Sclerotherapy is the injection of a chemical solution called sclerosing agent or sclerosant into a vein which damages the endothelial lining and causes vessel occlusion, leading to the development of fibrous tissue. With multiple uses in the medical field, sclerotherapy has not been widely practiced for dental purposes. The commonly used sclerosing agents are sodium tetradecyl sulfate (STS), polidocanol, sodium morrhuate, ethanolamine oleate, sodium silicate, pingyangmycin (PYM), OK-432, and ethanol. This being a noninvasive and simpler procedure, helps reduce the cost and complications associated with surgery of oral mucocele, a common salivary gland lesion. This review aims to enhance the knowledge of a dental practitioner regarding sclerotherapy and its benefits for the treatment of oral mucocele.
MATERIALS AND METHODS
We systematically searched the Google Scholar and PubMed database using the keywords oral mucocele, sclerotherapy, polidocanol, STS, ethanol, bleomycin (BLM), OK-432, hypertonic saline, and sclerosants published from the year 2010 to 2020. Articles with oral mucocele treated with sclerotherapy were selected. Our search was not limited to these terms only. We have also gone through the references of these articles and thoroughly studied them. A total of six relevant articles were found, whose salient features are shown in Table 1.
Sclerotherapy is the targeted elimination of intracutaneous, subcutaneous, and/or transfascial varicose veins as well as the sclerosation of subfascial varicose vessels in venous malformation cases by injecting sclerosing agents.
Sclerotherapy has been used widely in the medical field to treat:
- Varicose veins
- Venous malformations
- Lymph cysts
- Baker's cysts.
In recent years, it had a wide range of uses in the dental field also. It is commonly used nowadays for the treatment of:
- Pyogenic granulomas
- Arteriovenous vascular malformations.
The word mucocele is derived from a Latin term, mucus and coele which means cavity. Mucoceles are mucous-filled cavities that can appear at various locations on the oral mucosa, gallbladder, appendix, lacrimal sac, or paranasal sinuses. It is the 17th common salivary gland lesion seen on the oral mucosa. Two types of mucocele can appear [FIGURE DASH] extravasation and retention. Mucous retention phenomena are less frequent and seen majorly in the elderly population. With extravasation type showing a prevalence of 92%, the incidence of this lesion is approximately 0.25 lesions/100 patients. They can occur in any age group with a higher frequency in the second and third decades.
TYPES OF MUCOCELE
Extravasation mucoceles are caused by a leaking of fluid from surrounding tissue ducts or acini. This type of mucocele is commonly found on the minor salivary glands. Physical trauma can cause a leakage of salivary secretion into surrounding submucosal tissue. Inflammation becomes obvious due to stagnant mucous resulting from extravasation.
There is obstruction of the salivary gland duct which causes excessive accumulation of fluid in the salivary duct, which results in the formation of a small balloon, and with the progression of time, there is an increase in the balloon size which bulges inside the oral cavity.
The most affected region by mucoceles in the oral cavity is the lower lip. Rare cases of mucoceles in the upper lip, retromolar region, palate, lingual frenum, buccal mucosa, and dorsal surface of the tongue have been reported. They are mostly asymptomatic, but in some patients, they may cause discomfort due to interference in speech, chewing, or swallowing. Retention type of mucoceles have a slight bluish tinge and are soft and transparent cystic swellings that usually resolve spontaneously. Blue tinge is due to the vascular congestion and cyanosis of the tissue above, and accumulation of fluid below. However, color varies according to the size of the lesion, proximity to the overlying surface, and elasticity of mucosa. The extravasation type of mucocele appears more frequently on the lower lip, followed by the tongue, buccal mucosa, and palate, and is very rarely found on the retromolar region and posterior dorsal surface of the tongue.
Surgery, laser ablation, cryosurgery, micromarsupialization, laser surgery, and intralesional injection of corticosteroids or sclerosants are various modalities used for the treatment of oral mucoceles. Surgery is the most commonly used modality and has numerous disadvantages such as disfigurement of the lip and damage to adjacent salivary ducts, and further development of new satellite mucoceles. Therefore, the focus of interest has shifted toward nonsurgical treatment modalities including intralesional corticosteroid injection and sclerotherapy.
Types of sclerosants
Unfortunately, the ideal sclerosant is said not to exist. However, the sclerosing agents are divided into various types: hyperosmolar, detergent, and chemical [Table 2].
The main goal of hyperosmolar agents is to cause dehydration of target cells, which induces cell damage and death. The effect of these agents is purely based on concentration gradients. Various osmotic agents are present such as hypertonic saline and sodium chloride solution with dextrose (Sclerodex) [Table 2], but their use for dental treatment purposes is limited.
