Clinical Inquiries

EVIDENCE SUMMARY

A 2014 Cochrane meta-analysis of 5 RCTs with a total of 733 patients examined the effectiveness of any type of exercise in decreasing vasomotor symptoms in perimenopausal and postmenopausal women.¹ The studies compared exercise—defined as structured exercise or physical activity through active living—with no active treatment, yoga, or hormone therapy (HT) over a 3- to 24-month follow-up period.

Three trials of 454 women that compared exercise with no active treatment found no difference between groups in frequency or intensity of vasomotor symptoms (standard mean difference [SMD]= -0.10; 95% confidence interval [CI], -0.33 to 0.13).

Two trials with 279 women that compared exercise with yoga didn’t find a difference in reported frequency or intensity of vasomotor symptoms between the groups (SMD= -0.03; 95% CI, -0.45 to 0.38).

One small trial (14 women) of exercise and HT found that HT patients reported decreased frequency of flushes over 24 hours compared with the exercise group (mean difference [MD]=5.8; 95% CI, 3.17-8.43).

Overall, the evidence was of low quality because of heterogeneity in study design.¹

Two exercise interventions fail to reduce symptoms

A 2014 RCT, published after the Cochrane search date, investigated exercise as a treatment for VMS in 261 perimenopausal and postmenopausal women ages 48 to 57 years.² Patients had a history of at least 5 hot flashes or night sweats per day and hadn’t taken HT in the previous 3 months.

The women were randomized to one of 2 exercise interventions or a control group. The exercise interventions both entailed 2 one-on-one consultations with a physical activity facilitator and use of a pedometer. Patients were encouraged to perform 30 minutes of moderate-intensity exercise 3 days a week during Weeks 1 through 12, then increase the frequency to 3 to 5 days a week during Weeks 13 through 24. In one intervention arm, the women also received an informational DVD and 5 educational leaflets.

In the other arm, they were invited to attend 3 exercise support groups in their local community. The control group was offered an opportunity for exercise consultation and given a pedometer at the end of the study.

At the end of the 6-month intervention, neither exercise intervention significantly decreased self-reported hot flashes/night sweats per week compared with the control group (DVD exercise arm vs control: MD= -8.9; 95% CI, -20 to 2.2; social support exercise arm vs control: MD= -5.2; 95% CI, -16.7 to 6.3). The study also found no difference in hot flashes/night sweats per week at 12-month follow-up between the DVD exercise arm and controls (MD= -3.2; 95% CI, -12.7 to 6.4) and the social-support group and controls (MD= -3.5; 95% CI, -13.2 to 6.1).

Drug therapy relieves symptoms, but other methods—not so much

An analysis of pooled individual data from 3 RCTs compared exercise with 5 other interventions for VMS in 899 perimenopausal and postmenopausal women.³ Patients had at least 14 bothersome symptoms per week.

Exercise doesn't decrease the frequency or severity of vasomotor menopausal symptoms in perimenopausal and post-menopausal women.

The 6 interventions ranged from nonpharmacologic therapies, such as aerobic exercise and yoga, to pharmacologic treatments, including escitalopram 10 to 20 mg/d, venlafaxine 75 mg/d, oral estradiol (E2) 0.5 mg/d, and omega-3 supplementation 1.8 g/d. The primary outcome was a change in VMS frequency and bother as assessed by a symptom diary over the 4- to 12-week follow-up.

The analysis found a significant 6-week reduction in daily VMS frequency relative to placebo for escitalopram (MD= -1.4; 95% CI, -2.7 to -0.2), low-dose E2 (MD= -1.9; 95% CI, -2.9 to -0.9), and venlafaxine (MD= -1.3; 95% CI, -2.3 to -0.3). However, no difference in VMS frequency or bother was found with exercise (MD= -0.4; 95% CI, -1.1 to 0.3), yoga (MD= -0.6; 95% CI, -1.3 to 0.1), or omega-3 supplementation (MD= 0.2; 95% CI, -0.4 to 0.8).

RECOMMENDATIONS

The American College of Obstetricians and Gynecologists (ACOG) doesn’t offer specific recommendations regarding exercise as a treatment for symptoms of menopause. The 2014 ACOG guidelines for managing symptoms report that data don’t support phytoestrogens, supplements, or lifestyle modifications (Level B, based on limited or inconsistent evidence). ACOG recommends basic palliative measures such as drinking cool drinks and decreasing layers of clothing (Level B).⁴

The American Association of Clinical Endocrinologists’ recommendations don’t mention exercise as a menopause therapy.⁵

The North American Menopause Society’s 2015 statement regarding the nonhormonal treatment of menopause symptoms doesn’t recommend exercise as an effective therapy because of insufficient or inconclusive data.⁶

EVIDENCE SUMMARY

A 2014 Cochrane meta-analysis of 5 RCTs with a total of 733 patients examined the effectiveness of any type of exercise in decreasing vasomotor symptoms in perimenopausal and postmenopausal women.¹ The studies compared exercise—defined as structured exercise or physical activity through active living—with no active treatment, yoga, or hormone therapy (HT) over a 3- to 24-month follow-up period.

Three trials of 454 women that compared exercise with no active treatment found no difference between groups in frequency or intensity of vasomotor symptoms (standard mean difference [SMD]= -0.10; 95% confidence interval [CI], -0.33 to 0.13).

Two trials with 279 women that compared exercise with yoga didn’t find a difference in reported frequency or intensity of vasomotor symptoms between the groups (SMD= -0.03; 95% CI, -0.45 to 0.38).

One small trial (14 women) of exercise and HT found that HT patients reported decreased frequency of flushes over 24 hours compared with the exercise group (mean difference [MD]=5.8; 95% CI, 3.17-8.43).

Overall, the evidence was of low quality because of heterogeneity in study design.¹

Two exercise interventions fail to reduce symptoms

A 2014 RCT, published after the Cochrane search date, investigated exercise as a treatment for VMS in 261 perimenopausal and postmenopausal women ages 48 to 57 years.² Patients had a history of at least 5 hot flashes or night sweats per day and hadn’t taken HT in the previous 3 months.

The women were randomized to one of 2 exercise interventions or a control group. The exercise interventions both entailed 2 one-on-one consultations with a physical activity facilitator and use of a pedometer. Patients were encouraged to perform 30 minutes of moderate-intensity exercise 3 days a week during Weeks 1 through 12, then increase the frequency to 3 to 5 days a week during Weeks 13 through 24. In one intervention arm, the women also received an informational DVD and 5 educational leaflets.

In the other arm, they were invited to attend 3 exercise support groups in their local community. The control group was offered an opportunity for exercise consultation and given a pedometer at the end of the study.

At the end of the 6-month intervention, neither exercise intervention significantly decreased self-reported hot flashes/night sweats per week compared with the control group (DVD exercise arm vs control: MD= -8.9; 95% CI, -20 to 2.2; social support exercise arm vs control: MD= -5.2; 95% CI, -16.7 to 6.3). The study also found no difference in hot flashes/night sweats per week at 12-month follow-up between the DVD exercise arm and controls (MD= -3.2; 95% CI, -12.7 to 6.4) and the social-support group and controls (MD= -3.5; 95% CI, -13.2 to 6.1).

Drug therapy relieves symptoms, but other methods—not so much

An analysis of pooled individual data from 3 RCTs compared exercise with 5 other interventions for VMS in 899 perimenopausal and postmenopausal women.³ Patients had at least 14 bothersome symptoms per week.

Exercise doesn't decrease the frequency or severity of vasomotor menopausal symptoms in perimenopausal and post-menopausal women.

The 6 interventions ranged from nonpharmacologic therapies, such as aerobic exercise and yoga, to pharmacologic treatments, including escitalopram 10 to 20 mg/d, venlafaxine 75 mg/d, oral estradiol (E2) 0.5 mg/d, and omega-3 supplementation 1.8 g/d. The primary outcome was a change in VMS frequency and bother as assessed by a symptom diary over the 4- to 12-week follow-up.

The analysis found a significant 6-week reduction in daily VMS frequency relative to placebo for escitalopram (MD= -1.4; 95% CI, -2.7 to -0.2), low-dose E2 (MD= -1.9; 95% CI, -2.9 to -0.9), and venlafaxine (MD= -1.3; 95% CI, -2.3 to -0.3). However, no difference in VMS frequency or bother was found with exercise (MD= -0.4; 95% CI, -1.1 to 0.3), yoga (MD= -0.6; 95% CI, -1.3 to 0.1), or omega-3 supplementation (MD= 0.2; 95% CI, -0.4 to 0.8).

RECOMMENDATIONS

The American College of Obstetricians and Gynecologists (ACOG) doesn’t offer specific recommendations regarding exercise as a treatment for symptoms of menopause. The 2014 ACOG guidelines for managing symptoms report that data don’t support phytoestrogens, supplements, or lifestyle modifications (Level B, based on limited or inconsistent evidence). ACOG recommends basic palliative measures such as drinking cool drinks and decreasing layers of clothing (Level B).⁴

The American Association of Clinical Endocrinologists’ recommendations don’t mention exercise as a menopause therapy.⁵

The North American Menopause Society’s 2015 statement regarding the nonhormonal treatment of menopause symptoms doesn’t recommend exercise as an effective therapy because of insufficient or inconclusive data.⁶

EVIDENCE SUMMARY

A 2014 Cochrane meta-analysis of 5 RCTs with a total of 733 patients examined the effectiveness of any type of exercise in decreasing vasomotor symptoms in perimenopausal and postmenopausal women.¹ The studies compared exercise—defined as structured exercise or physical activity through active living—with no active treatment, yoga, or hormone therapy (HT) over a 3- to 24-month follow-up period.

Three trials of 454 women that compared exercise with no active treatment found no difference between groups in frequency or intensity of vasomotor symptoms (standard mean difference [SMD]= -0.10; 95% confidence interval [CI], -0.33 to 0.13).

