Same-side insufficiency fractures of the tibia and femur after denosumab discontinuation: a case report.

Osteoporosis (OP) is a common disease in the elderly that causes bone fractures and increases mortality. Denosumab (DMAB) is one of several medications to treat OP. DMAB not only reduces the risk of fractures, but also improves the quality of life. However, an increase in the risk of multiple vertebral fractures has been reported after DMAB discontinuation. We described the rare case of a 71-year-old woman with severe OP who experienced same-side insufficiency fractures of the tibia and femur at 18 months after DMAB discontinuation. Careful monitoring for both vertebral and lower limb fragility fractures is advised after DMAB cessation.

Remarkable loss of bone mineral density in 6 months after denosumab discontinuation: a case report.

In recent years, several studies have shown that multiple vertebral fractures sometimes occur after denosumab discontinuation. Herein, we report the case of a 63-year-old woman with osteoporosis who lost 60% of lumbar bone mineral density acquired during osteoporosis treatment after 6 months of denosumab discontinuation.

Fragility fractures and delayed wound healing after tooth extraction in Japanese older adults.

INTRODUCTION: Fragility fractures can cause delayed wound healing after tooth extraction, which contributes to an increased risk of osteomyelitis of the jaw. We evaluated whether a history of fragility fracture was associated with increased risk of delayed wound healing after tooth extraction in older adults in Japan. MATERIALS AND METHODS: Of 5352 people aged 50-89 years in the 2014 basic resident registry of the town of Obuse, the present study included 376 subjects (190 men and 186 women) who completed a structured questionnaire and measurement of the bone mineral densities (BMDs) of the bilateral femoral neck. Delayed wound healing after tooth extraction was self-reported. Fragility fractures were confirmed via examination of hospital medical records. Logistic regression analyses adjusted for age and gender were used to evaluate association of clinical variables with delayed would healing after tooth extractions. Odds ratios (ORs) and the 95% confidence intervals (CIs) of all possible associated variables for the presence of delayed wound healing were calculated. RESULTS: Subjects with a history of fragility fractures had a significantly higher risk of delayed wound healing compared with those without previous fragility fractures (OR 2.68; 95% CI 1.11-6.46, p = 0.028). This association still remained after adjusted for all other variables (OR 2.70; 95% CI 1.10-6.60, p = 0.030). Delayed wound healing was not significantly associated with the BMD of the femoral neck. CONCLUSIONS: History of fragility fracture may be associated with increased risk of delayed wound healing after tooth extraction in Japanese men and women aged 50-89 years.

Unexpected rapid increase in bone mineral density by bisphosphonate therapy after multiple spinal fractures: a case report.

BACKGROUND: Osteoporosis is a serious disease that causes bone fragility fractures and increases mortality. Bisphosphonates are the first-line drugs for osteoporosis. However, the gains in bone mineral density by use of bisphosphonates alone are limited. CASE PRESENTATION: We describe the clinical outcome of a Japanese woman with osteoporosis treated with bisphosphonates after multiple spinal fractures. After 3 years of treatment with the bisphosphonate alendronate, her lumbar bone mineral density and bilateral hip bone mineral density markedly increased by 61.9% and 32.5%, respectively. CONCLUSION: We considered that our patient's multiple fractures had caused a decrease in bone mineral density, which naturally improved with fracture healing to enhance the increase in bone mineral density with bisphosphonate treatment.

Additive effects of eldecalcitol in poorly responding long-term bisphosphonate treatment for osteoporosis.