Detergent agents, also known as fatty alcohols and fatty acids, were introduced between the years 1920 and 1930. They are the most promising sclerosing agents in the world. They can displace blood mechanically, by the ability to be agitated and foamed which results in increased potency by 2–4 times. The surface area and time of contact with the endothelium are increased. Various examples of detergent sclerosants are STS, polidocanol, sodium morrhuate, etc. [Table 2] STS and polidocanol are used widely for the management of pyogenic granuloma and oral mucocele.
Chemical sclerosants have a corrosive effect. They disrupt the intercellular cement. They also poison the cell surface proteins and affect chemical bonds on exposure to the vein wall, immediately. A few chemical sclerosants include chromated glycerin, polyiodinated iodine, OK-432, BLM, etc. [Table 2]. OK-432 and BLM have been used widely to treat mucoceles and ranulas.
MECHANISM OF ACTION
Detergent sclerosants cause sclerosing effects through differential cell injury depending on the concentration. Through sclerosant administration, cellular calcium signaling takes place, and nitric oxide pathways become activated which leads to the death of cells. The timing of endothelial cell death depends on the concentration of sclerosing agents which ultimately leads to the lysis of cells of the endothelium. It can involve red blood cells and platelets, and cause platelet-derived microparticle formation.
Polidocanol is a widely used nonionic detergent sclerosant that was first developed as an anesthetic. Its action is through endothelial overhydration, vascular injury, and closure. It causes damage to the endothelial vessels permanently which results in necrosis.
Sodium tetradecyl sulfate
It is a surface-active substance mainly composed of sodium 1-isobutyl-4-echyloctyl sulfate and benzyl alcohol 2% which is a phosphate buffer. The pH of this STS solution is 7.6. Necrosis and sloughing of the tissue occur when STS is used superficially in the lesion. Total or partial regression of the lesion is seen by injecting STS.
It was initially produced as an immunotherapeutic agent for cancer treatment. It is a Streptococcal preparation that is lyophilized. The Su-strain of group A Streptococcus is treated with penicillin for the preparation of this sclerosant. After its administration, a strong inflammatory reaction occurs locally due to monocytes and neutrophil activation, which further leads to the production of cytokine. OK-432 is responsible for the induction of a very strong inflammatory reaction at the injection site in the oral mucocele.
BLM is a multicomponent complex and has higher pulmonary toxicity than PYM which is a single BLM A5 component. The cytotoxic nature of BLM is basically due to deoxyribonucleic acid (DNA) damage directly. It is responsible for causing single- and double-stranded DNA breakage. It is seen in DNA as chromosomal gaps, deletions, and fragmentations. The mechanism of action of BLM in sclerotherapy of oral mucoceles is due to its cytotoxic nature and the inflammatory reaction induced by it locally. The cytotoxic nature of BLM destroys the cystic wall and associated glands with it which results in decreased production of saliva. Further, localized inflammation reactions can promote salivary absorption, causing the collapse of mucocele.
The mechanism of action of sclerotherapy is depicted in Figure 1.
Procedure for mucocele sclerotherapy
- A localized patch test should be done to rule out an allergy to the sclerosant
- Local anesthesia (LA) needs to be applied at the injection site
- Under aseptic conditions, injection of 0.5–1 mL of the sclerosant solution in the lesion cavity with an insulin syringe until blanching is seen or till the solution leaks out
- Few sclerosants such as STS, due to the side effects they produce, need to be diluted with distilled water or hypertonic saline in the ratio of 1:3 before injecting
- Compress the injection site with a gauze piece or cotton to avoid leaking of the sclerosant for about 3–5 min
- Regular follow-up is necessary at weekly intervals to check the healing
- Multiple injections need to be planned at weekly intervals until the lesion becomes necrotic and vanishes following the same protocol
- After completion of treatment, follow-up is necessary after every 1, 3, and 6 months to check for recurrence.
- Sclerosants are very easily available
- They are safe, reliable, and effective with the least side effects
- They cause decreased discomfort to the patient
- There is almost no blood loss
- Less surgical expertise is required
- They are economical cost wise
- There is no need for LA, postoperative dressing, or any particular care
- No reports of systemic complications were seen while treating oral mucocele
- Chances of mucocele recurrence are also reduced.
- It causes various local complications
- Multiple injections may be required if the lesion does not regress completely.
