35–40 years old, age-related physiological loss of bone mass begins, which in men reaches 0.5–2% per year. Cortical bone tissue accounts for 20%, trabecular bone tissue accounts for up to 30% [4].
Trabecular bone is most susceptible to pathological changes, since metabolic processes occur more actively in it [5]. Thus, the decrease in BMD per unit volume in trabecular bone begins earlier than in cortical bone.
There is an assumption that the high rate of bone turnover of the cancellous layer, along with maintaining mechanical strength (sufficient thickness and density of vertical and horizontal trabeculae) determine adequate resistance to standard loads and play an important role in bone homeostasis [6].
With AP, the trabeculae of the spongy substance become thinner and perforated, the integration of bone structures is disrupted until they disappear in certain areas. Free bone beams do not bear a functional load and undergo autolysis.
Pathogenesis
Refinement of bone structures, decrease in bone mass, as well as disruption of bone microarchitecture are a consequence of changes in the function of osteoblasts (OB), osteocytes (OC) and a decrease in their enzymatic activity.
An imbalance in bone remodeling processes can be expressed by increased activity of osteoclasts (OC) with normal OB function (high metabolic rate), normal OC activity with reduced functional activity of OC (low metabolic rate), reduced activity of OC and OB. Most often, with AP, an increase in the pool of active OCs is observed, accompanied by intensification of bone resorption and a decrease in bone mass [7, 8].
In addition, bone tissue is a target for systemic sex hormones, as well as for their local metabolism and synthesis. Androgens and estrogens directly regulate the activity of osteogenic cells and indirectly (through the metabolism of hormone D) - inhibition of parathyroid hormone [5].
Estrogen receptors have been identified on both OB and OC [9]. The results of many studies confirm the positive effect of estrogens on the differentiation, proliferation and functional activity of OB. Estrogens stimulate the synthesis of collagen proteins, promoting an increase in trabecular bone mass [10]. These steroids inhibit the differentiation and activity of TC, including apoptosis [11, 12].
EP Paschalis et al. (2003) using histomorphometry confirmed the positive effect of estrogens on the bone matrix. Namely: an increase in the percentage of minerals in the trabecular structure of the bone and the number of collagen cross-links. Significant signs of suppression of resorptive activity with a decrease in the number of osteoclastic resorptive lacunae have also been demonstrated [13].
The presence of androgen receptors (AR) in various bone tissue cells (on OB, OC and progenitor cells) [14] suggests the presence of widespread androgenic activity. Androgens stimulate proliferation and differentiation of OB and promote bone mineralization by increasing the production of alkaline phosphatase and collagen by these cells [15]. Evidence has been obtained that the possible indirect effect of androgens is associated with the influence on the synthesis of growth factors (transforming growth factor and insulin-like growth factor 1), which also indicates activation of the OB function [16].
Expression of AR on human OC has not been detected. Therefore, it has been suggested that androgens act on OCs indirectly – through cells of the osteoblastic phenotype [17]. At the same time, a number of studies have shown that sex steroids can also have a direct effect, causing apoptosis of TC. Thus, AG Ruetsche et al. (2005) demonstrated that androgens promote periosteal bone growth in men [18]. Androgens also reduce osteoclastogenesis through inhibition of interleukin 6 production by bone marrow stromal cells, which prevents the maturation and differentiation of TC [15].
In bone tissue, androgens can be converted to estrogens by the enzyme aromatase and influence it through both AR and estrogen receptors [15].
Treatment
Treatment for AP is aimed at:
- to prevent new fractures;
- slowing down or stopping bone loss (ideally, its gain);
- normalization of bone remodeling processes;
- reduction of pain, expansion of motor activity;
- improving the patient's quality of life.
Non-drug treatment
Non-drug treatment of AP includes educational programs, walking and exercises with body weight, strength, balance training (jumping and running are contraindicated), nutritional correction (consumption of foods rich in calcium (Ca)), cessation of smoking and alcohol abuse, in case of high risk falls – measures aimed at reducing them (treatment of concomitant diseases, vision correction, changing the home environment, teaching the correct pattern of movements, using a cane, wearing stable shoes, etc.).