OBJECTIVES: We examined whether eldecalcitol (ELD) provided additive bone mineral density (BMD) and bone turnover marker gains in patients undergoing long-term bisphosphonate (BP) usage, especially in osteoporotic individuals exhibiting a poor response to BPs. METHODS: Forty-two post-menopausal patients with primary osteoporosis and low lumbar BMD (L-BMD) and/or bilateral total hip BMD (H-BMD) values receiving long-term BP treatment were prospectively enrolled. Serum bone alkaline phosphatase (BAP) was measured as a bone formation marker and urinary N-terminal telopeptide of type I collagen (NTX) was assessed as a bone resorption marker. L-BMD, H-BMD, and femoral neck BMD (N-BMD) were recorded before, at the commencement of, and during ELD administration. RESULTS: BAP and urinary NTX were significantly decreased by BP therapy prior to ELD. ELD addition further significantly decreased the bone turnover markers (both p < 0.01). The mean L-BMD increase rate was 0.2% (p = 0.81) from 2 to 1 years before ELD administration, -0.7% (p = 0.30) during the year before ELD, and 2.9% (p < 0.01) during 1 year of ELD. Similar findings were observed for the mean increase rate of H-BMD, with values of 0.2% (p = 0.55), -0.7% (p < 0.01), and 1.2% (p < 0.01), respectively. The mean N-BMD increase rate was significantly increased after ELD administration (1.1%, p = 0.03) despite no gains by BP therapy alone. CONCLUSIONS: This study suggests that ELD addition may be useful for osteoporotic patients exhibiting a diminished long-term BP therapy response.

Efficacy of denosumab therapy for neurofibromatosis type 1 with osteoporosis and history of fractures: a case report.

BACKGROUND: The natural history and pathogenesis of the skeletal abnormalities found in neurofibromatosis type 1 (NF1) are poorly understood, and the therapeutic options for these manifestations remain limited. This report first describes the clinical outcomes of denosumab treatment for a patient with NF1 suffering from osteoporosis. METHODS: We enrolled a patient with NF1 under denosumab treatment for osteoporosis, prior fractures, and no improvement in bone mineral density (BMD) over 3 years of alendronate therapy. BMD was monitored by dual-energy X-ray absorptiometry. Tested laboratory data included bone-specific alkaline phosphatase, urinary type I collagen amino-terminal telopeptide, tartrate-resistant acid phosphatase 5b, 1-alpha, 25-dihydroxyvitamin D3, and parathyroid hormone. BMD and laboratory data were evaluated before, between 2 and 4 months, and at 6, 12, 18, and 24 months of treatment. CASE PRESENTATION: During 2 years of denosumab therapy for osteoporosis in a 58-year-old female NF1 patient with prior fractures, BMD increased by 6.5% in the lumbar spine and 10.6% in the total hips, and bone turnover markers were notably improved. No fractures occurred during the latter half of treatment. CONCLUSION: Denosumab represents an effective treatment option for osteoporosis in NF1 patients.

Denosumab significantly improves lumbar spine bone mineral density more in treatment-naïve than in long-term bisphosphonate-treated patients.

The purpose of our study was to compare the skeletal responses to 3-year denosumab treatment in bisphosphonate (BP)-naïve and long-term BP-treated patients with postmenopausal osteoporosis. Female patients who were BP treatment-naïve (treatment-naïve group: 25 cases) or who received long-term BPs (BP pre-treated group: 24 cases) were compared for serum bone alkaline phosphatase (BAP), tartrate-resistant acid phosphatase (TRACP)-5b, and urinary N-terminal telopeptide of type I collagen (NTX) at baseline and at 4, 8, 12, 15, 18, 21, 24, 27, 30, 33, and 36 months of denosumab therapy. Lumbar 1-4 (L) spine bone mineral density (BMD), total hip (H)-BMD, and femoral neck (FN)-BMD values were measured at baseline and at 4, 8, 12, 18, 24, 30, and 36 months. The percentage changes of bone turnover markers were significantly decreased throughout the study period by a larger margin in the treatment-naïve group than in the BP pre-treated group. L-BMD, H-BMD, and FN-BMD were all significantly increased in the treatment-naïve and BP pre-treated groups at 36 months (12.9% and 7.5%, 5.9% and 6.0%, and 7.6% and 4.5%, respectively), compared with pre-treatment levels. There were significant differences for L-BMD at 12, 24, 30, and 36 months between the groups. Our findings suggest that the BMD response to denosumab, especially that of L-BMD, was diminished following BP therapy relative to treatment-naïve patients, thus providing evidence supporting the use of denosumab as a first-line therapy.