Although sclerotherapy for oral mucocele has no reports of systemic complications, it should be performed with care, because it can cause various local complications intraorally such as:
- Nerve damage
- Increased pain
- Tissue necrosis and sloughing
- Postinjection swelling and scar
- Local discomfort
- Superficial ulceration.
Sclerotherapy for the treatment of oral mucocele is a nonsurgical treatment modality that has gained popularity recently due to less cost, no scar formation posttherapy, low chances of recurrence, and less suffering to the patient. This modality should be thought of while treating not only oral mucoceles but also other vascular lesions occurring in the oral cavity such as pyogenic granulomas and hemangiomas. Thorough knowledge of the good and ill effects of this therapy is, therefore, necessary to proceed with it.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
1. Khunger N, Sacchidanand S. Standard guidelines for care: Sclerotherapy in dermatology Indian J Dermatol Venereol Leprol. 2011;77:222–31
2. Shah JS, Ranghani AF. Sclerotherapy in pyogenic granuloma and mucocele J Indian Acad Oral Med Radiol. 2018;30:230–4
3. Liu JL, Zhang AQ, Jiang LC, Li KY, Liu FZ, Yuan DY, et al The efficacy of polidocanol sclerotherapy in mucocele of the minor salivary gland J Oral Pathol Med. 2018;47:895–9
4. Shetty VM, Rao R, Pai B S. Sclerotherapy in mucocele: A novel therapeutic approach J Cutan Med Surg. 2018;22:652–3
5. George A, Loganathan E. Oral mucocoele: The magic of sclerotherapy Skinmed. 2017;15:383–4
6. Zhang J, Wang C. The application of absolute ethanol in the treatment of mucocele of the glands of Blandin-Nuhn J Craniofac Surg. 2016;27:e641–2
7. Cai Y, Wang R, Yang SF, Zhao YF, Zhao JH. Sclerotherapy for the mucoceles of the anterior lingual salivary glands with pingyangmycin Oral Dis. 2014;20:473–6
8. Rabe E, Pannier-Fischer F, Gerlach H, Breu FX, Guggenbichler S, Zabel M, et al Guidelines for sclerotherapy of varicose veins (ICD 10: I83.0, I83.1, I83.2, and I83.9) Dermatol Surg. 2004;30:687–93
9. Petre Z, Barjica D, Duta C, Boglut A, Bernad E, Craina M, et al Sclerotherapy for varicose veins Mater Plastice. 2016;53:765–6
10. Rabe E, Pannier Ffor the Guideline Group. . Indications, contraindications and performance: European Guidelines for Sclerotherapy in Chronic Venous Disorders Phlebology. 2014;29:26–33
11. Zimmet SE. Sclerotherapy treatment of telangiectasias and varicose veins Tech Vasc Interv Radiol. 2003;6:116–20
12. Gorman J, Zbarsky SJ, Courtemanche RJ, Arneja JS, Heran MK, Courtemanche DJ. Image guided sclerotherapy for the treatment of venous malformations CVIR Endovasc. 2018;1:2
13. de Lorimier AA. Sclerotherapy for venous malformations J Pediatr Surg. 1995;30:188–93
14. Abdulmaaboud MR, Shokeir AA, Farage Y, Abd El-Rahman A, El-Rakhawy MM, Mutabagani H. Treatment of varicocele: A comparative study of conventional open surgery, percutaneous retrograde sclerotherapy, and laparoscopy Urology. 1998;52:294–300
15. Ghanem MA, Safan MA, Ghanem AA, Dohle GR. The role of varicocele sclerotherapy in men with severe oligo-astheno-teratozoospermia Asian J Androl. 2011;13:867–71
16. Wang YG, Seo HI, Kim HY. Sclerotheraphy with OK-432 for the treatment of lymphangiomas Cancer Res Treat. 2002;34:62–6
17. Chauhan V, Patel K, Anchalia M. Prospective comparative study of sclerotherapy by hypertonic saline and absolute alcohol for the treatment of hemorrhoids Gujarat Med J. 2014;69:82–6
18. Suskind DL, Tavill MA, Handler SD. Doxycycline sclerotherapy of benign lymphoepithelial cysts of the parotid: A minimally invasive treatment Int J Pediatr Otorhinolaryngol. 2000;52:157–61
19. Linetsky F. Sclerotherapy for Baker's cyst Pain Physician. 2008;11:375–6