Two trials with 279 women that compared exercise with yoga didn’t find a difference in reported frequency or intensity of vasomotor symptoms between the groups (SMD= -0.03; 95% CI, -0.45 to 0.38).

One small trial (14 women) of exercise and HT found that HT patients reported decreased frequency of flushes over 24 hours compared with the exercise group (mean difference [MD]=5.8; 95% CI, 3.17-8.43).

Overall, the evidence was of low quality because of heterogeneity in study design.¹

Two exercise interventions fail to reduce symptoms

A 2014 RCT, published after the Cochrane search date, investigated exercise as a treatment for VMS in 261 perimenopausal and postmenopausal women ages 48 to 57 years.² Patients had a history of at least 5 hot flashes or night sweats per day and hadn’t taken HT in the previous 3 months.

The women were randomized to one of 2 exercise interventions or a control group. The exercise interventions both entailed 2 one-on-one consultations with a physical activity facilitator and use of a pedometer. Patients were encouraged to perform 30 minutes of moderate-intensity exercise 3 days a week during Weeks 1 through 12, then increase the frequency to 3 to 5 days a week during Weeks 13 through 24. In one intervention arm, the women also received an informational DVD and 5 educational leaflets.

In the other arm, they were invited to attend 3 exercise support groups in their local community. The control group was offered an opportunity for exercise consultation and given a pedometer at the end of the study.

At the end of the 6-month intervention, neither exercise intervention significantly decreased self-reported hot flashes/night sweats per week compared with the control group (DVD exercise arm vs control: MD= -8.9; 95% CI, -20 to 2.2; social support exercise arm vs control: MD= -5.2; 95% CI, -16.7 to 6.3). The study also found no difference in hot flashes/night sweats per week at 12-month follow-up between the DVD exercise arm and controls (MD= -3.2; 95% CI, -12.7 to 6.4) and the social-support group and controls (MD= -3.5; 95% CI, -13.2 to 6.1).

Drug therapy relieves symptoms, but other methods—not so much

An analysis of pooled individual data from 3 RCTs compared exercise with 5 other interventions for VMS in 899 perimenopausal and postmenopausal women.³ Patients had at least 14 bothersome symptoms per week.

Exercise doesn't decrease the frequency or severity of vasomotor menopausal symptoms in perimenopausal and post-menopausal women.

The 6 interventions ranged from nonpharmacologic therapies, such as aerobic exercise and yoga, to pharmacologic treatments, including escitalopram 10 to 20 mg/d, venlafaxine 75 mg/d, oral estradiol (E2) 0.5 mg/d, and omega-3 supplementation 1.8 g/d. The primary outcome was a change in VMS frequency and bother as assessed by a symptom diary over the 4- to 12-week follow-up.

The analysis found a significant 6-week reduction in daily VMS frequency relative to placebo for escitalopram (MD= -1.4; 95% CI, -2.7 to -0.2), low-dose E2 (MD= -1.9; 95% CI, -2.9 to -0.9), and venlafaxine (MD= -1.3; 95% CI, -2.3 to -0.3). However, no difference in VMS frequency or bother was found with exercise (MD= -0.4; 95% CI, -1.1 to 0.3), yoga (MD= -0.6; 95% CI, -1.3 to 0.1), or omega-3 supplementation (MD= 0.2; 95% CI, -0.4 to 0.8).

RECOMMENDATIONS

The American College of Obstetricians and Gynecologists (ACOG) doesn’t offer specific recommendations regarding exercise as a treatment for symptoms of menopause. The 2014 ACOG guidelines for managing symptoms report that data don’t support phytoestrogens, supplements, or lifestyle modifications (Level B, based on limited or inconsistent evidence). ACOG recommends basic palliative measures such as drinking cool drinks and decreasing layers of clothing (Level B).⁴

The American Association of Clinical Endocrinologists’ recommendations don’t mention exercise as a menopause therapy.⁵

The North American Menopause Society’s 2015 statement regarding the nonhormonal treatment of menopause symptoms doesn’t recommend exercise as an effective therapy because of insufficient or inconclusive data.⁶

EVIDENCE SUMMARY

A 25-week double-blind, placebo-controlled RCT of 51 nursing home patients (mean age 76 years, range 50 to 95 years; 96% men) in 2000 found no difference in all-cause mortality between the MA treatment group and the placebo group (absolute risk reduction [ARR]=13.4%; 95% confidence interval [CI], -12.9% to 37.3%; number needed to harm [NNH]=7; 95% CI, -8 to 3).¹

A 2007 case-control study of 17,328 nursing home residents (mean age 84 years [standard deviation, 9]; 71% women) found increased mortality for residents treated with at least 6 days of MA (median survival=23.9 months; 95% CI, 20.2-27.5) compared with untreated residents (median survival=31.2 months; 95% CI, 27.8-35.9).² The decrease in median survival remained after adjusting for demographic variables, medical diagnoses, and cognitive and physical functioning (hazard ratio=1.37; 95% CI, 1.17-1.59). Follow-up ranged from 30 days to 44 months.

Risks related to megestrol acetate include deep vein thrombosis

The 2000 double-blind, placebo-controlled RCT of 51 nursing home patients found no difference in adverse events between the MA group and the placebo group (absolute risk increase=6.3%; 95% CI, -14.7% to 27.3%).¹ No DVTs were reported as adverse events.

A 2003 retrospective chart review of 246 nursing home residents (mean age 87 years, 77% women) who were given MA 400 mg/d found an overall incidence of DVT of 4.1% (10 residents); 3.2% (8) residents were on MA at the time of DVT occurrence.³

A 2000 retrospective chart review of 19 nursing home residents who were prescribed MA (mean age 83 years, range 66 to 92 years; 84% women) found 32% (6) who developed Doppler-confirmed DVT after 50 days of therapy.⁴ DVT was not associated with known risk factors, age, body mass index, numbers of medications, or other medical diagnoses. The authors didn’t report MA dosage.

Patients on megestrol acetate don’t gain weight...

The 2000 double-blind, placebo-controlled RCT of 51 nursing home patients found no difference between the MA (800 mg/d for 12 weeks) and placebo groups in percentage of patients who gained ≥1.82 kg (ARR=-6.6%; 95% CI, -30.2% to 18.2%).¹ At the 25-week follow-up (after the MA patients had been off the therapy for 13 weeks), a statistically, but not clinically, significant difference was observed in the number of MA patients who gained ≥1.82 kg (absolute benefit increase=40.2%; 95% CI, 13.4%-66.9%; number needed to treat [NNT]=2; 95% CI, 1-8). Of note, the authors based their statistics on a weight gain of ≥1.82 kg whereas 5 kg or 5% weight gain is the more commonly used definition for clinical significance.⁵

Megestrol acetate is neither safe nor effective for stimulating appetite in malnourished nursing home residents.

The 2007 case-control cohort study of 17,328 nursing home residents, who had lost 5% of total body weight in 3 months or 10% of total body weight in 6 months, also found no significant difference in weight gain between MA-treated patients (median dose=486 mg, range 20 to 2400 mg; median duration=90 days, range 7 to 934 days; median change=1 lb, interquartile range [IQR]=-8 to 10) and controls (median change=2 lb, IQR=-4 to 9) after 6 months of treatment.²

In a 2005 prospective case series of 17 nursing home residents (mean age 92 years [standard deviation, 6], 88% women), MA (400 mg/d for 63 days) was associated with weight loss (mean=-2.13±9.32 lb).⁶ Nine patients (53%) lost weight (mean=9.3±5.4 lb), and 8 patients (47%) gained weight (mean=5.9±4.9 lb).

A retrospective chart review in 2000 of 14 nursing home residents (mean age 84 years, range 74 to 97 years; 85% women) who received MA 40 to 800 mg/d for one to 15 weeks showed that 43% gained weight (mean=3.1 kg), 43% lost weight (mean=2.0 kg), and 14% had no weight change.⁷

A 2002 retrospective chart review of 50 nursing home residents (mean age 79 years, range 31 to 93 years; 74% women) who were treated with MA 200 to 2400 mg/d for at least 6 months found a mean weight loss of 1.1 to 2.2 kg.⁸ In the 6 months after MA discontinuation, weight gain for available subjects (5 to 16 patients) varied (mean monthly change=-0.17 kg to 3.07 kg). The study had a high attrition rate (26 patients were lost 6 months after MA initiation; 39 were lost 6 months after MA discontinuation).

RECOMMENDATIONS

The 2015 American Geriatrics Society Beers Criteria for potentially inappropriate medication use in older adults strongly advises against the use of MA because of limited increases in weight and increased risk of thrombotic events.⁹

EVIDENCE SUMMARY

A 25-week double-blind, placebo-controlled RCT of 51 nursing home patients (mean age 76 years, range 50 to 95 years; 96% men) in 2000 found no difference in all-cause mortality between the MA treatment group and the placebo group (absolute risk reduction [ARR]=13.4%; 95% confidence interval [CI], -12.9% to 37.3%; number needed to harm [NNH]=7; 95% CI, -8 to 3).¹

A 2007 case-control study of 17,328 nursing home residents (mean age 84 years [standard deviation, 9]; 71% women) found increased mortality for residents treated with at least 6 days of MA (median survival=23.9 months; 95% CI, 20.2-27.5) compared with untreated residents (median survival=31.2 months; 95% CI, 27.8-35.9).² The decrease in median survival remained after adjusting for demographic variables, medical diagnoses, and cognitive and physical functioning (hazard ratio=1.37; 95% CI, 1.17-1.59). Follow-up ranged from 30 days to 44 months.

Risks related to megestrol acetate include deep vein thrombosis

The 2000 double-blind, placebo-controlled RCT of 51 nursing home patients found no difference in adverse events between the MA group and the placebo group (absolute risk increase=6.3%; 95% CI, -14.7% to 27.3%).¹ No DVTs were reported as adverse events.