Adequate nutrition status important for bone mineral density improvement in a patient with anorexia nervosa.

Low bone mineral density (BMD) is one of the most frequent complications of anorexia nervosa (AN). We report the clinical outcomes of a female patient with severe AN, whose chest had become deformed due to thoracic fracture. Lumbar BMD was 0.358 g/cm2 (T-score = -6.3), and total hip BMD was 0.411 g/cm2 (T-score = -4.4). Active vitamin D increased these parameters by 81.0% and 57.4%, respectively, but a drop in her nutrition status afterward resulted in a sharp decrease in BMD values. These findings suggest that adequate nutrient intake is essential for effective osteoporosis treatment in patients with AN.

Efficacy of Denosumab for Glucocorticoid-Induced Osteoporosis in an Adolescent Patient with Duchenne Muscular Dystrophy: A Case Report.

CASE: We report the case of a 13-year-old boy with Duchenne muscular dystrophy (DMD) who sustained bilateral femoral neck fractures associated with glucocorticoid-induced osteoporosis. Denosumab therapy for 18 months markedly improved the lumbar bone mineral density and the bone turnover markers. No fractures or complications were recorded during the treatment period. CONCLUSION: To the best of our knowledge, this is the first description of denosumab treatment for glucocorticoid-induced osteoporosis in a patient with DMD. The drug merits additional testing as an effective therapy for osteoporosis in patients with DMD.

Pretreatment of daily teriparatide enhances the increase of bone mineral density in cortical bones by denosumab therapy.

BACKGROUND: While it is well known that teriparatide (TPTD) increases bone mineral density (BMD) in osteoporotic patients, it is unknown whether TPTD pretreatment affects BMD after denosumab (DMAb) therapy. METHODS: Fifty-seven patients in TPTD-pretreated group and 35 patients in DMAb-alone group had been further analyzed, all of whom were treated by DMAb for 1.5 years. Vitamin D (400 IU) and Ca (600 mg) supplementation was used in all patients. The BMD of lumbar 1-4 vertebrae (L-BMD), bilateral total hips (H-BMD), and bilateral femoral neck (FN-BMD) was quantified at first visit, and at 4, 8, 12, and 18 months after daily TPTD treatment following four times DMAb treatment. RESULTS: There were significant differences in L-BMD (p=0.004) and H-BMD (p=0.026) at baseline between TPTD-pretreated and DMAb-alone groups, although there was no significant difference in FN-BMD between the two groups. The increase of L-BMD by DMAb therapy was less in TPTD-pretreated group than in DMAb-alone group. There was no significant difference in H-BMD, although percent changes of H-BMD tended to be higher in the TPTD-pretreated group than those in the DMAb-alone group. Percent change in FN-BMD at 4 months (p=0.067) and 12 months (p=0.057) tended to be higher in TPTD-pretreated group than in DMAb-alone group. Percent change in FN-BMD at 18 months was significantly higher in TPTD-pretreated group (p=0.004) than in DMAb-alone group. CONCLUSION: These findings suggest that the pretreatment of TPTD might have enhanced the increase of BMD in cortical bones treated by DMAb. Thus, it is favorable that TPTD can be used for osteoporotic patients who have high fracture risks with cortical bones.

Significant improvement of bone mineral density by denosumab treatment in Japanese osteoporotic patients following breast cancer treatment.

