Skip to main content
eScholarship
Open Access Publications from the University of California

Lactic acid 5 percent mouthwash is an effective mode of therapy in treatment of recurrent aphthous ulcerations

  • Author(s): Sharquie, Khalifa E
  • Al-Tammimy, Sami M
  • Al-Mashhadani, Sabeeh
  • Hayani, Raafa K
  • Al-Nuaimy, Adil A
  • et al.
Main Content

Lactic acid 5 percent mouthwash is an effective mode of therapy in treatment of recurrent aphthous ulcerations
Khalifa E Sharquie MD PhD1, Sami M Al-Tammimy MD FIBMS2, Sabeeh Al-Mashhadani MD MSc1, Raafa K Hayani MD DDV2, Adil A Al-Nuaimy MD DDV FICMS3
Dermatology Online Journal 12 [7]: 2

1. Scientific Council of Dermatology and Venereology, Iraqi Board for Medical Specializations. ksharquie@yahoo.uk.co
2. Department of Dermatology and Venereology,Baghdad Teaching Hospital
3. Department of Dermatology and Venereology, College of Medicine, Baghdad University


Abstract

Background: Recurrent aphthous ulceration (RAU) is the most common oral mucosal disease among the general world population, including Iraq. There is no uniformly effective therapy for this disease. Objective: To evaluate the therapeutic efficacy and safety of 5-percent lactic acid mouthwash in the treatment of patients with recurrent aphthous ulcerations. Methods: This is a single-blind controlled therapeutic study. We recruited 80 subjects with early-onset oral aphthosis from patients who attended Baghdad Teaching Hospital Department of Dermatology and Venereology in the period between April 2004 and April 2005. Of those subjects, 10 defaulted; the remaining 70 patients were divided into two groups, A and B. Subjects in group A (36 patients) were instructed to use 5-percent lactic acid mouthwash, one teaspoonful three times daily before meals. Subjects in group B (34 patients) were instructed to use placebo (distilled water mouthwash) in a similar way. Assessment of each patient of both groups was done by using the oral clinical manifestation index (OCMI) before, after 3 days of therapy, and after 7 days of therapy. Results: The mean OCMI in group A started to decline after 3 days of therapy and attained a statistically significant lower level after 7 days of therapy (p <0.05). The change in the mean OCMI of group B after 3 and 7 days of therapy was also statistically significant (p <0.05). However, the response rate (percentage of change in the mean) after 3 days of therapy in group A was 63.6 percent and in group B was 8.8 percent; the response rate after 7 days of therapy in group A was 90.8 percent and in group B was 35.7 percent. The difference in the response rates after 3 and 7 days between groups A and B was statistically significant (p <0.05). No significant side effects were noticed apart from mild irritation in two patients using lactic acid. Conclusions: Lactic acid 5 percent mouthwash is a new effective mode of therapy for patients with RAU that significantly reduces the signs and symptoms of the disease, especially in comparison with placebo. The mechanism of action may be related to increasing spontaneous secretion of endothelial growth factor from keratinocytes.



Introduction

Recurrent aphthous stomatitis (RAS), also termed recurrent oral ulceration (RAU), is the most common oral mucosal disease in adolescents and adults affecting an estimated 20-25 percent of the general population [1]. It is characterized by repeated development of self-limited, single or multiple, discrete, painful ulcers. An outbreak generally requires 7-10 days to heal, but in more severe cases ulcers may persist for up to 6 weeks [2].

The etiology of RAS is not clear. A multifactorial pathogenesis has been suggested including genetic predisposition, trauma, infectious agents, and immunological dysfunction, but the exact etiology and pathogenesis are not known [3]. Accordingly, there is no uniformly effective therapy for this disease.

A large number of therapies both topical and systemic have been used in treatment of RAU, including chlorohexidine [4], tetracycline [3], honey [5], Benedryl and Maalox, sucrolfate [1], zinc sulfate [6], nigella sativa [7], corticosteroids (topical, intralesional, and oral) [1], dapsone [1], colchicine [8], oxypentifylline [9], thalidomide [10], low intensity ultrasound [2], etanercept [11], and BCG [12]. These therapies act through different mechanisms with variable success rates and most of them are associated with a variety of side effects.