A 2003 retrospective chart review of 246 nursing home residents (mean age 87 years, 77% women) who were given MA 400 mg/d found an overall incidence of DVT of 4.1% (10 residents); 3.2% (8) residents were on MA at the time of DVT occurrence.³

A 2000 retrospective chart review of 19 nursing home residents who were prescribed MA (mean age 83 years, range 66 to 92 years; 84% women) found 32% (6) who developed Doppler-confirmed DVT after 50 days of therapy.⁴ DVT was not associated with known risk factors, age, body mass index, numbers of medications, or other medical diagnoses. The authors didn’t report MA dosage.

Patients on megestrol acetate don’t gain weight...

The 2000 double-blind, placebo-controlled RCT of 51 nursing home patients found no difference between the MA (800 mg/d for 12 weeks) and placebo groups in percentage of patients who gained ≥1.82 kg (ARR=-6.6%; 95% CI, -30.2% to 18.2%).¹ At the 25-week follow-up (after the MA patients had been off the therapy for 13 weeks), a statistically, but not clinically, significant difference was observed in the number of MA patients who gained ≥1.82 kg (absolute benefit increase=40.2%; 95% CI, 13.4%-66.9%; number needed to treat [NNT]=2; 95% CI, 1-8). Of note, the authors based their statistics on a weight gain of ≥1.82 kg whereas 5 kg or 5% weight gain is the more commonly used definition for clinical significance.⁵

Megestrol acetate is neither safe nor effective for stimulating appetite in malnourished nursing home residents.

The 2007 case-control cohort study of 17,328 nursing home residents, who had lost 5% of total body weight in 3 months or 10% of total body weight in 6 months, also found no significant difference in weight gain between MA-treated patients (median dose=486 mg, range 20 to 2400 mg; median duration=90 days, range 7 to 934 days; median change=1 lb, interquartile range [IQR]=-8 to 10) and controls (median change=2 lb, IQR=-4 to 9) after 6 months of treatment.²

In a 2005 prospective case series of 17 nursing home residents (mean age 92 years [standard deviation, 6], 88% women), MA (400 mg/d for 63 days) was associated with weight loss (mean=-2.13±9.32 lb).⁶ Nine patients (53%) lost weight (mean=9.3±5.4 lb), and 8 patients (47%) gained weight (mean=5.9±4.9 lb).

A retrospective chart review in 2000 of 14 nursing home residents (mean age 84 years, range 74 to 97 years; 85% women) who received MA 40 to 800 mg/d for one to 15 weeks showed that 43% gained weight (mean=3.1 kg), 43% lost weight (mean=2.0 kg), and 14% had no weight change.⁷

A 2002 retrospective chart review of 50 nursing home residents (mean age 79 years, range 31 to 93 years; 74% women) who were treated with MA 200 to 2400 mg/d for at least 6 months found a mean weight loss of 1.1 to 2.2 kg.⁸ In the 6 months after MA discontinuation, weight gain for available subjects (5 to 16 patients) varied (mean monthly change=-0.17 kg to 3.07 kg). The study had a high attrition rate (26 patients were lost 6 months after MA initiation; 39 were lost 6 months after MA discontinuation).

RECOMMENDATIONS

The 2015 American Geriatrics Society Beers Criteria for potentially inappropriate medication use in older adults strongly advises against the use of MA because of limited increases in weight and increased risk of thrombotic events.⁹

EVIDENCE SUMMARY

A 25-week double-blind, placebo-controlled RCT of 51 nursing home patients (mean age 76 years, range 50 to 95 years; 96% men) in 2000 found no difference in all-cause mortality between the MA treatment group and the placebo group (absolute risk reduction [ARR]=13.4%; 95% confidence interval [CI], -12.9% to 37.3%; number needed to harm [NNH]=7; 95% CI, -8 to 3).¹

A 2007 case-control study of 17,328 nursing home residents (mean age 84 years [standard deviation, 9]; 71% women) found increased mortality for residents treated with at least 6 days of MA (median survival=23.9 months; 95% CI, 20.2-27.5) compared with untreated residents (median survival=31.2 months; 95% CI, 27.8-35.9).² The decrease in median survival remained after adjusting for demographic variables, medical diagnoses, and cognitive and physical functioning (hazard ratio=1.37; 95% CI, 1.17-1.59). Follow-up ranged from 30 days to 44 months.

Risks related to megestrol acetate include deep vein thrombosis

The 2000 double-blind, placebo-controlled RCT of 51 nursing home patients found no difference in adverse events between the MA group and the placebo group (absolute risk increase=6.3%; 95% CI, -14.7% to 27.3%).¹ No DVTs were reported as adverse events.

A 2003 retrospective chart review of 246 nursing home residents (mean age 87 years, 77% women) who were given MA 400 mg/d found an overall incidence of DVT of 4.1% (10 residents); 3.2% (8) residents were on MA at the time of DVT occurrence.³

A 2000 retrospective chart review of 19 nursing home residents who were prescribed MA (mean age 83 years, range 66 to 92 years; 84% women) found 32% (6) who developed Doppler-confirmed DVT after 50 days of therapy.⁴ DVT was not associated with known risk factors, age, body mass index, numbers of medications, or other medical diagnoses. The authors didn’t report MA dosage.

Patients on megestrol acetate don’t gain weight...

The 2000 double-blind, placebo-controlled RCT of 51 nursing home patients found no difference between the MA (800 mg/d for 12 weeks) and placebo groups in percentage of patients who gained ≥1.82 kg (ARR=-6.6%; 95% CI, -30.2% to 18.2%).¹ At the 25-week follow-up (after the MA patients had been off the therapy for 13 weeks), a statistically, but not clinically, significant difference was observed in the number of MA patients who gained ≥1.82 kg (absolute benefit increase=40.2%; 95% CI, 13.4%-66.9%; number needed to treat [NNT]=2; 95% CI, 1-8). Of note, the authors based their statistics on a weight gain of ≥1.82 kg whereas 5 kg or 5% weight gain is the more commonly used definition for clinical significance.⁵

Megestrol acetate is neither safe nor effective for stimulating appetite in malnourished nursing home residents.

The 2007 case-control cohort study of 17,328 nursing home residents, who had lost 5% of total body weight in 3 months or 10% of total body weight in 6 months, also found no significant difference in weight gain between MA-treated patients (median dose=486 mg, range 20 to 2400 mg; median duration=90 days, range 7 to 934 days; median change=1 lb, interquartile range [IQR]=-8 to 10) and controls (median change=2 lb, IQR=-4 to 9) after 6 months of treatment.²

In a 2005 prospective case series of 17 nursing home residents (mean age 92 years [standard deviation, 6], 88% women), MA (400 mg/d for 63 days) was associated with weight loss (mean=-2.13±9.32 lb).⁶ Nine patients (53%) lost weight (mean=9.3±5.4 lb), and 8 patients (47%) gained weight (mean=5.9±4.9 lb).

A retrospective chart review in 2000 of 14 nursing home residents (mean age 84 years, range 74 to 97 years; 85% women) who received MA 40 to 800 mg/d for one to 15 weeks showed that 43% gained weight (mean=3.1 kg), 43% lost weight (mean=2.0 kg), and 14% had no weight change.⁷

A 2002 retrospective chart review of 50 nursing home residents (mean age 79 years, range 31 to 93 years; 74% women) who were treated with MA 200 to 2400 mg/d for at least 6 months found a mean weight loss of 1.1 to 2.2 kg.⁸ In the 6 months after MA discontinuation, weight gain for available subjects (5 to 16 patients) varied (mean monthly change=-0.17 kg to 3.07 kg). The study had a high attrition rate (26 patients were lost 6 months after MA initiation; 39 were lost 6 months after MA discontinuation).

RECOMMENDATIONS

The 2015 American Geriatrics Society Beers Criteria for potentially inappropriate medication use in older adults strongly advises against the use of MA because of limited increases in weight and increased risk of thrombotic events.⁹

EVIDENCE SUMMARY

A Cochrane review of 16 RCTs (2144 patients) compared pain relief and return to function with oral NSAIDs and other oral analgesics (acetaminophen, opioids, or opioids plus acetaminophen) in patients who had suffered a soft tissue injury within the past 48 hours.¹ No differences between NSAIDs and acetaminophen were seen in pain relief at fewer than 24 hours on a 100-point visual analog scale (VAS) (4 trials; 359 patients; mean difference [MD]=1.56; 95% confidence interval [CI], -3.9 to 7.0). Nor were differences observed in return to function at 7 days (3 trials, 386 patients; risk ratio [RR]=0.99; 95% CI, 0.90-1.09).

No differences in pain relief between NSAIDs and oral opioids were seen at fewer than 24 hours (2 trials, 757 patients; MD=-0.02; 95% CI, -3.71 to 3.68) nor at days 4 to 6 (one trial, 706 patients; MD=-2.9; 95% CI, -6.06 to 0.26). Compared with NSAIDs, opioids showed a small increase in return to function at 7 days (2 trials, 749 patients; RR=1.13; 95% CI, 1.03-1.25), but the combination of acetaminophen and opioids didn’t show a difference (one trial, 89 patients; RR= 1.28; 95% CI, 0.90-1.81).

Adverse gastrointestinal events (not defined) were no different between NSAIDs and acetaminophen (7 trials, 627 patients; RR=1.76; 95% CI, 0.99-3.14) and occurred less often with NSAIDs than with oral opioids (2 trials, 769 patients; RR=0.51; 95% CI, 0.37-0.69). Overall, the authors concluded that low-quality evidence consistently showed NSAIDs were at least equal to other oral analgesics in efficacy of pain relief and return to function.

Naproxen vs oxycodone: The opioid has more adverse effects

A double-blind, noninferiority, randomized trial (published after the Cochrane review search date) compared the effects of treatment with a single dose of oxycodone with a single dose of naproxen in 150 adult emergency department (ED) patients in a tertiary care academic center who had acute soft tissue injury and pain scores between 3 and 7 (on a 1-to-10 scale).² Injuries included sprains, strains, contusions, low-back injury, and intervertebral disk problems. The authors didn’t clearly define “acute” with regard to time from injury.