Non-drug treatment also includes taking calcium and vitamin D supplements. These drugs are used to prevent AP and complement basic therapy.
Calcium is actively involved in physiological processes occurring in bone tissue (mineralization, remodeling). According to clinical recommendations, adequate consumption of this microelement with food helps maintain BMD, slows down age-dependent bone loss, enhances the antiresorptive effect of sex steroids, and therefore should be an important part of the treatment and prevention of AP [1, 5, 19]. During a screening program conducted in several regions of Russia, O.A. Nikitinskaya and N.V. Toroptsova (2012), it was found that the usual daily human diet does not contain enough Ca2+ - no more than 600–800 mg [20]. Similar data were obtained in other European countries [21, 22]. At the same time, the lowest level of microelement intake from food was recorded in men and women over 55 years of age [23].
L. D. McCabe et al. (2004) showed that the use of Ca2+ supplements in persons over 60 years of age reduces bone loss in the femur [24]. The work of BL Riggs et al. (1998) demonstrated that Ca2+ supplementation at a dose of 1600 mg per day for four years reduced the rate of bone loss in the proximal skeleton [25]. F. Scopacasa et al. (1998) found that the administration of 1000 mg Ca2+ per day helps to reduce the level of bone resorption markers and can have an effect on BMD with long-term use [26].
It should be noted that to date, a large number of studies have been conducted to determine the dose of calcium that causes side effects: the formation of stones, calcification of the vascular wall. Data from recent systemic reviews indicate that additional consumption of Ca2+ does not cause the formation of stones in organs, and the process of calcification of the vascular wall does not depend on the level of Ca2+ in the blood or its consumption, it is a consequence of passive deposition in areas of active inflammation. This protective effect, according to the authors, is due to calcium binding of oxalates and phosphates in the intestine, preventing their excessive excretion in the urine, which contributes to the formation of stones [27].
It has been proven that Ca2+ monotherapy is less effective in preventing bone loss than combination therapy with vitamin D. Vitamin D preparations promote better absorption of calcium salts. In their absence, no more than 10% of the macronutrient entering the body can be absorbed [28].
Vitamin D is fat soluble and is stored in adipose tissue. An increase in the number of overweight individuals leads to an increase in the prevalence of vitamin D deficiency, which is explained by its deposition in subcutaneous fat and inaccessibility to the central bloodstream.
In addition, the global trend towards reducing sun exposure and the use of sunscreens, as well as low levels of insolation in some regions of residence, reduce vitamin D synthesis in the skin by 95–98%.
Drug treatment
Many previously recommended drugs for AP are limited in use (strontium ranelate) or discontinued (calcitonin drugs) due to non-compliance with modern safety criteria.
Currently, bisphosphonates are considered the gold standard for drug treatment of AP.
Bisphosphonates were developed at the beginning of the 19th century, but it was only in 1960 that the first study of their effect on bone metabolism was conducted; since 1990, they have been included in treatment regimens for AP [29].
The mechanism of action of bisphosphonates is physicochemical binding to hydroxyapatite on the resorptive surface; accumulation around the OC and creating a high concentration in resorption lacunae. Absorption of bisphosphonates by OCs leads to suppression of the mevalone pathway of cholesterol biosynthesis. In this case, the formation of the cytoskeleton and corrugated border is disrupted, adhesion to the bone matrix is suppressed and the secretion of lysosomal enzymes is reduced. As a consequence, inhibition of OC migration, disruption of metabolism, functional activity, reduction of chemotaxis to sites of resorption and induction of their apoptosis [30–33].
Thus, the main pharmacological effect of this group of drugs is to reduce the rate of bone remodeling with inhibition of the resorption phase [34, 35].
Among the anabolic effects of bisphosphonates, they include the ability to increase the survival of BC and OB by blocking their apoptosis, and increase the synthesis of OB collagen type 1. This is accompanied by positive changes in bone microarchitecture and an increase in the mineral component. As a result, bone trabeculae thicken and bone loss is prevented [36, 37].