BACKGROUND: The aim of this study was to evaluate the effects of denosumab in patients with osteoporosis (OP) and non-metastatic breast cancer following treatment of 1) surgery, 2) surgery and aromatase inhibitors, and 3) surgery, aromatase inhibitors, and anti-cancer agents, compared with those in primary OP patients. PATIENTS AND METHODS: In this retrospective 24-month study, patients were divided into the primary OP group (34 cases) or OP receiving breast cancer treatment group (breast cancer group; 17 cases). We measured serum calcium, whole parathyroid hormone (PTH), 1,25OH2D3, bone alkaline phosphatase (BAP), tartrate-resistant acid phosphatase-5b (TRACP-5b), and bone mineral density (BMD) of the lumbar 1-4 vertebrae (L-BMD) and bilateral total hips (H-BMD) for 24 months. RESULTS: The percent changes of serum calcium in the breast cancer group were significantly lower than those in the primary OP group at 1 week, 1 and 12 months. The percent changes of whole PTH in the primary OP group were significantly lower than those in the breast cancer group at 2 and 4 months. Significant differences were found between the groups at 18 months (-34.5% in the primary OP group and -52.6% in the breast cancer group, respectively) for the percent changes of BAP. Significant differences were found between the groups at 12, 18, and 24 months (-39.7% in the primary OP group and -64.0% in the breast cancer group at 24 months, respectively) for the percent changes of TRACP-5b. The percent changes of L-BMD and H-BMD were significantly increased at 12, 18, and 24 months in both the primary OP group (7.0% and 4.7% at 24 months, respectively) and breast cancer group (8.0% and 5.4% at 24 months, respectively), compared with pre-treatment levels. Significant differences were not found between the groups for the percent changes of L-BMD and H-BMD. CONCLUSION: Denosumab significantly increased L-BMD and H-BMD to comparable degrees in both groups; therefore, it represents a good therapeutic option for OP receiving breast cancer treatment as well as primary OP. Also, vitamin D supplementation is required due to the potential hypocalcemia, and estrogen may be responsible for the decrease of serum calcium in the breast cancer patients.

Comparison of the effects of denosumab with either active vitamin D or native vitamin D on bone mineral density and bone turnover markers in postmenopausal osteoporosis.

Osteoporosis is a worldwide health concern. Although treatment with denosumab plus the active vitamin D alfacalcidol has been found to improve femoral neck (FN) and distal forearm bone mineral density (BMD), there have been no reports on the efficacy or adverse effects of denosumab plus eldecalcitol (ELD) in primary osteoporosis patients. Fifty-six treatment-naïve post-menopausal women with primary osteoporosis were recruited and divided into denosumab plus native vitamin D or denosumab plus ELD. Ultimately, 26 subjects in the native vitamin D group and 24 in the ELD group were analyzed. Lumbar and total hip BMD significantly increased in both groups. However, there was no significant difference in the percent increase of lumbar and total hip BMD between two groups. FN-BMD was significantly increased from 6 to 12 months in the ELD group compared with baseline. This study revealed that combination therapy with denosumab and ELD could improve FN-BMD more effectively than denosumab plus native vitamin D. Thus, the addition of ELD may enhance the effects of denosumab treatment for primary osteoporosis.

Vitamin D and calcium are required at the time of denosumab administration during osteoporosis treatment.

To evaluate the differences in outcomes of treatment with denosumab alone or denosumab combined with vitamin D and calcium supplementation in patients with primary osteoporosis. Patients were split into a denosumab monotherapy group (18 cases) or a denosumab plus vitamin D supplementation group (combination group; 23 cases). We measured serum bone alkaline phosphatase (BAP), tartrate-resistant acid phosphatase (TRACP)-5b and urinary N-terminal telopeptide of type-I collagen (NTX) at baseline, 1 week, as well as at 1 month and 2, 4, 8 and 12 months. We also measured bone mineral density (BMD) of L1-4 lumbar vertebrae (L)-BMD and bilateral hips (H)-BMD at baseline and at 4, 8 and 12 months. There was no significant difference in patient background. TRACP-5b and urinary NTX were significantly suppressed in both groups from 1 week to 12 months (except at 12 months for NTX). In the combination group, TRACP-5b was significantly decreased compared with the denosumab monotherapy group at 2 and 4 months (P<0.05). BAP was significantly suppressed in both groups at 2-12 months. L-BMD significantly increased at 8 and 12 months (8.9%) in the combination group and at 4, 8 and 12 months (6.0%) in the denosumab monotherapy group, compared with those before treatment. H-BMD was significantly increased in the combination group (3.6%) compared with the denosumab group (1.2%) at 12 months (P<0.05). Compared with denosumab monotherapy, combination therapy of denosumab with vitamin D and calcium stopped the decrease in calcium caused by denosumab, inhibited bone metabolism to a greater extent, and increased BMD (especially at the hips).

