Study (year) | Sample (size) | Treatment group (size) | Methodology | Parameter | Outcome |
---|---|---|---|---|---|
Cai et al. (2015) [22] | New Zealand white rabbits (nā=ā18). Implant inserted into calvaria (nā=ā18). | Control (nā=ā6) Diclofenac (nā=ā6) Parecoxib (nā=ā6) | Treatments were administered for 7Ā days: Diclofenac, 2Ā mg/kg/day orally Parecoxib, 1.5Ā mg/kg/day subcutaneous injection | Parameters observed at week 4 and 12 after implantation: Micro-CT: bone volume ratio, mean trabecular thickness, and mean trabecular separation. Histomorphometric: bone-to-implant contact. | No statistically significant differences between the three separate groups, nor between the different time points. |
Chikazu et al. (2007) [30] | 9-week old male mice (nā=ā72). Implant inserted in femur (nā=ā72). | Mice with the original C57BL6/129S7 hybrid background were generated and maintained: Wild-type (nā=ā36) COX-2-knockout (nā=ā36) | No drug was administered | mRNA levels were observed at days 0, 1, 2, 4, 7, and 56 after implant insertion: expression of COX-2 and osteocalcin mRNA. Histomorphometric analysis at weeks 4 and 8: bone-to-implant contact. | Expression of COX-2 and osteocalcin mRNA was induced in bone surrounding implants in wild-type mice, but not in knockout mice. Bone-to-implant contact was minimal in knockout mice. |
Goodman et al. (2002) [29] | New Zealand white rabbits (nā=ā8). Titanium bone harvest chamber inserted in tibia (nā=ā8). | Control Naproxen Rofecoxib | Treatments administered: Control: weeks 0ā4 and 9ā12. Naproxen, 110Ā mg/kg: weeks 5ā8 orally. Rofecoxib, 12.5Ā mg/kg: week 13ā16 orally. | Immunohistochemistry observed: total tissue area, total bone area, ratio of bone area, and total number of osteoblasts and osteoclast-like cells per section area | Naproxen and rofecoxib decreased bone ingrowth significantly. Rofecoxib decreased the area of osteoblasts per area compared with controls, and naproxen sodium did not reach statistical significance. |
Goodman et al. (2005) [26] | New Zealand white rabbits (nā=Ā 8). Titanium bone harvest chamber implanted bilaterally in tibia (nā=ā16). | Control Rofecoxib | Treatments were administered for 6Ā weeks each: control-no drug; rofecoxib (12.5Ā mg/day) for the first 2Ā weeks of a 6-week trial, or the last 2Ā weeks or given continuously for all 6Ā weeks washout periods | Immunohistochemistry observed: total tissue area, total bone area, ratio of bone area, and the total number of osteoblasts and osteoclast-like cells per section area. | Rofecoxib given continuously for 6Ā weeks had less bone ingrowth, osteoclast-like cells and osteoblasts per area compared to the control treatment. Rofecoxib given for 2 of a 6-weeks cycle did not interfere with the parameters. |
Pablos et al. (2008) [31] | Male Sprague-Dawley rats, 3-month-old, weighing 250-300Ā g (nā=ā30). Implant inserted in tibia (nā=ā30). | Control (nā=ā10) Diclofenac (nā=ā10) Meloxicam (nā=ā10) | Diclofenac, 1.07Ā mg/kg b.i.d. for 5Ā days. Meloxicam, 0.2Ā mg/kg daily for 5Ā days. | Histomorphometric analysis at 28Ā days after implant insertion: bone-to-implant contact, cortical bone area, and trabecular bone area within the implant threads | The bone-to-implant contact was lower in diclofenac compared with the meloxicam and control. The trabecular bone area was greater in diclofenac compared with meloxicam and control. |
Ribeiro et al. (2006) [27] | Male Wistar rats, aged 10Ā weeks (nā=ā31). Implant inserted in tibia (nā=Ā 31). | Control (nā=ā14) Meloxicam (nā=ā17) | Daily subcutaneous injections for 60Ā days: control, 1Ā mL/kg of saline Meloxicam, 3Ā mg/kg | Histomorphometric analysis at 60Ā days after implant insertion: bone-to-implant contact, bone area, and bone density in the cortical and cancellous bone areas | Meloxicam reduced bone-to-implant contact, bone area, and bone density in both the cortical and cancellous bone areas. |
Ribeiro et al. (2009) [28] | Male Wistar rats, aged 10Ā weeks (nā=ā30). Implant inserted in tibia (nā=ā30). | Control (nā=ā14) Meloxicam (nā=ā16) | Daily subcutaneous injections for 60Ā days: control, 1Ā mL/kg of saline Meloxicam, 3Ā mg/kg | Histomorphometric analysis at 60Ā days after implant insertion: bone-to-implant contact, bone area, and bone density in the cortical and cancellous bone areas | Blasting implant surface with aluminium oxide can increase bone-to-implant contact; however, it does not reverse the negative effects caused by a selective COX-2 inhibitor on bone healing around implants. |
Salduz et al. (2017) [32] | New Zealand white rabbits, skeletally mature weighing 3.5ā4Ā kg (nā=ā40). Titanium rods implanted bilaterally in femur (nā=ā80). | Control Diclofenac Celecoxib | Treatments were administered for 8Ā weeks: control, regular food Diclofenac, 5Ā mg/kg/day intramuscularly Celecoxib, 3Ā mg/kg/day orally | Biomechanical and histomorphometric analysis at 8Ā weeks after implant insertion: interface failure load, bone quality, bone implant interface, host reaction, total bone area, and bone-to-implant contact rate | No significant difference in the biomechanical and histological results between the groups. |