Patients were randomized and given a single dose of oxycodone 10 mg or naproxen 250 mg with water. Pain scores and adverse effects were reassessed at 30 minutes and 60 minutes after administration, and a follow-up phone call was placed at 24 hours to evaluate further need for analgesics and adverse effects.

Baseline pain scores before medication administration were similar in the 2 groups (6.21 for the oxycodone group, 6 for the naproxen group). No difference in pain scores between oxycodone and naproxen was seen at 30 minutes (4.5 vs 4.4; P=.76) or 60 minutes (2.5 vs 2.6; P=.45). The number of patients who required more analgesics within 24 hours after administration didn’t differ significantly between the oxycodone group and the naproxen group (12 patients vs 5 patients; P=.07).

The study evaluated adverse effects, including nausea, vomiting, dizziness, drowsiness, pruritus, and epigastric pain. Overall, 22% of patients (33) from both groups combined experienced at least one adverse effect. The oxycodone group reported more adverse effects overall (36% vs 8%; RR=4.5; 95% CI, 2.0-10.2;). Ten patients experienced nausea, 6 vomiting, 4 dizziness, 3 drowsiness, and 2 pruritis. In the naproxen group, 4 patients experienced nausea; no other adverse effects were reported.

A double-blind RCT in a university hospital ED in Hong Kong compared patients older than 16 years with “isolated painful limb injury” after trauma who received combinations of analgesics or placebo.³ Patients were recruited during typical work-week hours (Monday to Friday, 9 am to 5 pm) and randomized into 4 groups: acetaminophen 1 g plus placebo (66 patients), placebo plus indomethacin 25 mg (71 patients), placebo plus diclofenac 25 mg (69 patients), or acetaminophen 1 g plus diclofenac 25 mg (94 patients).

Each patient was given the group’s designated combination of analgesics in the ED and asked to rate pain on a 0-to-100 visual analog pain scale (VAPS) at 0, 30, 60, 90, and 120 minutes after administration. Patients then left the ED with a 3-day course of their analgesic combination and were instructed to take the medication 4 times daily on the first day and 3 times daily thereafter. Patients recorded pain scores on the VAPS 3 times daily after discharge and at follow-up 5 to 8 days after initial presentation. Intention-to-treat analysis was done for patients lost to follow-up. A change in VAPS of 13 was considered clinically significant.

NSAIDs are at least as effective as opioids and acetaminophen in relieving pain from acute musculoskeletal injury.

All groups started with similar pain scores (30 at rest and 70 with activity) and didn’t achieve clinically significant pain relief within the first hour (mean change in VAPS <13). At 90 minutes, all groups achieved a mean change in VAPS >13, with no statistically significant difference between the groups. Adverse effects were rare (7% total), and none were severe (no gastrointestinal hemorrhage or renal damage).

Outside the ED, the acetaminophen-diclofenac combination group showed the greatest pain score reduction at every time point at rest and with activity, but none of the reductions were statistically or clinically significant (results presented graphically). No difference was found between the groups in number of patients who completed the course of analgesics, took additional analgesia, tried Chinese medicine, or returned to the ED within 30 days.

Limitations to the study included that the medication dosages may be much lower than typical dosages given in the United States and therefore lack applicability. The study also didn’t include a true placebo arm.

EVIDENCE SUMMARY

A Cochrane review of 16 RCTs (2144 patients) compared pain relief and return to function with oral NSAIDs and other oral analgesics (acetaminophen, opioids, or opioids plus acetaminophen) in patients who had suffered a soft tissue injury within the past 48 hours.¹ No differences between NSAIDs and acetaminophen were seen in pain relief at fewer than 24 hours on a 100-point visual analog scale (VAS) (4 trials; 359 patients; mean difference [MD]=1.56; 95% confidence interval [CI], -3.9 to 7.0). Nor were differences observed in return to function at 7 days (3 trials, 386 patients; risk ratio [RR]=0.99; 95% CI, 0.90-1.09).

No differences in pain relief between NSAIDs and oral opioids were seen at fewer than 24 hours (2 trials, 757 patients; MD=-0.02; 95% CI, -3.71 to 3.68) nor at days 4 to 6 (one trial, 706 patients; MD=-2.9; 95% CI, -6.06 to 0.26). Compared with NSAIDs, opioids showed a small increase in return to function at 7 days (2 trials, 749 patients; RR=1.13; 95% CI, 1.03-1.25), but the combination of acetaminophen and opioids didn’t show a difference (one trial, 89 patients; RR= 1.28; 95% CI, 0.90-1.81).

Adverse gastrointestinal events (not defined) were no different between NSAIDs and acetaminophen (7 trials, 627 patients; RR=1.76; 95% CI, 0.99-3.14) and occurred less often with NSAIDs than with oral opioids (2 trials, 769 patients; RR=0.51; 95% CI, 0.37-0.69). Overall, the authors concluded that low-quality evidence consistently showed NSAIDs were at least equal to other oral analgesics in efficacy of pain relief and return to function.

Naproxen vs oxycodone: The opioid has more adverse effects

A double-blind, noninferiority, randomized trial (published after the Cochrane review search date) compared the effects of treatment with a single dose of oxycodone with a single dose of naproxen in 150 adult emergency department (ED) patients in a tertiary care academic center who had acute soft tissue injury and pain scores between 3 and 7 (on a 1-to-10 scale).² Injuries included sprains, strains, contusions, low-back injury, and intervertebral disk problems. The authors didn’t clearly define “acute” with regard to time from injury.

Patients were randomized and given a single dose of oxycodone 10 mg or naproxen 250 mg with water. Pain scores and adverse effects were reassessed at 30 minutes and 60 minutes after administration, and a follow-up phone call was placed at 24 hours to evaluate further need for analgesics and adverse effects.

Baseline pain scores before medication administration were similar in the 2 groups (6.21 for the oxycodone group, 6 for the naproxen group). No difference in pain scores between oxycodone and naproxen was seen at 30 minutes (4.5 vs 4.4; P=.76) or 60 minutes (2.5 vs 2.6; P=.45). The number of patients who required more analgesics within 24 hours after administration didn’t differ significantly between the oxycodone group and the naproxen group (12 patients vs 5 patients; P=.07).

The study evaluated adverse effects, including nausea, vomiting, dizziness, drowsiness, pruritus, and epigastric pain. Overall, 22% of patients (33) from both groups combined experienced at least one adverse effect. The oxycodone group reported more adverse effects overall (36% vs 8%; RR=4.5; 95% CI, 2.0-10.2;). Ten patients experienced nausea, 6 vomiting, 4 dizziness, 3 drowsiness, and 2 pruritis. In the naproxen group, 4 patients experienced nausea; no other adverse effects were reported.

A double-blind RCT in a university hospital ED in Hong Kong compared patients older than 16 years with “isolated painful limb injury” after trauma who received combinations of analgesics or placebo.³ Patients were recruited during typical work-week hours (Monday to Friday, 9 am to 5 pm) and randomized into 4 groups: acetaminophen 1 g plus placebo (66 patients), placebo plus indomethacin 25 mg (71 patients), placebo plus diclofenac 25 mg (69 patients), or acetaminophen 1 g plus diclofenac 25 mg (94 patients).

Each patient was given the group’s designated combination of analgesics in the ED and asked to rate pain on a 0-to-100 visual analog pain scale (VAPS) at 0, 30, 60, 90, and 120 minutes after administration. Patients then left the ED with a 3-day course of their analgesic combination and were instructed to take the medication 4 times daily on the first day and 3 times daily thereafter. Patients recorded pain scores on the VAPS 3 times daily after discharge and at follow-up 5 to 8 days after initial presentation. Intention-to-treat analysis was done for patients lost to follow-up. A change in VAPS of 13 was considered clinically significant.

NSAIDs are at least as effective as opioids and acetaminophen in relieving pain from acute musculoskeletal injury.

All groups started with similar pain scores (30 at rest and 70 with activity) and didn’t achieve clinically significant pain relief within the first hour (mean change in VAPS <13). At 90 minutes, all groups achieved a mean change in VAPS >13, with no statistically significant difference between the groups. Adverse effects were rare (7% total), and none were severe (no gastrointestinal hemorrhage or renal damage).

Outside the ED, the acetaminophen-diclofenac combination group showed the greatest pain score reduction at every time point at rest and with activity, but none of the reductions were statistically or clinically significant (results presented graphically). No difference was found between the groups in number of patients who completed the course of analgesics, took additional analgesia, tried Chinese medicine, or returned to the ED within 30 days.

Limitations to the study included that the medication dosages may be much lower than typical dosages given in the United States and therefore lack applicability. The study also didn’t include a true placebo arm.

EVIDENCE SUMMARY

A Cochrane review of 16 RCTs (2144 patients) compared pain relief and return to function with oral NSAIDs and other oral analgesics (acetaminophen, opioids, or opioids plus acetaminophen) in patients who had suffered a soft tissue injury within the past 48 hours.¹ No differences between NSAIDs and acetaminophen were seen in pain relief at fewer than 24 hours on a 100-point visual analog scale (VAS) (4 trials; 359 patients; mean difference [MD]=1.56; 95% confidence interval [CI], -3.9 to 7.0). Nor were differences observed in return to function at 7 days (3 trials, 386 patients; risk ratio [RR]=0.99; 95% CI, 0.90-1.09).

No differences in pain relief between NSAIDs and oral opioids were seen at fewer than 24 hours (2 trials, 757 patients; MD=-0.02; 95% CI, -3.71 to 3.68) nor at days 4 to 6 (one trial, 706 patients; MD=-2.9; 95% CI, -6.06 to 0.26). Compared with NSAIDs, opioids showed a small increase in return to function at 7 days (2 trials, 749 patients; RR=1.13; 95% CI, 1.03-1.25), but the combination of acetaminophen and opioids didn’t show a difference (one trial, 89 patients; RR= 1.28; 95% CI, 0.90-1.81).

