Table 2.
Anti-tumor necrosis factor (anti-TNF) therapy and bone mineral density in Spondyloarthropaties
| Ref | Study | FU time | Treatment groups (n) | Spine BMD | Hip BMD | Findings |
|---|---|---|---|---|---|---|
| [83] | Obs SpA | 6 months | T1: INF (29) | BMD increased (+3.6%,P=0.001) | BMD total hip increased (+2.2%, p=0.0012) BMD trochanter increased (+2.3%, P=0.00012) BMD total neck stable (+1.1%, P=0.19) |
No changes in BMD with concomitant use of glucocorticoids. Osteocalcin increased at 6 weeks but no differences at 6 months. |
| [84] | Obs CD | Mean 23±11months | T1: INF (15) T2: conventional treatment (30) |
BMD increased T1≫T2 (+8.1% vs.+ 1.0%, P<0.01) |
BMD increased Left hip T1≈T2 (+2.7% vs. +1.3%, P>0.05) Right hip T1≫T2 (+5.6% vs. −0.2%, P<0.05) |
In the INF treated group, ΔBMD in spine was not associated with glucocorticoid use |
| [85] | Obs CD | Mean 2.2 ± 0.99 y | T1: INF (23) T2: conventional treatment (38) |
No biphosphonate, BMD loss T1≈T2 (−4.1% vs. −3.3%, P>0.05) Biphosphonate , BMD loss T1≈T2 (+4.4% vs. +2.0%, P>0.068) Biphosphonate users vs. non-users (+4.0% vs. −3.7%, P<0.001) |
ND | Biphosphonates was associated with spine BMD gain, but effect was partially inhibited by concomitant use of glucocorticoids. INF had a marginal effect in BMD only in those patients that used bisphosphonates |
| [86] | Obs AS | Mean range 13.5 to 15.6 months | T1: conventional treatment (40) T2: biphosphonate (20) T3: anti-TNF (19) T4: anti-TNF+biphosphonate (11) |
BMD increased in all treatment, but marginally significant in T2. | BMD remained stable in all treatment groups, but in T4 BMD increased at trochanter | ΔBMD at trochanter correlate with Δinflammatory markers. In patients without syndesmophytes, ΔBMD at spine and total hip was different between treatments, ΔBMD at femoral neck correlate with Δinflammatory markers. |
| [87] | OL CD | 1 year | T1: INF (46) | ΔBMD similar in all groups BMD increased (2.4%, P=0.002) | BMD increased at trochanter and femoral neck (+2.8%, P=0.03 and +2.6%, P=0.001 respectively) | ΔBMD at spine and femoral neck was independent of glucocorticoids use. |
| [88] | OL SpA | 6 months | T1: ETA (10) T2: SSZ/NSAIDs (10) |
ΔBMD T1≈T2 (+1.1% vs. −1.4%, P=0.19) | ΔBMD femoral neck T1≈T2 (+0.2% vs. −1.5%, P=0.34) ΔBMD total hip T1>T2 (+1.6% vs. −1.3%, P=0.027) |
Measures of disease activity improved in ETA treated group but not in controls. |
| [89] [90] | OL SpA | 1 -2 years | T1:INF/ETA ( n=19) T1:INF/ETA ( n=106) |
BMD increased | BMD hip increased | Markers of bone resorption decreased early and remained low during treatment, but markers of bone formation only increase temporarily (3 months) but return to baseline thereafter. |
| [91] | RCT AS | 24 weeks | T1: INF (201) T2: placebo (78) |
BMD increased T1≫T2 (+2.5% vs. +0.5%, P<0.001) | BMD increased T1≫T2 (0.5% vs. +0.2%, P=0.033) | In the INF treated group ΔBMD in spine was not associated with Δmarkers of bone turnover; but ΔBMD in hip was associated with baseline osteocalcin and bone alkaline phosphatase, and inversely correlated with changes in carboxy –terminal collagen crosslinks |
| [92] | RCT | 30 weeks | T1 : MTX +INF (28) T2 : MTX+ Placebo (14) |
ΔBMD T1≈T2 (+3.6% vs. −1.3%, P=0.06) | ΔBMD total hip T1≈T2 (+1.9% vs. +0.1%, P=0.14) ΔBMD femoral neck T1≈T2 (+2.5% vs. −1.3%, P=0.09) |
BMD increased significantly in INF but not in the MTX monotherapy treated group, ΔBMD were similar in spine, hip and femoral neck |
Abbreviations: Ref, references; FU, follow-up; BMD, bone mineral density; ND, not done; Δ, changes; ≈, similar; Obs, observational; OL, open label; RCT, randomized clinical trial; SpA, spondyloarthropathies; CD, Crohn’s disease;AS, ankylosing spondylitis; INF, infliximab; ETA, etanercept; SSZ, sulfasalazine; NSAIDs, non steroidal anti-inflammatory drugs; MTX, methotrexate; Rx, treatment; vs., versus;