Mode of Action

The mechanism of action of Traumeel as a bioregulatory medicine and the immune response triggered by low concentration molecules have been translated into an animated, highly realistic movie that is presented here.

The Inflammation Cascade

The inflammation process is really a complex cascade of different steps. According to research results, Traumeel® is postulated to act on the first stages of the inflammation cascade and thus optimizes the whole process towards recovery. Contrarily, NSAIDS block the cascade at one of its essential steps at the end which results in masking the injury and the pain. The blockade of this central pathway is also the reason for the common side effects of NSAIDs.

Synergy of Ingredients

As with many other commonly used therapeutic agents, the exact mechanism of action of Traumeel® is not fully understood. However, the product’s ingredients appear to modulate various cellular and biochemical pathways.

Placebo-controlled studies, drug monitoring studies, and in vitro experimental models (including the carragenean-induced edema test and the adjuvant arthritis test) have all demonstrated the inflammation regulating, anti-edematous and anti-exudative effects of Traumeel® [1][2][3][4][5][6]. Various in vitro and in vivo studies offer a possible mechanism for Traumeel’s inflammation regulating effects as observed in clinical practice.

In resting as well as activated immune cells, Traumeel® inhibits pro-inflammatory mediators such as IL-1β, TNF-α and IL-8 [7].

The ingredients of Traumeel® are non-cytotoxic to granulocytes, lymphocytes, platelets, and endothelial cells, indicating that the defensive functions of these cells are preserved during treatment with Traumeel® [3]. Components of Traumeel® raise levels of the anti-inflammatory cytokine TGF-β, indicating that the “immunological bystander reaction” may play a role in the medication’s inflammation regulating effect [8].

Although Traumeel® appears to be as effective as NSAIDs, it differs in its mechanism of action from NSAIDs, COX-2 inhibitors and steroids and is therefore better tolerated and free of the side effects associated with these agents.

References

[1] Böhmer D et al. Biological Therapy 1992; X(4): 290-300.
[2] Zenner S et al. Biomedical Therapy 1997; XV(1): 22-26.
[3] Conforti A et al. Biomedical Therapy 1997; XV(1): 28-31.
[4] Zell J et al. Biological Therapy 1989; VII(1): 1-6.
[5] Thiel W. Biological Therapy 1994; XII(4): 242-248.
[6] Zenner S et al. Biological Therapy 1992; X(4): 301-310.
[7] Porozov S et al. Clin Dev Immunol. 2004; 11(2): 143-149.
[8] Heine H. Biologische Medizin 1998; 12-14.