Adverse gastrointestinal events (not defined) were no different between NSAIDs and acetaminophen (7 trials, 627 patients; RR=1.76; 95% CI, 0.99-3.14) and occurred less often with NSAIDs than with oral opioids (2 trials, 769 patients; RR=0.51; 95% CI, 0.37-0.69). Overall, the authors concluded that low-quality evidence consistently showed NSAIDs were at least equal to other oral analgesics in efficacy of pain relief and return to function.

Naproxen vs oxycodone: The opioid has more adverse effects

A double-blind, noninferiority, randomized trial (published after the Cochrane review search date) compared the effects of treatment with a single dose of oxycodone with a single dose of naproxen in 150 adult emergency department (ED) patients in a tertiary care academic center who had acute soft tissue injury and pain scores between 3 and 7 (on a 1-to-10 scale).² Injuries included sprains, strains, contusions, low-back injury, and intervertebral disk problems. The authors didn’t clearly define “acute” with regard to time from injury.

Patients were randomized and given a single dose of oxycodone 10 mg or naproxen 250 mg with water. Pain scores and adverse effects were reassessed at 30 minutes and 60 minutes after administration, and a follow-up phone call was placed at 24 hours to evaluate further need for analgesics and adverse effects.

Baseline pain scores before medication administration were similar in the 2 groups (6.21 for the oxycodone group, 6 for the naproxen group). No difference in pain scores between oxycodone and naproxen was seen at 30 minutes (4.5 vs 4.4; P=.76) or 60 minutes (2.5 vs 2.6; P=.45). The number of patients who required more analgesics within 24 hours after administration didn’t differ significantly between the oxycodone group and the naproxen group (12 patients vs 5 patients; P=.07).

The study evaluated adverse effects, including nausea, vomiting, dizziness, drowsiness, pruritus, and epigastric pain. Overall, 22% of patients (33) from both groups combined experienced at least one adverse effect. The oxycodone group reported more adverse effects overall (36% vs 8%; RR=4.5; 95% CI, 2.0-10.2;). Ten patients experienced nausea, 6 vomiting, 4 dizziness, 3 drowsiness, and 2 pruritis. In the naproxen group, 4 patients experienced nausea; no other adverse effects were reported.

A double-blind RCT in a university hospital ED in Hong Kong compared patients older than 16 years with “isolated painful limb injury” after trauma who received combinations of analgesics or placebo.³ Patients were recruited during typical work-week hours (Monday to Friday, 9 am to 5 pm) and randomized into 4 groups: acetaminophen 1 g plus placebo (66 patients), placebo plus indomethacin 25 mg (71 patients), placebo plus diclofenac 25 mg (69 patients), or acetaminophen 1 g plus diclofenac 25 mg (94 patients).

Each patient was given the group’s designated combination of analgesics in the ED and asked to rate pain on a 0-to-100 visual analog pain scale (VAPS) at 0, 30, 60, 90, and 120 minutes after administration. Patients then left the ED with a 3-day course of their analgesic combination and were instructed to take the medication 4 times daily on the first day and 3 times daily thereafter. Patients recorded pain scores on the VAPS 3 times daily after discharge and at follow-up 5 to 8 days after initial presentation. Intention-to-treat analysis was done for patients lost to follow-up. A change in VAPS of 13 was considered clinically significant.

NSAIDs are at least as effective as opioids and acetaminophen in relieving pain from acute musculoskeletal injury.

All groups started with similar pain scores (30 at rest and 70 with activity) and didn’t achieve clinically significant pain relief within the first hour (mean change in VAPS <13). At 90 minutes, all groups achieved a mean change in VAPS >13, with no statistically significant difference between the groups. Adverse effects were rare (7% total), and none were severe (no gastrointestinal hemorrhage or renal damage).

Outside the ED, the acetaminophen-diclofenac combination group showed the greatest pain score reduction at every time point at rest and with activity, but none of the reductions were statistically or clinically significant (results presented graphically). No difference was found between the groups in number of patients who completed the course of analgesics, took additional analgesia, tried Chinese medicine, or returned to the ED within 30 days.

Limitations to the study included that the medication dosages may be much lower than typical dosages given in the United States and therefore lack applicability. The study also didn’t include a true placebo arm.

EVIDENCE SUMMARY

A 2015 network meta-analysis of 137 RCTs with 33,243 patients (ages 45-76 years) with knee OA compared the effectiveness of a variety of treatments including intra-articular CS and HA.¹ At 3 months, the effect on pain was not significantly different between the CS and HA groups (12 trials; effect size [ES]=0.02; 95% confidence interval [CI], -0.12 to 0.17). However, a small but significant improvement in function was noted (scoring system not defined) at 3 months favoring HA (ES=0.24; 95% CI, 0.06-0.43; number of trials not specified).

At 3 and 6 months, HA improves pain, but not function, more than CS

Another meta-analysis published in 2015 examined the effectiveness of intra-articular CS and HA in 7 RCTs with 583 patients with knee OA.² All 7 trials were included in the network meta-analysis and discussed separately to evaluate different time points.

Pain at one month wasn’t significantly different using a visual analog score (VAS) of one to 100 (4 trials; 245 patients; mean difference [MD]=1.66 points; 95% CI, -0.90 to 4.23). At 3 and 6 months, the HA group reported significantly reduced pain compared with the CS group (3 months: 3 trials; 320 patients; MD=12.58 points; 95% CI, -17.76 to -7.40; 6 months: 5 trials; 411 patients; MD=9.01 points; 95% CI, -12.62 to -5.40). There were no significant differences in function outcomes (Index of severity for OA of the knee by Lequesne et al; The Knee Society Clinical Rating System), maximum flexion, or adverse events.

Triamcinolone improves pain, function, but not for long

A 2016 double-blind RCT of 110 patients with knee OA compared intra-articular HA and triamcinolone, assessing pain and function at intervals between 24 hours and 6 months.³ Patients in the HA group received a single injection of 6 mL hylan G-F 20 (Synvisc); patients in the CS group received 1 mL of triamcinolone acetonide 40 mg and 5 mL of 1% lidocaine with epinephrine.

The CS group reported significantly less pain (VAS score 1 to 100) at 24 hours than the HA group (24 points vs 36 points; P=.002); relief lasted as long as one week (14 points vs 23 points; P=.018). After the first week, no difference was seen in pain between groups for as long as 6 months.

Function, assessed by a modified Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC 1 to 100; higher score indicates worse pain, stiffness, and function) showed a significant improvement with CS at 2 weeks (25 points vs 31 points; P=.03), but no difference at any other time point up to 6 months.

A 2015 RCT of 200 patients with knee OA compared the effectiveness of intra-articular HA and betamethasone.⁴ Evaluators were blinded and assessments were made at 3, 6, 9, and 12 months. The HA group received 2.5 mL of 1% HA (Suprahyal); the CS group received betamethasone dipropionate 5 mg plus betamethasone sodium phosphate 2 mg in 1 mL.

Inconsistent evidence shows a small amount of pain relief at one week to 3 months with corticosteroid injections.

The CS group had significantly less pain (VAS 1 to 10) at 3 months compared with the HA group (2.2 points vs 3.1 points; P=.004), but the HA group had less pain at all other time points (6 months: 3.9 points vs 2.4 points; P=.0001; 9 months: 5.5 points vs 3.6 points; P=.0001; 12 months: 6 points vs 4.1 points; P=.0001).

The WOMAC function subscores (0 to 68; lower indicates more function) were significantly better at all follow-up points in the HA group compared with the CS group (3 months: 19 vs 25; P=.0001; 6 months: 17 vs 29; P=.0001; 9 months: 25 vs 42; P=.0001; 12 months: 28 vs 42; P=.0001).⁴

RECOMMENDATIONS

The American Academy of Orthopaedic Surgeons 2013 work group couldn’t recommend for or against using intra-articular CS for patients with symptomatic knee OA based on inconclusive evidence.⁵ They also couldn’t recommend using HA (SOR: strong).

The National Institute for Health and Care Excellence (NICE) stated in 2008 that intra-articular CS injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with OA.⁶ In 2014, NICE recommended against offering intra-articular HA injections for managing OA.

The US Veterans Administration and Department of Defense have issued guidelines stating that clinicians may consider intra-articular CS injections for patients with symptomatic knee OA (US Preventive Services Task Force [USPSTF] Grade B).⁷ They report insufficient evidence to recommend for or against the use of intra-articular HA with the caveat that HA may be considered for patients who don’t respond adequately to nonpharmacologic measures and who have an inadequate response, intolerable adverse events, or contraindications to other pharmacologic therapies (USPSTF Grade I).

EVIDENCE SUMMARY

A 2015 network meta-analysis of 137 RCTs with 33,243 patients (ages 45-76 years) with knee OA compared the effectiveness of a variety of treatments including intra-articular CS and HA.¹ At 3 months, the effect on pain was not significantly different between the CS and HA groups (12 trials; effect size [ES]=0.02; 95% confidence interval [CI], -0.12 to 0.17). However, a small but significant improvement in function was noted (scoring system not defined) at 3 months favoring HA (ES=0.24; 95% CI, 0.06-0.43; number of trials not specified).

At 3 and 6 months, HA improves pain, but not function, more than CS

Another meta-analysis published in 2015 examined the effectiveness of intra-articular CS and HA in 7 RCTs with 583 patients with knee OA.² All 7 trials were included in the network meta-analysis and discussed separately to evaluate different time points.

Pain at one month wasn’t significantly different using a visual analog score (VAS) of one to 100 (4 trials; 245 patients; mean difference [MD]=1.66 points; 95% CI, -0.90 to 4.23). At 3 and 6 months, the HA group reported significantly reduced pain compared with the CS group (3 months: 3 trials; 320 patients; MD=12.58 points; 95% CI, -17.76 to -7.40; 6 months: 5 trials; 411 patients; MD=9.01 points; 95% CI, -12.62 to -5.40). There were no significant differences in function outcomes (Index of severity for OA of the knee by Lequesne et al; The Knee Society Clinical Rating System), maximum flexion, or adverse events.

