Main Article Content



  1. Sodium diclofenac is one of NSAID a common treatment to relieve pain associated with bone fractures.

  2. Sodium diclofenac with a some dose of body weight could decrease the callus quality on fracture healing.



Non-steroidal anti-inflammatory drugs (NSAIDs), such as diclofenac sodium, are standard treatments to relieve pain associated with bone fractures. The bone healing process consists of four stages: inflammation, soft callus formation, complex callus formation, and bone remodeling. Previous studies mentioned that intake of NSAIDs (sodium diclofenac) could inhibit the bone healing process. This study examined the effect of diclofenac sodium intake on callus formation in fracture healing. In this study, thirty-six rats (Rattus Norvegicus) with fractures were used and divided into two groups, namely 18 rats for the control and 18 rats for the treatment group. In the treatment group, each rat was given 1.8 mg sodium diclofenac/150 grams of body weight per day. In the control group, each rat was given CMC-Na 0.5% with equal volume as diclofenac sodium in the treatment group. After 28 days, all the rats were stunned until dead, and the diameter and strength of their calluses were measured. In the treatment group with diclofenac sodium1.8 mg/ 150 grams BW/ 28 days after the tibia bone callus was pressed using the Shimadzu tool, the lowest callus strength was found to be 56.500 N, and the highest callus strength was 59.000 N. The lowest callus diameter in the treatment group was 4 mm, the highest was 5 mm. In the control group, the lowest callus strength was 76 N, and the highest callus strength was 77 N. The lowest callus diameter in the control group was 6 mm, and the highest was 8 mm. The strongest callus in the treatment group was found in the sixth observation, with a value of 59 N and a diameter of 4 mm. In the control group, the highest callus strength was 77 N, with a diameter of 7-8 mm. These measurements were found on the 5th, 7th, 8th, 9th, 16th, and 17th observations. Diclofenac sodium with a dose of 1.8 mg/150 grams of body weight could decrease the callus quality parameters, such as callus strength and diameter on fracture healing.


Bone fracture sodium diclofenac rattus norvegicus callus strength callus diameter

Article Details

How to Cite
Wibowo, H., & Widiyanti, P. (2022). The Effect of Diclofenac Sodium on Callus Formation in White Male Rat (Rattus norvegicus) Cruris Fracture Healing. Folia Medica Indonesiana, 58(2), 108–112.


  1. Akman S, Gögüs A, Sener N, el al (2002). Effect of diclofenac sodium on union of tibial fractures in rats. Adv. Ther. 19, 119–125.
  2. Beck A, Krischak G, Sorg T, et al (2003). Influence of diclofenac (group of nonsteroidal anti-inflammatory drugs) on fracture healing. Arch. Orthop. Trauma Surg. 123, 327–332.
  3. Bissinger O, Kreutzer K, Götz C, et al (2016). A biomechanical, micro-computertomographic and histological analysis of the influence of diclofenac and prednisolone on fracture healing in vivo. BMC Musculoskelet. Disord. 17, 1–11.
  4. Donatus I, Nurlaila N (1986). Obat tradisional dan fitoterapi uji toksikologi. Universitas Gadjah Mada, Yogyakarta.
  5. Hadjicharalambous C, Alpantaki K, Chatzinikolaidou M (2021). Effects of NSAIDs on pre‑osteoblast viability and osteogenic differentiation. Exp. Ther. Med. 22, 1–7.
  6. Harder A, An Y (2003). The mechanisms of the inhibitory effects of nonsteroidal anti-inflammatory drugs on bone healing: A concise review. J. Clin. Pharmacol. 43, 807–815.
  7. Kress H, Baltov A, Basinski A, et al (2016). Acute pain: A multifaceted challenge – the role of nimesulide. Curr. Med. Res. Opin. 32, 23–36.
  8. Krischak G, Augat P, Sorg T, et al (2007). Effects of diclofenac on periosteal callus maturation in osteotomy healing in an animal model. Arch. Orthop. Trauma Surg. 127, 3–9.
  9. Lisowska B, Kosson D, Domaracka K (2018). Lights and shadows of NSAIDs in bone healing: The role of prostaglandins in bone metabolism. Drug Des. Devel. Ther. 12, 1753–1758.
  10. Maroon J, Bost J, Maroon A (2010). Natural anti-inflammatory agents for pain relief. Surg. Neurol. Int. 1, 1–10.
  11. Moro M, Sánchez P, Lupepsa A, et al (2017). Cyclooxygenase biology in renal function – Literature review. Rev. Colomb. Nefrol. 4, 27–37.
  12. Painter S, Kleerekoper M, Camacho P (2006). Secondary osteoporosis: A review of the recent evidence. Endocr. Pract. 12, 436–445.
  13. Pountos I, Georgouli T, Blokhuis T, et al (2008). Pharmacological agents and impairment of fracture healing: What is the evidence? Injury 39, 384–394.
  14. Pratiwi W, Kertia N (2019). The effect of curcuminoid turmeric rhizome extract on interleukin 1β concentration in osteoarthritis patient. J. Kedokt. dan Kesehat. Indones. 10, 162–170.
  15. Reynolds J (1993). The extra pharmacopoeia (Martindale). Pharmaceutical Press, London.
  16. Santos SDL, Garcia-Perez V, Hernández-Reséndiz S, et al (2017). ‘(-)-Epicatechin induces physiological cardiac growth by activation of the PI3K/Akt pathway in mice. Mol Nutr Food Res 61, 1–32.
  17. Shapiro I, Layfield R, Lotz M, et al (2014). Boning up on autophagy: The role of autophagy in skeletal biology. Autophagy 10, 7–19.
  18. Suhana R (2002). Pengaruh pemberian natrium diklofenak terhadap pembentukan kalus dilihat dari jumlah osteoblast pada penyembuhan patah tulang tibia kelinci. Universitas Padjadjaran.
  19. Zhou J, Li T, Li L, et al (2018). Clinical efficacy of calcitonin compared to diclofenac sodium in chronic nonspecific low back pain with type I Modic changes: A retrospective study. J. Pain Res. 11, 1335—1342.