Lactic acid has been used in treatment of many skin diseases including warts, xerosis, ichthyosis, seborrheic keratosis, and actinic keratosis. Lactic acid is used in chemical peeling for treatment of wrinkling, roughness and mottled pigmentation of photodamaged skin [13]. Lactic acid has antioxidant action that may help in repigmentation of vitiligo [14]. It is also reported that lactic acid can be used as a safe and effective topical antibacterial agent [15]. Topically applied lactic acid increases spontaneous secretion of vascular endothelial growth factor by human reconstructed epidermis [16]. Vascular endothelial growth factor is a multifunctional angiogenic cytokine involved in angiogensis and wound healing, and its level is low in early active-stage RAS when compared with its level in late remission stage [17].

This is the first work to evaluate the therapeutic efficacy and safety of lactic acid in the treatment of RAS.


Patients and methods

This is a single blind-controlled therapeutic study to evaluate the therapeutic efficacy and safety of 5-percent lactic acid mouthwash in the treatment of patients with recurrent aphthous ulcerations.

Patients with RAS included in this study were those who attended Baghdad teaching hospital department of dermatology and venereology from April 2004 to April 2005.

Recruited patients had oral ulcerations that were early onset (less than 3 days duration) and who had little benefit from other conventional therapy in previous attacks. Patients were requested to avoid the use of any other medicaments throughout the trial.

The diagnosis of RAS was based on history and clinical examination. A detailed history was obtained and included age, sex, occupation, history of disease, recurrence rate, general health, previous medical history, and history of oral ulcers or other illness in the family. Patients were asked about associated symptoms and aggravating factors including food, stress, trauma, and smoking. All patients were fully examined regarding shape, size, edge, surface, number, and site of the lesions.

To exclude patients with Behçet disease and other internal causes of oral ulcerations, all patients were evaluated with a pathergy test, complete blood count, erythrocyte sedimentation rate, and HLA typing for HLA-B51 and HLA-B27.

Lactic acid (C3H6O3 88%, pH 3.1) was obtained from Hopkin and Williams LTD Company and was prepared at a concentration of 5 percent in distilled water.

The 80 patients included in the study were divided into two groups, group A (40 patients) and group B (40 patients). Patients in group A were instructed to use 5 percent lactic acid mouth wash, 3 times daily 15 minutes before meals. One teaspoonful (5ml) of mouthwash was retained in the mouth for 5 minutes. Patients in group B were instructed to use a placebo (distilled water mouthwash).

An oral clinical manifestations index (OCMI) [7, 12], (Table 1), for each patient was calculated before therapy. Assessment of each patient was performed on days 3 and 7 from starting therapy. The data were analyzed, and the student's t-test was used to compare the means of OCMI before, after 3 days, and after 7 days of therapy for both group A and group B. The response rate was estimated by calculating the percentage of change in the means of OCMI after 3 and 7 days of treatment from the baseline mean of OCMI before treatment. The student's t test was used also to compare the response rates after 3 and 7 days of therapy between group A and group B. A probability of α = 0.05 was considered to be statistically significant.


Results


Sex and age

Of the 80 patients included in this study, 10 patients defaulted for unknown reasons; the remaining 70 patients completed the study, 41 males (58.5 percent) and 29 females (41.5 percent). The male to female ratio was 1.4:1. Their ages ranged between 7 and 64 years (mean and standard deviation 29.6 ± 9.6 years).


Ulcer type

There were 43 patients (61.4 %) with minor aphthous ulcers, 25 patients (35.7 %) with major apthous ulcers, and 2 patients (2.4 %) with herpetiform aphthous ulcers (see Table 2).


The effect of lactic acid on OCMI in group A

For this group of 36 patients, the pre-therapy OCMI ranged between 6 and 14 (mean ± SD 11.5 ± 1.81). The mean OCMI declined significantly after 3 days of treatment (4.3 ± 2.56). After 7 days of treatment the mean OCMI was 1.02 (± 1.71. p < 0.05, see Table 3).

