AYURVEDIC APPROACH TO LEUKOPLAKIA – A CASE STUDY
Thirty five years obese male patient came from kharadi reported to our branch for complaints of Oral leukoplakia. He had history of white plaques in the oral cavity along with inability to open mouth along with inability to consume hot meal ,liquid along with difficulty in opening of mouth also since 1 yrs.
He had taken medicines from physician for at least 1 yr such as multivitamins ,oral antibiotics and anti fungal treatment for 4 to 5 times, but it was inversely relapsed, so he consulted our sanjeevani ayurveda center.
Patient was young man belonging to healthy family. He liked to salty and spicy food, he used to consume non veg. 4-5 times a week at nighttime. He was working with busy and hectic duty schedule. He used to addict for tobacco. He had history of chronic fissure for that he took homeopathic treatment 4 yrs back.
He had history of iron deficiency anemia for that he took oral iron supplementation.
He fails to exercise daily and his lifestyle was sedentary.
A) Nidan /Hetu:
- Tobacco chewing (1 packet daily)
- Weekly 4-5 times non veg
- Fast food-junk food daily at evening time
- Stress factor, oily spicy food,cold drinks,Tea(5-7 times per day)
B) SAMPRAPTI: Pittaj Mukhapak (AYURVEDIYA NIDAN)
RUGNA PRAKRUTI: PITTA KAPHA
RUGNA JANAM DIN: 11/12/1980 (KSHAR ANDAMLADHARMI )
DOSHA: PITTA KAPHA ANUBANDH
DUSHYA: RAKTA, MANSA
C) TREATMENT PLAN:
1) SHAMAN CHIKITSA
2) SWARNAMAKSHIK - 125 MG+PRAWAL BHASMA-125MG+GUDUCHI SATVA- 250MG for 25 days given
3) MOUKTIK YUKTA KAMDUDHA -125 MG prat and say bhojnottar for 1 month
4) GULOOCHYADI KASHAYAM -50 prat say bhojanottar for 20 days
5) IRIMEDADI TAILA for kawal and gandusharth for 1 month
6) MAHATIKTAKAM GHRUTAM-Used as pitta shaman (Bhrajaka pittam). Local applicaton
7) GANDHARVA HARITAKI 3 gm bhojanottar ratrou
8) TURMGEL LOZENGES 1qid
SHODHAN CHIKITSA:
VIRECHAN
Virechan with TRIVRUTHA LEHYAM: 50gms after snehapan with mahatiktakam ghrutam for 2 times given during treatment course.
3) Bahiparimarjan chikitsa:
1) Kawal of Irimedadi tailam forthrice a day.
2) Yastimadhu ghrutam for kawaldharan for one in a day.
3) Mukha dhavan by haridra+triphala+nimb choorna kwatha twice a day after meal..
Pitta shaman chikitsa along with agnivardhan chikitsa done by kashay and choornas. Anuloman is given for vatanuloman. Diet is corrected by specific diet prescribed at ayusanjiavni. The treatment continued for 3months.now patient is on diet only.
Three stages of OL have been described:
1. The earliest lesion is non palpable, faintly translucent,and has white discoloration.
2. These lesions are localized or diffuse, slightly elevated plaques with an irregular development. These lesions are opaque white and may have a fine, granular texture’
3. In some instances, the lesions progress to thickened, white lesions, showing induration, fissuring, and ulcer formation.
Clinically, OL falls into 1 of 2 main groups.
1. The most common are uniformly white plaques (homogenous OL) prevalent in the buccal mucosa, which usually have low premalignant potential.
2. Far more serious is speckled or verrucous leukoplakia,which has a stronger malignant potential than homogenous leukoplakia. Speckled leukoplakia consists of white flecks or fine nodules on an atrophicerythematous base.These lesions can be regarded as a combination of or a transition between leukoplakia and erythroplasia, which is flat or depressed below the level of the surrounding mucosal red patch, is uncommon in the mouth,and carries the highest risk of malignant transformation.
Five clinical criteria demonstrate a particularly high risk of malignant change.
1. The verrucous type is considered high risk.
2. Erosion or ulceration within the lesion is highly suggestive of malignancy.
3. The presence of a nodule indicates malignant potential.
4. A lesion that is hard in its periphery is predictive of malignant change.
5. OL of the anterior floor of the mouth and undersurface of the tongue is strongly associated with malignant potential.
In all cases, the relative risk of malignant potential is determined by the presence of epithelial dysplasia upon histological examination.
Causes:
· In persons who smoke (eg, tobacco tars and resins) are irritating substances capable of producing leukoplakic alterations of the oral mucosa. Years of heavy pipe, cigar, and cigarette smoking can lead to a characteristic type of benign keratosis in the hard palate, called stomatitis nicotina leukoplakia.
· The use of alcohol has been suggested as a possible etiology because alcohol may irritate the mucosa. Persons who habitually consume considerable quantities of alcohol usually also smoke inveterately; therefore, establishing the effects of alcohol alone is difficult.
· Malocclusion; chronic cheek biting;ill-fitting dentures; and sharp, broken-down teeth that constantly irritate the mucosa are considered extremely important in the etiology of OL.
· Patients who have had syphilitic gloss it is have a higher prevalence of OL than individuals with a non syphilitic background.
· The presence of Candida albicans, a relatively common oral fungus, has been reported to be very frequently associated with OL.
· Deficiency of vitamins A and B has been suggested as an inciting factor in the development of OL.
Diagnostics consideration/differential diagnosis:
These include the following:
· Leukoedema
· Lichen planus
· Chemical burn
· Morsicatio buccarum (habitual cheek biting)
· Candidosis
· Psoriasis
· Lupus erythematosus
· White sponge nevus
Treatment and management:
Surgical excision of oral leukoplakia (OL) may be considered. Frequent clinical observation accompanied by photographic records is recommended. Because of the unpredictable behavior of dysplastic lesions, immediately obtain a biopsy on any areas that are suggestive or that change in appearance. Cryotherapy ablation and carbon dioxide laser ablation are also used. The area heals rapidly, and apparently healthy mucosa is left behind. However, uncertainty remains regarding the risk of invasive carcinomas subsequently arising in sites previously treated.