Triamcinolone improves pain, function, but not for long

A 2016 double-blind RCT of 110 patients with knee OA compared intra-articular HA and triamcinolone, assessing pain and function at intervals between 24 hours and 6 months.³ Patients in the HA group received a single injection of 6 mL hylan G-F 20 (Synvisc); patients in the CS group received 1 mL of triamcinolone acetonide 40 mg and 5 mL of 1% lidocaine with epinephrine.

The CS group reported significantly less pain (VAS score 1 to 100) at 24 hours than the HA group (24 points vs 36 points; P=.002); relief lasted as long as one week (14 points vs 23 points; P=.018). After the first week, no difference was seen in pain between groups for as long as 6 months.

Function, assessed by a modified Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC 1 to 100; higher score indicates worse pain, stiffness, and function) showed a significant improvement with CS at 2 weeks (25 points vs 31 points; P=.03), but no difference at any other time point up to 6 months.

A 2015 RCT of 200 patients with knee OA compared the effectiveness of intra-articular HA and betamethasone.⁴ Evaluators were blinded and assessments were made at 3, 6, 9, and 12 months. The HA group received 2.5 mL of 1% HA (Suprahyal); the CS group received betamethasone dipropionate 5 mg plus betamethasone sodium phosphate 2 mg in 1 mL.

Inconsistent evidence shows a small amount of pain relief at one week to 3 months with corticosteroid injections.

The CS group had significantly less pain (VAS 1 to 10) at 3 months compared with the HA group (2.2 points vs 3.1 points; P=.004), but the HA group had less pain at all other time points (6 months: 3.9 points vs 2.4 points; P=.0001; 9 months: 5.5 points vs 3.6 points; P=.0001; 12 months: 6 points vs 4.1 points; P=.0001).

The WOMAC function subscores (0 to 68; lower indicates more function) were significantly better at all follow-up points in the HA group compared with the CS group (3 months: 19 vs 25; P=.0001; 6 months: 17 vs 29; P=.0001; 9 months: 25 vs 42; P=.0001; 12 months: 28 vs 42; P=.0001).⁴

RECOMMENDATIONS

The American Academy of Orthopaedic Surgeons 2013 work group couldn’t recommend for or against using intra-articular CS for patients with symptomatic knee OA based on inconclusive evidence.⁵ They also couldn’t recommend using HA (SOR: strong).

The National Institute for Health and Care Excellence (NICE) stated in 2008 that intra-articular CS injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with OA.⁶ In 2014, NICE recommended against offering intra-articular HA injections for managing OA.

The US Veterans Administration and Department of Defense have issued guidelines stating that clinicians may consider intra-articular CS injections for patients with symptomatic knee OA (US Preventive Services Task Force [USPSTF] Grade B).⁷ They report insufficient evidence to recommend for or against the use of intra-articular HA with the caveat that HA may be considered for patients who don’t respond adequately to nonpharmacologic measures and who have an inadequate response, intolerable adverse events, or contraindications to other pharmacologic therapies (USPSTF Grade I).

EVIDENCE SUMMARY

A 2015 network meta-analysis of 137 RCTs with 33,243 patients (ages 45-76 years) with knee OA compared the effectiveness of a variety of treatments including intra-articular CS and HA.¹ At 3 months, the effect on pain was not significantly different between the CS and HA groups (12 trials; effect size [ES]=0.02; 95% confidence interval [CI], -0.12 to 0.17). However, a small but significant improvement in function was noted (scoring system not defined) at 3 months favoring HA (ES=0.24; 95% CI, 0.06-0.43; number of trials not specified).

At 3 and 6 months, HA improves pain, but not function, more than CS

Another meta-analysis published in 2015 examined the effectiveness of intra-articular CS and HA in 7 RCTs with 583 patients with knee OA.² All 7 trials were included in the network meta-analysis and discussed separately to evaluate different time points.

Pain at one month wasn’t significantly different using a visual analog score (VAS) of one to 100 (4 trials; 245 patients; mean difference [MD]=1.66 points; 95% CI, -0.90 to 4.23). At 3 and 6 months, the HA group reported significantly reduced pain compared with the CS group (3 months: 3 trials; 320 patients; MD=12.58 points; 95% CI, -17.76 to -7.40; 6 months: 5 trials; 411 patients; MD=9.01 points; 95% CI, -12.62 to -5.40). There were no significant differences in function outcomes (Index of severity for OA of the knee by Lequesne et al; The Knee Society Clinical Rating System), maximum flexion, or adverse events.

Triamcinolone improves pain, function, but not for long

A 2016 double-blind RCT of 110 patients with knee OA compared intra-articular HA and triamcinolone, assessing pain and function at intervals between 24 hours and 6 months.³ Patients in the HA group received a single injection of 6 mL hylan G-F 20 (Synvisc); patients in the CS group received 1 mL of triamcinolone acetonide 40 mg and 5 mL of 1% lidocaine with epinephrine.

The CS group reported significantly less pain (VAS score 1 to 100) at 24 hours than the HA group (24 points vs 36 points; P=.002); relief lasted as long as one week (14 points vs 23 points; P=.018). After the first week, no difference was seen in pain between groups for as long as 6 months.

Function, assessed by a modified Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC 1 to 100; higher score indicates worse pain, stiffness, and function) showed a significant improvement with CS at 2 weeks (25 points vs 31 points; P=.03), but no difference at any other time point up to 6 months.

A 2015 RCT of 200 patients with knee OA compared the effectiveness of intra-articular HA and betamethasone.⁴ Evaluators were blinded and assessments were made at 3, 6, 9, and 12 months. The HA group received 2.5 mL of 1% HA (Suprahyal); the CS group received betamethasone dipropionate 5 mg plus betamethasone sodium phosphate 2 mg in 1 mL.

Inconsistent evidence shows a small amount of pain relief at one week to 3 months with corticosteroid injections.

The CS group had significantly less pain (VAS 1 to 10) at 3 months compared with the HA group (2.2 points vs 3.1 points; P=.004), but the HA group had less pain at all other time points (6 months: 3.9 points vs 2.4 points; P=.0001; 9 months: 5.5 points vs 3.6 points; P=.0001; 12 months: 6 points vs 4.1 points; P=.0001).

The WOMAC function subscores (0 to 68; lower indicates more function) were significantly better at all follow-up points in the HA group compared with the CS group (3 months: 19 vs 25; P=.0001; 6 months: 17 vs 29; P=.0001; 9 months: 25 vs 42; P=.0001; 12 months: 28 vs 42; P=.0001).⁴

RECOMMENDATIONS

The American Academy of Orthopaedic Surgeons 2013 work group couldn’t recommend for or against using intra-articular CS for patients with symptomatic knee OA based on inconclusive evidence.⁵ They also couldn’t recommend using HA (SOR: strong).

The National Institute for Health and Care Excellence (NICE) stated in 2008 that intra-articular CS injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with OA.⁶ In 2014, NICE recommended against offering intra-articular HA injections for managing OA.

The US Veterans Administration and Department of Defense have issued guidelines stating that clinicians may consider intra-articular CS injections for patients with symptomatic knee OA (US Preventive Services Task Force [USPSTF] Grade B).⁷ They report insufficient evidence to recommend for or against the use of intra-articular HA with the caveat that HA may be considered for patients who don’t respond adequately to nonpharmacologic measures and who have an inadequate response, intolerable adverse events, or contraindications to other pharmacologic therapies (USPSTF Grade I).

EVIDENCE SUMMARY

A systematic review analyzed 30 predominantly US studies with more than 8000 patients published between 1990 and 2012 (4 RCTs, 7 nonrandomized clinical trials, 13 before/after intervention trials, and 6 evaluation studies) to evaluate interventions that decreased parental vaccine refusal and hesitancy.¹ Interventions included: change in state law, changes in state and school policies, and family-centered education initiatives.

Four studies that evaluated the impact of state laws concerning personal exemption (in addition to religious exemption) consistently found that total nonmedical exemption rates were higher in states that allowed personal exemptions. One nationwide survey found that total nonmedical exemption rates were 2.54 times higher (95% confidence interval [CI], 1.68-3.83) in states that allowed personal exemption than in states where only religious nonmedical exemption was allowed.

Fifteen studies evaluated the impact of educational initiatives on parental attitude towards vaccination; 8 of them reported statistically significant changes. None of the studies demonstrated a change in vaccination rates, however. Citing the generally low quality of the studies, the review authors concluded that they didn’t have convincing evidence that educational interventions reduced vaccine hesitancy.

Herd immunity is an iffy motivator

A systematic review analyzed 29 studies from western nations (17 qualitative and 12 quantitative, 4650 patients) regarding willingness to immunize children for the benefit of the community.² Of the 17 qualitative studies, only 2 (164 patients) identified benefit to others as a motivating factor in parents’ decisions to immunize their children. In the 12 quantitative studies, a wide range of parents (1% to 60%) rated the concept of benefit to others as a reason for immunization. Overall, approximately one-third of parents listed herd immunity as a motivating reason. The authors concluded that the high heterogeneity of the studies made it unclear whether herd immunity was a motivating factor in childhood immunizations.

Multifaceted interventions, education, and tailored approaches may all work

A systematic review of international studies published between 2007 and 2013 investigated interventions to increase uptake of routinely recommended immunizations in groups with vaccine hesitancy and reduced use.³ Authors identified 189 articles (trial types and number of patients not given) that provided outcome measures.

Interventions that resulted in at least a 25% increase in vaccine uptake were primarily multifaceted, including elements of: targeting undervaccinated populations, improving access or convenience, educational initiatives, and mandates. Interventions that produced a greater than 20% increase in knowledge were generally educational interventions embedded in routine processes such as clinic visits.