E.V. Rudenko et al. (2011) showed that 20–50% of the drug entering the body is deposited in bone tissue [28].
Bisphosphonates have a protective effect on the vascular wall: they suppress the uptake of low-density lipoproteins involved in the development of atherosclerosis [7].
A large number of large randomized clinical trials have been devoted to the use of bisphosphonates in AP. It has been established that with their use, a significant increase in BMD is observed after three months in the area of the vertebral bodies and after a year in the area of the femur [34]. In studies by DM Black et al. (2006–2007) treatment with bisphosphonates for three to five years was associated with a significant increase in BMD and a 70% reduction in vertebral fractures. On the contrary, cessation of therapy led to an increase in bone turnover markers over the next five years [35].
Today, nitrogen-containing bisphosphonates (alendronate, ibandronate) are recognized as one of the most effective drugs for AP in both women and men [34]. The presence of a nitrogen atom in the side chain of drugs determines their ability to inhibit the modification of proteins in the TC, which leads to specific changes and apoptosis of the latter. In addition, preosteoclasts, under the influence of nitrogen-containing ibandronates, lose the ability to differentiate and mature, as a result of which the OC population decreases.
The antiresorptive activity of individual drugs in this group varies significantly, which is associated with the characteristics of their chemical structure and reflects the levels of effective pharmacological and therapeutic doses [7, 38]. In accordance with the increase in antiresorptive potential, the relative activity of alendronate is 100–1000, ibandronate – 1000–10,000.
Monitoring treatment effectiveness
The effectiveness of treatment is assessed using dual-energy X-ray absorptiometry one to three years after the start of therapy, but not more than once a year (it is recommended to use a device from the same manufacturer). Peripheral dual-energy X-ray absorptiometry should not be used for monitoring.
In addition, markers of bone resorption are analyzed.
Treatment is considered effective if BMD increases or remains at the original level. Continued loss of BMD on dual-energy x-ray absorptiometry or a new fracture may indicate poor patient adherence to treatment.
Bonviva
Bonviva (ibandronate) is a third-generation nitrogen-containing bisphosphonate. The drug is taken orally at a dose of 150 mg once a month. After absorption, 40–50% of the drug dose in the systemic circulation binds to bone tissue and accumulates in it, which corresponds to the concept of a high affinity of the drug for bone hydroxyapatite. Once bound, the release of the drug occurs extremely slowly.
It should be noted that when Bonviva is taken one hour before meals, there is no significant decrease in bioavailability.
Like other bisphosphonates, Bonviva is not metabolized in the body and is excreted unchanged in the urine. Clearance of ibandronate depends on renal function. The part of the drug that is bound to bone tissue is not eliminated from the body until the remodeling process is completed in the bone area. The half-life of Bonviva from bones is about a year.
The clinical effectiveness of ibandronate is confirmed by data from a number of multicenter studies that studied its effect on BMD and bone quality, the risk of developing new fractures, and tolerability. In total, 13,000 patients took part in them.
After a year of monthly administration of Bonviva at a dose of 150 mg, BMD in the lumbar spine significantly increased by 4.3%, and after two years – by 6.6%. A significant increase in BMD in the general hip, femoral neck and greater trochanter area was noted after a year of therapy. The achieved values were maintained during the second year of treatment. Thus, on average, BMD relative to the initial level after two years in the femoral neck increased by 3.1%, the greater trochanter - by 6.2%, and in the general hip - by 4.2%. A decrease in the level of bone turnover markers was recorded after three months of treatment and continued throughout the entire observation period.
The results of the multicenter, randomized, double-blind MOBILE trial showed that BMD in the lumbar spine in patients with postmenopausal AP increased with ibandronate administered once a month as effectively as with daily dosing of the drug at a dose of 2.5 mg [39].
Bonviva 150 mg once a month was associated with the largest and most progressive increase in BMD at all proximal femoral sites (at two years p
After three years of ibandronate therapy, the increase in BMD in the femoral neck was 3.5%, in the greater trochanter - 6.2%, in the total hip - 4.1%, in the lumbar spine - 7.6%.