The response rate was estimated by calculating the percentage of change from baseline in the mean of OCMI after 3 and 7 days of treatment; it was 63.6 percent (± 22.5 %) after 3 days and 90.8 percent (± 15.2 %) after 7 days of treatment (see Table 4).

The mean duration of the minor aphthous ulcers before lactic acid therapy was 8.95 (± 1.23 days). With lactic acid therapy it was 4.3 ± 1.92 days. The mean duration of the major type before lactic acid therapy was 16.33 (± 3.03 days), and that decreased to 5.6 (± 1.68 days) with therapy (p < 0.05).

The mean of the number of minor ulcers before therapy was 2.75 (± 1.01). After 3 days of therapy it was 0.60 ± 0.88 and after 7 days it was 0.10 (± 0.30, p < 0.05) (see Table 5). The mean of the number of major ulcers before therapy was 3.00 (± 0.92). After 3 and 7 days of therapy it was 1.33 (± 0.72) and 0.13 (± 0.35), respectively (p < 0.05, see Table 5).

The mean pain score of minor ulcers before therapy was 2.90 (± 0.78). After 3 and 7 days of therapy it was 0.50 (± 0.76) and 0.10 (± 0.30), respectively. The mean pain score of major ulcers before therapy was 3.26 (± 0.79). After 3 and 7 days of therapy it was 1.33 (± 0.72) and 0.13 (± 0.35), respectively (p < 0.05, see Table 6).


The effect of placebo (distilled water) on OCMI in group B

This group (34 patients) showed a slight decline of mean OCMI. Before therapy the OCMI ranged between 10-14 with a mean of 10.8 (± 2.30). After 3 days of treatment the mean was 9.3 (± 2.80) and after 7 days the mean was 7.2 (± 3.07, p < 0.05, see Table 7).

The response rate was 8.8 (± 40.4) after 3 days of therapy and 35.7 (± 24.3) after 7 days (see Table 4).

The mean of number of minor ulcers before therapy was 2.65 (± 1.15). After 3 and 7 days of therapy it became 2.43 (± 1.44) and 1.00 (± 1.16) respectively (p < 0.05, see Table 5). The mean of number of major ulcers before therapy was 2.90 (± 0.99), and after 3 and 7 days of therapy it was 2.90 (± 0.99) and 2.30 (± 0.94) respectively (p = 0.302 was insignificant, see Table 6).

The mean of the pain scores of minor ulcers before therapy was 2.82 (± 0.65), and after 3 and 7 days of therapy it was 2.08 (± 0.90) and 0.82 (± 0.93), respectively. The mean pain score of major ulcers before therapy was 3.30 (± 0.64), and after 3 and 7 days of therapy it was 2.90 (± 0.56) and 2.00 (± 0.81), respectively (p < 0.05, see Table 6).

When the percentage of change in the means of ulcer number and pain scores of minor and major ulcers after 3 and 7 days of therapy were compared between groups A and B, the differences were statistically significant (p < 0.05).

When the response rates after 3 and 7 days of treatment were compared between groups A and B, there was a statistically significant difference (p < 0.05, see Table 4).


Side effects

No significant side effects were noticed apart from mild irritation in two patients of group A.


Discussion

Recurrent aphthous ulceration (RAU) is the most common oral mucosal disease among the general world population, including Iraq [12]. There is no uniformly effective therapy for this disease. Lactic acid has been used in the treatment of many skin diseases and it has been demonstrated to stimulate keratinocytes to release cytokines to help in angiogenesis and wound healing [16].

This is the first attempt to evaluate the therapeutic efficacy and safety of lactic acid in the treatment of RAS. This work shows that 5 percent lactic acid mouthwash produced a significant reduction in the duration, number, and associated pain of aphthous ulcers in comparison to a placebo mouthwash.

The effect of lactic acid on the duration of aphthous ulcers was more obvious in the major aphthous ulcers. These ulcers generally need 2-3 weeks for spontaneous healing; the use of lactic acid 5 percent mouthwash reduced the healing process to 5-7 days. The healing time was also shortened for minor aphthous and herpetiform ulcers. The effect of lactic acid was clearly evident in the reduction of the number of ulcers and associated pain in all clinical types of RAS. The slight response to placebo could not specifically be explained. There were no significant side effects noticed during the study apart from mild irritation in two patients using lactic acid.