Increased Serum 25(OH)D3 Levels in Post-Menopausal Japanese Women with Osteoporosis after 3-Year Bisphosphonate Treatment.

Osteoporosis is characterized by the systemic impairment of bone mass, strength, and microarchitecture, leading to an increased risk of fragility fracture. Bisphosphonates (BPs) are the first-line drugs for osteoporosis. Vitamin D is considered to be essential for osteoporotic treatment. However, long-term effects of BPs on the serum levels of 25-hydroxyvitamin D3 (25(OH)D3) are unknown. Accordingly, in this retrospective study, we collected clinical data of 41 post-menopausal Japanese women with osteoporosis treated with BP for over 3 years, without vitamin D supplementation. We measured lumbar and femoral neck bone mineral density (BMD) and serum levels of bone specific alkaline phosphatase (BAP) as a bone formation marker, and tartrate-resistant acid phosphatase (TRACP)-5b as a bone resorption marker, before and after the 3-year treatment. Serum 25(OH)D3, 1,25(OH)2D3, and whole parathyroid hormone (PTH) were also measured. Notably, no fracture occurred during the treatment. Compared with baseline values, 25(OH)D3 levels were significantly increased from 21.6 to 26.4 ng/mL (P = 0.006), despite no vitamin D supplementation. 1,25(OH)2D3 and whole PTH levels tended to be decreased from 62.6 to 57.8 pg/mL and 27.3 to 25.1 pg/mL, respectively. Both bone formation and resorption markers were significantly suppressed (P < 0.01). Both lumbar BMD (7.3% increase) and femoral neck BMD (4.1% increase) were significantly improved (P < 0.0001) after 3 years of the treatment. Thus, even without vitamin D supplementation, serum 25(OH)D3 levels were significantly increased after 3-year BP therapy. These results suggest that vitamin D supplementation might not be required in the long-term BP therapy for osteoporosis.

Two-year clinical outcome of denosumab treatment alone and in combination with teriparatide in Japanese treatment-naive postmenopausal osteoporotic women.

This randomized prospective study aimed to evaluate the clinical outcome of denosumab treatment alone and in combination with teriparatide in treatment-naive postmenopausal Japanese female patients with osteoporosis. Thirty patients were randomly assigned to two groups: (1) denosumab group (denosumab alone, n=13); and (2) combination group (denosumab+teriparatide, n=17). Serum bone-specific alkaline phosphatase (BAP), serum tartrate-resistant acid phosphatase (TRACP)-5b, urinary cross-linked N-terminal telopeptides of type I collagen (NTX), and bone mineral density (BMD) of L1-4 lumbar vertebrae (L-BMD) and bilateral total hips (H-BMD) were determined at the first visit and at various time points up to 24 months post-treatment to determine percentage changes. Serum TRACP-5b and urinary NTX were equally suppressed in both groups and maintained at low levels, with slight increases at 12, 18 and 24 months. BAP was significantly decreased in both groups from 4 to 24 months, with significant differences between the groups at 4, 8 and 15 months (P<0.05). L-BMD was significantly increased at most time points in both groups, with a significant difference between the combination group and denosumab group at 24 months (17.2% increase versus 9.6% increase; P<0.05). There was no significant difference in H-BMD between the two groups, although the levels tended to be higher in the combination group than in the denosumab group (9.5% increase versus 5.6% increase). These findings suggest that denosumab+teriparatide combination therapy may represent an important treatment for primary osteoporotic patients at high risk of vertebral fracture.