20. Castillo CD. The use of OK-432 (Picibanil) as a non-surgical alternative for the management of ranula and mucoceles Rev ADM. 2011;68:215–21
21. Reddy GS, Reddy GV, Reddy KS, Priyadarshini BS, Sree PK. Intralesional sclerotherapy – A novel approach for the treatment of intraoral haemangiomas J Clin Diagn Res. 2016;10:ZD13–4
22. Khaitan T, Sinha R, Sarkar S, Kabiraj A, Ramani D, Sharma M. Conservative approach in the management of oral pyogenic granuloma by sclerotherapy J Indian Acad Oral Med Radiol. 2018;30:46–51
23. Deepa V, David CM, Lidiya A. Management of arterio venous vascular malformation masquerading as a mucocele using sclerotherapy-review of literature and a case report Int J Pharm Sci Invent. 2013;9:1–6
24. Laller S, Saini RS, Malik M, Jain R. An appraisal of oral mucous extravasation cyst case-mini review J Adv Med Dent Sci. 2014;2:166–70
25. Hayashida AM, Zerbinatti DC, Balducci I, Cabral LA, Almeida JD. Mucus extravasation and retention phenomena: A 24-year study BMC Oral Health. 2010;10:15
26. Delbem AC, Cunha RF, Vieira AE, Ribeiro LL. Treatment of mucus retention phenomena in children by the micro-marsupialization technique: Case reports Pediatr Dent. 2000;22:155–8
27. Agrawal S, Koirala B, Dali M, Shrestha S. Oral mucocele: Various treatment modalities J Kathmandu Med Coll. 2018;7:110–3
28. Ata-Ali J, Carrillo C, Bonet C, Balaguer J, Peñarrocha M, Peñarrocha M. Oral mucocele: Review of the literature J Clin Exp Dent. 2010;2:e18–21
29. More CB, Bhavsar K, Varma S, Tailor M. Oral mucocele: A clinical and histopathological study J Oral Maxillofac Pathol. 2014;18:S72–7
30. Sagari SK, Vamsi KC, Shah D, Singh V, Patil GB, Saawarn S. Micro-marsupialization: A minimally invasive technique for mucocele in children and adolescents J Indian Soc Pedod Prev Dent. 2012;30:188–91
31. Rao PK, Hegde D, Shetty SR, Chatra L, Shenai P. Oral mucocele-diagnosis and management J Dent Med Med Sci. 2012;2:26–30
32. Sinha R, Sarkar S, Khaitan T, Kabiraj A, Maji A. Nonsurgical management of oral mucocele by intralesional corticosteroid therapy Int J Dent. 2016;2016:2896748
33. Dietzek CL. Sclerotherapy: Introduction to solutions and techniques Perspect Vasc Surg Endovasc Ther. 2007;19:317–24
34. Albanese G, Kondo KL. Pharmacology of sclerotherapy Semin Intervent Radiol. 2010;27:391–9
35. Chhabra N, Chhabra S, Kapila SA. Use of hypertonic saline in the management of parotid fistulae and sialocele: A report of 2 cases J Maxillofac Oral Surg. 2009;8:64–7
36. Duffy DM. Sclerosants: A comparative review Dermatol Surg. 2010;36(Suppl 2):1010–25
37. Trivedi K, Soni A, Meshack R, Kulthya RS. Intraoral hemangioma: An overview of the clinical entity J Int Clin Dent Res Organ. 2015;7:79–81
38. Subramanyam S, Shivhare P. Pyogenic granuloma – A simple treatment approach with sclerotherapy Acta Sci Dent Sci. 2021;5:111–4
39. Ohta N, Fukase S, Suzuki Y, Aoyagi M. Treatment of salivary mucocele of the lower lip by OK-432 Auris Nasus Larynx. 2011;38:240–3
40. Eckmann DM. Polidocanol for endovenous microfoam sclerosant therapy Expert Opin Investig Drugs. 2009;18:1919–27
41. Parsi K, Exner T, Connor DE, Herbert A, Ma DD, Joseph JE. The lytic effects of detergent sclerosants on erythrocytes, platelets, endothelial cells and microparticles are attenuated by albumin and other plasma components in vitro
Eur J Vasc Endovasc Surg. 2008;36:216–23
42. Rohit, Singh A, Kumar P. A new concept in the treatment of oral venous malformation using sclerotherapy Int J Contemp Med Res. 2017;4:1104–7
43. Ahmad S. Efficacy of percutaneous sclerotherapy in low flow venous malformations – A single center series Neurointervention. 2019;14:53–60
44. Bansal N, Belgaumkar VA, Chavan RB, Doshi BR. Successful treatment of pyogenic granuloma with sclerotherapy Indian J Drugs Dermatol. 2019;5:30–3