The authors noted wide variation between studies in effect size, settings, and target populations. They concluded that interventions tailored to specific populations and concerns were likely to work best.

Corrective information doesn’t help with the most worried parents

A subsequent RCT tested whether correcting the myth that the flu vaccine can give people the flu would reduce belief in the misconception, increase perceptions that the flu vaccine is safe, and increase vaccination intent.⁴ Respondents to a national online poll of 1000 people received one of 3 interventions: correctional education (information debunking the myth), risk education (information about the risks of influenza infection), or no additional education.

Although about a third of parents cite herd immunity as a motivation to vaccinate, its efficacy in addressing vaccine hesitancy isn't clear.

Corrective information about the flu vaccine reduced the false belief that the vaccine can cause the flu by 15% to 20% and that the flu vaccine is unsafe by 5% to 10% (data from graphs; P<.05 for both effects). However, corrective information actually decreased parental intention to vaccinate among the group most concerned about the adverse effects of the vaccine (data from graph and text: +5% in the low-concern group vs −18% in the high-concern group; P<.05).

A presumptive approach works—but at a cost

A subsequent observational study videotaped 111 patient-provider vaccine discussions.⁵ Researchers categorized the initiation of the vaccine discussion as presumptive (eg, “We have to do some shots.”) or participatory (eg, “What do you want to do about shots?”). Using a presumptive style was more likely to result in acceptance of all recommended vaccines by the end of the visit (90% vs 17%; P<.05), but it decreased the chance of a highly rated visit experience (63% vs 95%; P<.05).

RECOMMENDATIONS

The 2015 Centers for Disease Control and Prevention (CDC) Pink Book recommends a combination of strategies, aimed at both providers and the public, for increasing and maintaining high immunization rates. The Pink Book advises providers to be ready to address vaccine safety concerns raised by parents.⁶

In a 2012 guideline, the CDC encouraged providers to listen attentively, be ready with scientific information and reliable resources, and use appropriate anecdotes in communicating with vaccine-hesitant parents.⁷ The guideline recommended against excluding families who refuse vaccination from the practice.

EVIDENCE SUMMARY

A systematic review analyzed 30 predominantly US studies with more than 8000 patients published between 1990 and 2012 (4 RCTs, 7 nonrandomized clinical trials, 13 before/after intervention trials, and 6 evaluation studies) to evaluate interventions that decreased parental vaccine refusal and hesitancy.¹ Interventions included: change in state law, changes in state and school policies, and family-centered education initiatives.

Four studies that evaluated the impact of state laws concerning personal exemption (in addition to religious exemption) consistently found that total nonmedical exemption rates were higher in states that allowed personal exemptions. One nationwide survey found that total nonmedical exemption rates were 2.54 times higher (95% confidence interval [CI], 1.68-3.83) in states that allowed personal exemption than in states where only religious nonmedical exemption was allowed.

Fifteen studies evaluated the impact of educational initiatives on parental attitude towards vaccination; 8 of them reported statistically significant changes. None of the studies demonstrated a change in vaccination rates, however. Citing the generally low quality of the studies, the review authors concluded that they didn’t have convincing evidence that educational interventions reduced vaccine hesitancy.

Herd immunity is an iffy motivator

A systematic review analyzed 29 studies from western nations (17 qualitative and 12 quantitative, 4650 patients) regarding willingness to immunize children for the benefit of the community.² Of the 17 qualitative studies, only 2 (164 patients) identified benefit to others as a motivating factor in parents’ decisions to immunize their children. In the 12 quantitative studies, a wide range of parents (1% to 60%) rated the concept of benefit to others as a reason for immunization. Overall, approximately one-third of parents listed herd immunity as a motivating reason. The authors concluded that the high heterogeneity of the studies made it unclear whether herd immunity was a motivating factor in childhood immunizations.

Multifaceted interventions, education, and tailored approaches may all work

A systematic review of international studies published between 2007 and 2013 investigated interventions to increase uptake of routinely recommended immunizations in groups with vaccine hesitancy and reduced use.³ Authors identified 189 articles (trial types and number of patients not given) that provided outcome measures.

Interventions that resulted in at least a 25% increase in vaccine uptake were primarily multifaceted, including elements of: targeting undervaccinated populations, improving access or convenience, educational initiatives, and mandates. Interventions that produced a greater than 20% increase in knowledge were generally educational interventions embedded in routine processes such as clinic visits.

The authors noted wide variation between studies in effect size, settings, and target populations. They concluded that interventions tailored to specific populations and concerns were likely to work best.

Corrective information doesn’t help with the most worried parents

A subsequent RCT tested whether correcting the myth that the flu vaccine can give people the flu would reduce belief in the misconception, increase perceptions that the flu vaccine is safe, and increase vaccination intent.⁴ Respondents to a national online poll of 1000 people received one of 3 interventions: correctional education (information debunking the myth), risk education (information about the risks of influenza infection), or no additional education.

Although about a third of parents cite herd immunity as a motivation to vaccinate, its efficacy in addressing vaccine hesitancy isn't clear.

Corrective information about the flu vaccine reduced the false belief that the vaccine can cause the flu by 15% to 20% and that the flu vaccine is unsafe by 5% to 10% (data from graphs; P<.05 for both effects). However, corrective information actually decreased parental intention to vaccinate among the group most concerned about the adverse effects of the vaccine (data from graph and text: +5% in the low-concern group vs −18% in the high-concern group; P<.05).

A presumptive approach works—but at a cost

A subsequent observational study videotaped 111 patient-provider vaccine discussions.⁵ Researchers categorized the initiation of the vaccine discussion as presumptive (eg, “We have to do some shots.”) or participatory (eg, “What do you want to do about shots?”). Using a presumptive style was more likely to result in acceptance of all recommended vaccines by the end of the visit (90% vs 17%; P<.05), but it decreased the chance of a highly rated visit experience (63% vs 95%; P<.05).

RECOMMENDATIONS

The 2015 Centers for Disease Control and Prevention (CDC) Pink Book recommends a combination of strategies, aimed at both providers and the public, for increasing and maintaining high immunization rates. The Pink Book advises providers to be ready to address vaccine safety concerns raised by parents.⁶

In a 2012 guideline, the CDC encouraged providers to listen attentively, be ready with scientific information and reliable resources, and use appropriate anecdotes in communicating with vaccine-hesitant parents.⁷ The guideline recommended against excluding families who refuse vaccination from the practice.

EVIDENCE SUMMARY

A systematic review analyzed 30 predominantly US studies with more than 8000 patients published between 1990 and 2012 (4 RCTs, 7 nonrandomized clinical trials, 13 before/after intervention trials, and 6 evaluation studies) to evaluate interventions that decreased parental vaccine refusal and hesitancy.¹ Interventions included: change in state law, changes in state and school policies, and family-centered education initiatives.

Four studies that evaluated the impact of state laws concerning personal exemption (in addition to religious exemption) consistently found that total nonmedical exemption rates were higher in states that allowed personal exemptions. One nationwide survey found that total nonmedical exemption rates were 2.54 times higher (95% confidence interval [CI], 1.68-3.83) in states that allowed personal exemption than in states where only religious nonmedical exemption was allowed.

Fifteen studies evaluated the impact of educational initiatives on parental attitude towards vaccination; 8 of them reported statistically significant changes. None of the studies demonstrated a change in vaccination rates, however. Citing the generally low quality of the studies, the review authors concluded that they didn’t have convincing evidence that educational interventions reduced vaccine hesitancy.

Herd immunity is an iffy motivator

A systematic review analyzed 29 studies from western nations (17 qualitative and 12 quantitative, 4650 patients) regarding willingness to immunize children for the benefit of the community.² Of the 17 qualitative studies, only 2 (164 patients) identified benefit to others as a motivating factor in parents’ decisions to immunize their children. In the 12 quantitative studies, a wide range of parents (1% to 60%) rated the concept of benefit to others as a reason for immunization. Overall, approximately one-third of parents listed herd immunity as a motivating reason. The authors concluded that the high heterogeneity of the studies made it unclear whether herd immunity was a motivating factor in childhood immunizations.

Multifaceted interventions, education, and tailored approaches may all work

A systematic review of international studies published between 2007 and 2013 investigated interventions to increase uptake of routinely recommended immunizations in groups with vaccine hesitancy and reduced use.³ Authors identified 189 articles (trial types and number of patients not given) that provided outcome measures.

Interventions that resulted in at least a 25% increase in vaccine uptake were primarily multifaceted, including elements of: targeting undervaccinated populations, improving access or convenience, educational initiatives, and mandates. Interventions that produced a greater than 20% increase in knowledge were generally educational interventions embedded in routine processes such as clinic visits.

The authors noted wide variation between studies in effect size, settings, and target populations. They concluded that interventions tailored to specific populations and concerns were likely to work best.

Corrective information doesn’t help with the most worried parents

A subsequent RCT tested whether correcting the myth that the flu vaccine can give people the flu would reduce belief in the misconception, increase perceptions that the flu vaccine is safe, and increase vaccination intent.⁴ Respondents to a national online poll of 1000 people received one of 3 interventions: correctional education (information debunking the myth), risk education (information about the risks of influenza infection), or no additional education.

Although about a third of parents cite herd immunity as a motivation to vaccinate, its efficacy in addressing vaccine hesitancy isn't clear.

Corrective information about the flu vaccine reduced the false belief that the vaccine can cause the flu by 15% to 20% and that the flu vaccine is unsafe by 5% to 10% (data from graphs; P<.05 for both effects). However, corrective information actually decreased parental intention to vaccinate among the group most concerned about the adverse effects of the vaccine (data from graph and text: +5% in the low-concern group vs −18% in the high-concern group; P<.05).