Efficacy of Denosumab for Osteoporosis in Three Female Patients with Osteogenesis Imperfecta.

Osteogenesis imperfecta (OI) is an inherited bone disorder that causes fractures due to impaired production of collagen type I. In recent years, denosumab, a human monoclonal antibody against receptor activator of nuclear factor κB ligand (RANKL), has become widely used as an anti-osteoclastic agent for osteoporosis. This study investigated osteoporotic cases of OI to examine effects of denosumab on bone fragility. This was a retrospective, consecutive case series that included 3 female patients aged 42, 40, and 14 years, respectively. One patient carries a point mutation (c.G769A) in the COL1A1 gene, encoding collagen type I alpha 1 chain, which causes an amino-acid substitution (p.G257R). By contrast, no mutation was found in the analyzed regions of the OI responsive genes in another two patients (mother and daughter). These three patients underwent subcutaneous injection of denosumab every 6 months. All patients underwent dual-energy X-ray absorptiometry for bone mineral density (BMD) measurement of the lumbar 1-4 spine (L-BMD) and bilateral hips (H-BMD) before and during treatment. BMD and laboratory data were evaluated before, between 2 and 4 months, and at 6, 12, 18, and 24 months of therapy. No fractures or severe side effects, such as hypocalcemia, were observed during denosumab treatment. Both L-BMD and H-BMD were increased by denosumab. At 24 months, the mean percentage changes in L-BMD and H-BMD were 14.7% and 15.1%, respectively. In conclusion, no bone fragility fractures occurred during 2 years of denosumab administration in OI patients. Denosumab therefore is a good therapeutic option in the OI patients.

Alfacalcidol Increases the Therapeutic Efficacy of Ibandronate on Bone Mineral Density in Japanese Women with Primary Osteoporosis.

Bisphosphonates (BPs) increase bone mineral density (BMD) through the inhibition of osteoclast activity. Among BPs, ibandronate (IBN) is a strong inhibitor of bone resorption. However, the effects of a vitamin D analogue, alfacalcidol (ALF), on IBN treatment for osteoporosis is unknown. Fifty-three treatment-naïve post-menopausal women with primary osteoporosis were recruited and divided into IBN-treatment group (IBN group) and IBN with ALF group (IBN/ALF group). IBN (1.0 mg) was intravenously injected once a month, with or without oral ALF (1.0 µg/day). Ultimately, 19 subjects in IBN group and 26 in IBN/ALF group were analyzed. Bone turnover markers were examined at 4, 6, 12, and 18 months, and BMD was measured at 6, 12, and 18 months. Compared with pre-treatment, bone turnover markers significantly decreased in both groups after 4 months. The levels of serum N-terminal propeptide of type-1 procollagen and tartrate-resistant acid phosphatase-5b, and urinary N-terminal telopeptide of type-I collagen were significantly lower in IBN/ALF group than those in IBN group at 12 months. Lumbar 1-4 (L)-BMD significantly increased from 6 months in IBN/ALF group and at 18 months in IBN group. L-BMD was significantly higher in IBN/ALF group (6.6% increase) than in IBN group (3.4%) at 18 months. Total hip (H)-BMD significantly increased from 6 months in IBN/ALF group and tended to improve in IBN group. H-BMD was significantly higher in IBN/ALF group (4.8%) than in IBN group (3.2%) at 18 months. In conclusion, treatment with ALF in combination with IBN improves BMD in post-menopausal women with osteoporosis.

Short-term bisphosphonate treatment reduces serum 25(OH) vitamin D3 and alters values of parathyroid hormone, pentosidine, and bone metabolic markers.