As part of the BONE study, histological and histomorphometric analyzes of bone biopsies were performed to evaluate the effect of ibandronate on the quality and microarchitecture of bone tissue [40]. Oral Bonviva was associated with new bone formation without evidence of impaired bone matrix mineralization (Figure 1). At the same time, an improvement in its microarchitecture was noted (Fig. 2).
The results of numerous studies have shown that taking aminobisphosphonates increases BMD in the lumbar spine and proximal femur and reduces the incidence of fractures by 40−70% [38, 41]. An increase in BMD and a reduction in bone loss are largely associated with an increase in the mineral component of bone, which contributes to the thickening of trabeculae [37, 42].
It should be noted that the effectiveness of therapy for any chronic disease is largely determined by the patient’s adherence to treatment. The results of the multicenter BALTO study on the comparative assessment of patient adherence to treatment showed that 66.1% of patients with postmenopausal AP preferred monthly administration of Bonviva at a dose of 150 mg to weekly administration of alendronate at a dose of 70 mg [43].
The results of the studies showed that a relatively large dose of Bonviva did not have a significant effect on the tolerability of therapy. Additionally, Bonviva was not associated with an increased risk of upper gastrointestinal side effects [44].
The literature describes cases of osteonecrosis of the jaw in patients receiving bisphosphonates. Their frequency is 6.5–12.5% [45–47]. Osteonecrosis of the jaw is a condition characterized by exposure of the bone of the lower and/or upper jaw and persists for at least eight weeks, in the absence of previous radiation or metastases to the jaw [48]. Moreover, only 4% of all cases of osteonecrosis of the jaw were recorded in patients with AP [7]. This complication was more often observed with intravenous administration of long-acting drugs (pamidronate, zoledronic acid) than with oral administration [47, 49].
The pathogenesis of osteonecrosis of the jaw is not fully understood. Some authors associate its development with an imbalance in bone remodeling processes, increased formation of proinflammatory cytokines, and the presence of pathogenic microflora in the oral cavity [46, 47]. Other authors believe that with long-term use, bisphosphonates block OB function by inhibiting OC activity [50].
A cause-and-effect relationship between necrotic changes in the jaw and treatment of AP with bisphosphonates has not been established [48, 51].
One of the advantages of aminobisphosphonates is the minimal risk of jaw necrosis [34].
The above allows us to conclude: Bonviva is an effective drug for the treatment of AP. Its long-term use promotes an increase in BMD in the lumbar spine and proximal femur, as well as a reduction in the risk of fractures.
Bonviva, 1 piece, 150 mg, film-coated tablets
Ibandronic acid is a highly active nitrogen-containing bisphosphonate, an inhibitor of bone resorption and osteoclast activity. Ibandronic acid prevents bone destruction caused by gonadal blockade, retinoids, tumors and tumor extracts in vivo
. Inhibits endogenous resorption in young (fast-growing) rats, which is manifested by higher bone mass compared to intact animals.
Does not interfere with bone mineralization when administered in doses more than 5000 times higher than doses for the treatment of osteoporosis and does not affect the process of replenishment of the osteoclast pool. The selective effect of ibandronic acid on bone tissue is due to its high affinity for hydroxyapatite, which constitutes the mineral matrix of bone.
Ibandronic acid inhibits bone resorption in a dose-dependent manner and does not have a direct effect on bone formation. In menopausal women, it reduces the increased rate of bone tissue turnover to the level of reproductive age, which leads to a general progressive increase in bone mass, a decrease in the breakdown of bone collagen (concentrations of deoxypyridinoline and cross-linked C- and N-telopeptides of type I collagen) in urine and blood serum , incidence of fractures and increased BMD.
High activity and therapeutic range provide the possibility of a flexible dosage regimen and intermittent administration of the drug with a long period without treatment in relatively low doses.
Efficiency
Film-coated tablets, 2.5 mg.
Both continuous and intermittent (one 9-10 week break per quarter) long-term oral use of Bonviva® in the form of 2.5 mg film-coated tablets in menopausal women is accompanied by dose-dependent inhibition of bone resorption, incl. a decrease in the breakdown of bone collagen (the concentration of deoxypyridinoline and cross-linked C- and N-telopeptides of type I collagen) in urine and blood serum, an increase in BMD and a decrease in the incidence of fractures.