A presumptive approach works—but at a cost

A subsequent observational study videotaped 111 patient-provider vaccine discussions.⁵ Researchers categorized the initiation of the vaccine discussion as presumptive (eg, “We have to do some shots.”) or participatory (eg, “What do you want to do about shots?”). Using a presumptive style was more likely to result in acceptance of all recommended vaccines by the end of the visit (90% vs 17%; P<.05), but it decreased the chance of a highly rated visit experience (63% vs 95%; P<.05).

RECOMMENDATIONS

The 2015 Centers for Disease Control and Prevention (CDC) Pink Book recommends a combination of strategies, aimed at both providers and the public, for increasing and maintaining high immunization rates. The Pink Book advises providers to be ready to address vaccine safety concerns raised by parents.⁶

In a 2012 guideline, the CDC encouraged providers to listen attentively, be ready with scientific information and reliable resources, and use appropriate anecdotes in communicating with vaccine-hesitant parents.⁷ The guideline recommended against excluding families who refuse vaccination from the practice.

EVIDENCE SUMMARY

A systematic review featured a single RCT (n=185) comparing the effect of a 12-month vs 24-month interval between dental visits on dental caries in low-risk 3- to 5-year-old children with primary teeth and young adults, ages 16 to 20 years, with permanent teeth.¹ The outcomes of caries (ie, decayed, missing, filled surfaces increment) between the 12- and 24-month visits both in younger children (mean difference [MD]= -0.90; 95% confidence interval [CI], -1.96 to 0.16) and young adults (MD= -0.86; 95% CI, -1.75 to 0.03) did not differ.

Gingivitis: Not an issue when visits were delayed in healthy adults

Another systematic review (3 RCTs; N=836) evaluated the benefits associated with scaling and polishing in the prevention of gingivitis (primary outcome measure).² One RCT (n=207) compared scaling and polishing at 6- and 12-month intervals to no treatment for 24 months in adults with healthy dental histories. There was no difference in the percentage of index teeth with bleeding in the 6-month or 12-month treatment groups compared to the group that received no treatment for 24 months (MD= -2%; 95% CI, -10% to 6% and MD= -1%; 95% CI, -9% to 7%, respectively).

2 visits/year prevents tooth loss in high-risk patients

A retrospective cohort study (N=5117) using 16 years of data evaluated the association between one or 2 preventive dental visits per year and tooth extraction events in adults at low risk and those at high risk for progressive periodontitis.³ Those at high risk had at least one of the following risk factors: smoking, diabetes, or interleukin-1 genotype. Low-risk patients had no difference in tooth loss with one visit compared to 2 visits annually (absolute risk reduction [ARR]=2.6%; 95% CI, 0.5%-5.8%; P=.092); however, high-risk patients had fewer events with 2 annual visits (number needed to treat [NNT]=19; ARR 5.2%; 95% CI, 1.8%-8.4%; P=.002).

Visits before age 3 likely benefit only those at high risk

A systematic review of 4 retrospective cohort studies (N=77,291) analyzed the impact of early preventive dental visits (EPDV) on the frequency of future preventive and non-preventive dental visits and related expenditures using data from insurance claims and a kindergarten state dental registry.⁴ One study (n=11,394) used dental disease status at kindergarten (defined as the count of decayed, missing [molar teeth only], and filled primary teeth) as an outcome measure. Children who received EPDV before age 24 months had a comparable number of caries to those who had EPDV at 24 to 36 months. The authors concluded that EPDV before age 3 years is likely to benefit only children at high risk, and that evidence for a first dental visit by age one year is weak.

RECOMMENDATIONS

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk.

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk (12 months as the longest interval under age 18 years and 24 months as the longest interval for those 18 years and older at low risk).⁵ The American Dental Association recommends preventive dental visits at intervals determined by individual risk.⁶ The American Academy of Pediatric Dentistry recommends a first exam by age one year and preventive dental visits every 6 months through adolescence or as indicated by individual risk.⁷ The US Preventive Services Task Force states there is insufficient evidence to recommend routine dental screening by primary care physicians in children up to age 5 years.⁸

EVIDENCE SUMMARY

A systematic review featured a single RCT (n=185) comparing the effect of a 12-month vs 24-month interval between dental visits on dental caries in low-risk 3- to 5-year-old children with primary teeth and young adults, ages 16 to 20 years, with permanent teeth.¹ The outcomes of caries (ie, decayed, missing, filled surfaces increment) between the 12- and 24-month visits both in younger children (mean difference [MD]= -0.90; 95% confidence interval [CI], -1.96 to 0.16) and young adults (MD= -0.86; 95% CI, -1.75 to 0.03) did not differ.

Gingivitis: Not an issue when visits were delayed in healthy adults

Another systematic review (3 RCTs; N=836) evaluated the benefits associated with scaling and polishing in the prevention of gingivitis (primary outcome measure).² One RCT (n=207) compared scaling and polishing at 6- and 12-month intervals to no treatment for 24 months in adults with healthy dental histories. There was no difference in the percentage of index teeth with bleeding in the 6-month or 12-month treatment groups compared to the group that received no treatment for 24 months (MD= -2%; 95% CI, -10% to 6% and MD= -1%; 95% CI, -9% to 7%, respectively).

2 visits/year prevents tooth loss in high-risk patients

A retrospective cohort study (N=5117) using 16 years of data evaluated the association between one or 2 preventive dental visits per year and tooth extraction events in adults at low risk and those at high risk for progressive periodontitis.³ Those at high risk had at least one of the following risk factors: smoking, diabetes, or interleukin-1 genotype. Low-risk patients had no difference in tooth loss with one visit compared to 2 visits annually (absolute risk reduction [ARR]=2.6%; 95% CI, 0.5%-5.8%; P=.092); however, high-risk patients had fewer events with 2 annual visits (number needed to treat [NNT]=19; ARR 5.2%; 95% CI, 1.8%-8.4%; P=.002).

Visits before age 3 likely benefit only those at high risk

A systematic review of 4 retrospective cohort studies (N=77,291) analyzed the impact of early preventive dental visits (EPDV) on the frequency of future preventive and non-preventive dental visits and related expenditures using data from insurance claims and a kindergarten state dental registry.⁴ One study (n=11,394) used dental disease status at kindergarten (defined as the count of decayed, missing [molar teeth only], and filled primary teeth) as an outcome measure. Children who received EPDV before age 24 months had a comparable number of caries to those who had EPDV at 24 to 36 months. The authors concluded that EPDV before age 3 years is likely to benefit only children at high risk, and that evidence for a first dental visit by age one year is weak.

RECOMMENDATIONS

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk.

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk (12 months as the longest interval under age 18 years and 24 months as the longest interval for those 18 years and older at low risk).⁵ The American Dental Association recommends preventive dental visits at intervals determined by individual risk.⁶ The American Academy of Pediatric Dentistry recommends a first exam by age one year and preventive dental visits every 6 months through adolescence or as indicated by individual risk.⁷ The US Preventive Services Task Force states there is insufficient evidence to recommend routine dental screening by primary care physicians in children up to age 5 years.⁸

EVIDENCE SUMMARY

A systematic review featured a single RCT (n=185) comparing the effect of a 12-month vs 24-month interval between dental visits on dental caries in low-risk 3- to 5-year-old children with primary teeth and young adults, ages 16 to 20 years, with permanent teeth.¹ The outcomes of caries (ie, decayed, missing, filled surfaces increment) between the 12- and 24-month visits both in younger children (mean difference [MD]= -0.90; 95% confidence interval [CI], -1.96 to 0.16) and young adults (MD= -0.86; 95% CI, -1.75 to 0.03) did not differ.

Gingivitis: Not an issue when visits were delayed in healthy adults

Another systematic review (3 RCTs; N=836) evaluated the benefits associated with scaling and polishing in the prevention of gingivitis (primary outcome measure).² One RCT (n=207) compared scaling and polishing at 6- and 12-month intervals to no treatment for 24 months in adults with healthy dental histories. There was no difference in the percentage of index teeth with bleeding in the 6-month or 12-month treatment groups compared to the group that received no treatment for 24 months (MD= -2%; 95% CI, -10% to 6% and MD= -1%; 95% CI, -9% to 7%, respectively).

2 visits/year prevents tooth loss in high-risk patients

A retrospective cohort study (N=5117) using 16 years of data evaluated the association between one or 2 preventive dental visits per year and tooth extraction events in adults at low risk and those at high risk for progressive periodontitis.³ Those at high risk had at least one of the following risk factors: smoking, diabetes, or interleukin-1 genotype. Low-risk patients had no difference in tooth loss with one visit compared to 2 visits annually (absolute risk reduction [ARR]=2.6%; 95% CI, 0.5%-5.8%; P=.092); however, high-risk patients had fewer events with 2 annual visits (number needed to treat [NNT]=19; ARR 5.2%; 95% CI, 1.8%-8.4%; P=.002).

Visits before age 3 likely benefit only those at high risk

A systematic review of 4 retrospective cohort studies (N=77,291) analyzed the impact of early preventive dental visits (EPDV) on the frequency of future preventive and non-preventive dental visits and related expenditures using data from insurance claims and a kindergarten state dental registry.⁴ One study (n=11,394) used dental disease status at kindergarten (defined as the count of decayed, missing [molar teeth only], and filled primary teeth) as an outcome measure. Children who received EPDV before age 24 months had a comparable number of caries to those who had EPDV at 24 to 36 months. The authors concluded that EPDV before age 3 years is likely to benefit only children at high risk, and that evidence for a first dental visit by age one year is weak.

RECOMMENDATIONS

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk.

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk (12 months as the longest interval under age 18 years and 24 months as the longest interval for those 18 years and older at low risk).⁵ The American Dental Association recommends preventive dental visits at intervals determined by individual risk.⁶ The American Academy of Pediatric Dentistry recommends a first exam by age one year and preventive dental visits every 6 months through adolescence or as indicated by individual risk.⁷ The US Preventive Services Task Force states there is insufficient evidence to recommend routine dental screening by primary care physicians in children up to age 5 years.⁸