This study aimed to clarify the effects of short-term bisphosphonate (BP) administration in Japanese osteoporotic patients retrospectively. Daily minodronate (MIN) at 1 mg/day (MIN group) or weekly risedronate (RIS) at 17.5 mg/week (RIS group) was primarily prescribed for each patient. We analyzed the laboratory data of 35 cases (18 of MIN and 17 of RIS) before the start of treatment and at 4 months afterward. The changes in 25(OH)D3, whole parathyroid hormone (PTH), serum pentosidine, and the bone turnover markers urinary cross-linked N-telopeptide of type I collagen (NTX), serum tartrate-resistant acid phosphatase (TRACP)-5b, bone-specific alkaline phosphatase (BAP), and undercarboxylated osteocalcin were evaluated. Overall, serum 25(OH)D3 was significantly decreased from 21.8 to 18.4 ng/mL at 4 months, with a percent change of -14.7%. Whole PTH increased significantly from 23.4 to 30.0 pg/mL, with a percent change of 32.1%. Serum pentosidine rose from 0.0306 to 0.0337 µg/mL, with a percent change of 15.2%. In group comparisons, 25(OH)D3 and pentosidine showed comparable changes in both groups after 4 months of treatment, whereas whole PTH became significantly more increased in the MIN group. All bone turnover markers were significantly decreased at 4 months in both groups. Compared with the RIS group, the MIN group exhibited significantly larger value changes for urinary NTX, serum TRACP-5b, and BAP at the study end point. This study demonstrated that serum 25(OH)D3 became significantly decreased after only 4 months of BP treatment in Japanese osteoporotic patients and confirmed that MIN more strongly inhibited bone turnover as compared with RIS.

Compliance and discontinuation of denosumab treatment in postmenopausal Japanese women with primary osteoporosis or rheumatoid arthritis and osteoporosis.

OBJECTIVES: The aim of this study was to examine the discontinuation and occurrence of fracture during denosumab treatment in Japanese women with primary osteoporosis or rheumatoid arthritis (RA) with osteoporosis. METHODS: This retrospective study included 143 patients with primary osteoporosis and 96 patients with RA and osteoporosis who were treated with denosumab. Treatment discontinuation, fracture occurrence, lumbar spine (L1-4) bone mineral density (LS-BMD), and bilateral total hip BMD (TH-BMD) were examined before and at 1 and 2 years after treatment commencement. RESULTS: In the primary osteoporosis group, 32 cases dropped out and no fractures occurred from 0 to 1 year. Eighteen cases were lost to follow-up and no fractures were noted from 1 to 2 years. In the RA with osteoporosis group, 7 cases dropped out and no fracture occurred from 0 to 1 year. Twenty-one cases were lost to follow-up and 2 nonvertebral fractures were noted from 1 to 2 years. In this group, 13 cases dropped out from 1 to 2 years and 16 cases dropped out during the 2-year study period due to economic reasons. LS-BMD and TH-BMD values increased continuously for 2 years of treatment in both primary osteoporosis and RA with osteoporosis groups. CONCLUSIONS: These results suggest that during denosumab therapy, the discontinuation rate is expected to remain low during 2 years of treatment in primary osteoporotic patients. In RA patients with osteoporosis, however, the discontinuation rate may increase due to economic reasons from 1 to 2 years of therapy.

Bony findings detected by MRI may reflect the pathophysiology of osteoarthritis with thumb carpometacarpal joint pain.

BACKGROUND: Osteoarthritis (OA) is the most common skeletal disease worldwide. Although thumb carpametacarpal joint (CMJ) OA is also frequently encountered, the etiologies remain largely unknown. METHOD: We analyzed 20 patients who had thumb CMJ OA with accompanying joint pain and categorized a total of 37 thumbs according to the Eaton and Littler staging system. RESULTS: In patients with advanced OA, bone alterations as detected by magnetic resonance imaging (MRI) were observed in almost all of the painful joints. The frequency of bone alterations in the thumb CMJ increased with OA severity. In contrast, MRI revealed no bone alterations in thumbs with no pain and less pain in bilateral thumb basal pain, even in radiographically advanced OA. CONCLUSIONS: While the incidence of bone cysts in the CMJ was higher with OA staging, OA severity had no apparent correlation with pain. Thus, it is possible that the cause of thumb CMJ pain in advanced OA is bone alterations.