The mechanism of action of lactic acid in treatment of RAS cannot be clearly explained, but could be due to the following:

  • increase in secretion of endothelial growth factor from keratinocytes [16]
  • antibacterial action and improvement of oral hygiene especially against Streptococcus sanguis, which is considered as a possible pathogenic agent that may be associated with RAU [15]

In conclusion, lactic acid 5 percent mouthwash is a new effective mode of therapy for patients with RAU. It significantly reduces the signs and symptoms of the disease. A long-term extended study is needed to evaluate the prophylactic role of lactic acid mouthwash in RAS.

References

1. Andrews M D. Diseases of the skin, clinical dermatology. W. B. Saunders Company. Philadelphia. 9th Edition. Recurrent aphthous stomatitis. 2000. Chapter 34: 1006-8.

2. Sylvia Brice. Clinical evaluation of the use of low intensity ultrasound in the treatment of recurrent aphthous stomatitis. Oral surg. Oral med. Oral pathol. Endod. 1997. 83: 14-20.

3. Champion R H, Burton and Ebling DSC. Textbook of dermatology. Blackwell Scientific Publications. Oxford. Fifth edition. Recurrent aphthous stomatitis. 1992. Chapter 65: 2709-12.

4. Addy M, Seal M and Lorna T J. Trial of astringent and antibacterial mouthwashes in management of recurrent aphthous ulceration. Brit. Dent. J. 1974. 136: 462.

5. Sharquie K E and Najim R A. Honey as a new skin tissue preservative. J. Pan-Arab League Dermatol. 2001. 12: 49-54.

6. Merchant H W, Gangarosa L P, Glossman AB and Sobel R E. Zinc sulphate supplementation for treatment of recurrent aphthous ulceration. South Med. Journal 1997. 70: 559-561.

7. Abdoli S, Hadi N, Ali A, Waiz M and Hayani R. A comparative study in the effect of nigella sativa oil, eugenol and betamethasone in the treatment of recurrent oral ulcerations. Clinical and experimental Rheum. Journal. 2004. 22: 120.

8. Fontes V, Machet L, Huttenberger B, Lorette G and Vaillant L. Recurrent aphthous stomatitis: treatment with Colchicine. Ann. Dermatol. Venereol. 2002. 129: 1365-9.

9. Chandrasekhar J, Liem A A, Cox N H and Paterson A W. Oxypentifylline in the management of recurrent aphthous stomatitis. Oral surg. Oral med. Oral pathol. Oral radiol. Endod. 1999. 87: 564-7.

10. Grinspan D. Significant response of oral aphthosis with thalidomide. J. Am. Acad. Dermatol. 1985. 12: 85.

11. Robinson N D, Guitart J. Recalicitrant, recurrent aphthous stomatitis treated with etanercept. Arch. Dermatol. 2003. 139: 1259-1262.

12. Sharquie K E and Hayani R K. BCG as a new therapeutic and prophylactic agent in patients with sever oral aphthosis. Clinical Experimental Rheum. Journal. 2004. 22: 120.

13. Van-Scott E and Yu R. Alpha hydroxy acids: procedure for use in clinical practice. Cutis 1989. 43: 222-8.

14. Sharquie K E and Abdulla M S. Treatment of Vitiligo with Topical 15% Lactic Acid Solution in Combination with Ultraviolet-A. Saudi Med. J. 2005. 26: 1013-14.

15. Pasricha A, Bhalla P and Sharma K B. Evaluation of lactic acid as an antibacterial agent.Indian J of Dermatol.1979.45:149-161.

16. Rendle M, Myer C, Weniger W and Tehochler. Topically applied lactic acid increase spontaneous secretion of vascular endothelial growth factor by human reconstructed epidermis. Br. J. Dermatol. 2001. 145: 3-9.

17. Brozovic S, Vucicevic Boros V, Mrovak Stipetic M and Jukic S. Salivory levels of vascular endothelial growth factor (VEGF) in recurrent aphthous ulceration. J. Oral. Pathol. Med. 2002. 31: 106-8.

© 2006 Dermatology Online Journal