Recovery from Abobotulinum Toxin A-Induced Paralysis Following Ozone Injection in a Split-Body Rabbit Model

Although previous studies have demonstrated that ozone gas can inactivate botulinum toxin in liquid solutions, evidence regarding its effects under in vivo conditions remains limited. This exploratory study investigated whether local ozone injection is associated with earlier functional recovery from abobotulinum toxin A-induced muscle paralysis in a rabbit model. Three New Zealand White rabbits received bilateral intramuscular injections of 15 U abobotulinum toxin A into the anterior auricular muscles. After maximal paralysis was established, the right anterior auricular muscle received 1 mL ozone gas at a concentration of 10 µg/mL twice weekly for two weeks (four sessions in total), while the left side received room air injections as the concurrent control. Ear positions were assessed by twice-weekly imaging using a four-grade visual paralysis scale (Grade 0-III) until baseline position was restored. All ozone-treated ears improved from Grade III to Grade II by day 7 and returned to their baseline positions (Grade 0) by day 10, remaining at Grade 0 thereafter. In contrast, the room-air control ears remained at Grade III through week 3, showed progressive improvement during weeks 4 and 5, and returned to Grade 0 by week 6. Previous findings using the same experimental model without additional intervention reported persistence of paralysis for approximately 16 weeks. This study provides the first in vivo experimental evidence suggesting that local ozone administration may be associated with earlier functional recovery from abobotulinum toxin A-induced paralysis. However, larger, randomized, and objectively assessed studies are required to confirm this observation and clarify the underlying mechanisms.