After cessation of treatment, there is a return to the pre-treatment increased rate of bone resorption in postmenopausal osteoporosis.
Histological analysis of bone tissue samples obtained after 2 and 3 years of treatment in menopausal women showed normal bone tissue characteristics and no signs of mineralization disorders.
Daily administration of Bonviva® in the form of film-coated tablets, 2.5 mg for 3 years (randomized, double-blind, placebo-controlled study MF4411) is accompanied by a statistically significant reduction in the incidence of radiographic and morphometrically confirmed vertebral fractures by 62%, and clinically confirmed vertebral body fractures by 49%. The reduction in bone loss was accompanied by a significantly less pronounced decrease in the height of patients compared to placebo.
Prevention of fractures was maintained throughout the study, and there was no evidence of the effect fading over time.
A similar reduction in the relative risk of non-vertebral fractures was revealed by 69% in patients from the high-risk group (BMD T coefficient for the femoral neck less than -3.0 SD). These data are consistent with the results of clinical studies of other bisphosphonates.
With daily use of Bonviva® for 3 years, the BMD of the lumbar vertebrae increases by 6.5% compared to the baseline.
Film-coated tablets, 150 mg each, and solution for intravenous administration. Bone Mineral Density (BMD)
Taking Bonviva® 150 mg once a month for a year increases the average BMD of the lumbar vertebrae, hip, femoral neck and trochanter by 4.9, 3.1, 2.2 and 4.6%; IV administration of Bonviva® 3 mg once every 3 months for 1 year increases the average BMD of the femur, femoral neck and trochanter by 2.4, 2.3 and 3.8%, respectively.
Regardless of the duration of menopause and the degree of initial bone loss, the use of Bonviva® leads to a significantly more pronounced change in BMD than placebo. The effect of treatment within a year, defined as an increase in BMD, is observed in 83.9% (when taking film-coated tablets) and 92.1% (when administered intravenously) of patients.
Biochemical markers of bone resorption
Film-coated tablets, 2.5 mg.
Biochemical markers of bone resorption (urinary concentrations of type I procollagen C-terminal peptide (CTX) and serum osteocalcin) decline to their levels during reproductive age; the maximum reduction is observed after 3-6 months of treatment. Just one month after starting the use of Bonviva 2.5 mg daily and 20 mg intermittently, a clinically significant reduction in biochemical markers of bone resorption was achieved by 50 and 78%, respectively; Moreover, a slight decrease in these indicators was noted after a week of treatment. A clinically significant decrease in biochemical markers of bone resorption (urinary CTX concentrations) is observed one month after the start of treatment.
Bonviva 2.5 mg daily for the prevention of postmenopausal osteoporosis (study MF4499) increased mean lumbar spine BMD by 1.9% compared with baseline. Regardless of the duration of menopause and the degree of initial loss of basic bone tissue, the use of Bonviva® leads to a significantly more pronounced change in the BMD of the lumbar vertebrae. When using the drug Bonviva®, the treatment effect, defined as an increase in BMD compared to the baseline, is observed in 70% of patients.
Film-coated tablets, 150 mg each, and solution for intravenous administration.
A 28% decrease in serum CTX concentration was noted within 24 hours after the first dose of 150 mg Bonviva®, with a maximum decrease of 68% after 6 days. After the third and fourth doses of Bonviva® 150 mg, the maximum decrease in serum CTX by 74% was observed after 6 days. 28 days after taking the fourth dose, a decrease in the suppression of biochemical markers of bone resorption was noted to 56%.
A clinically significant decrease in serum CTX was obtained after 3, 6 and 12 months of therapy. After a year of therapy with Bonviva® 150 mg, the reduction was 76%; compared with the initial value, when using 3 mg IV - 58.6%.
A decrease in CTX of more than 50% compared to the initial value was observed in 83.5% of patients receiving Bonviva® 150 mg once every 28 days.
