1. A CLINICAL STUDY ON PALITYA W.S.R. TO
PREMATURE GRAYING OF HAIR AND ITS
MANAGEMENT WITH NIMBABEEJA TAILA NASYA
AND BHRUNGARAJADI RASAYANA
2. INTRODUCTION
Palitya is derived from the word palita, which means kasha
paka.
Heefueleb kesÀMem³e MegkeÌuelee e
(Yo.ratra. 61/1)
Graying of hair or whitening of hair is termed as palita.
Acharya Charaka described in trimarmiya adhyaya, Acharya
Vagbhata & Sarangadhara described in sirokapalagata roga
and Acharya sushruta, Madhavakara, Yogaratnakara,
Bhavaprakasha described under Kshudraroga adhikara.
5. The sign and symptoms are
Sphutita
Shyaba
Khara
Ruksha
Jalaprabha
Daha
Pittabha
Snigdha
Vivrudhasthula
Sukla
6. Ayurveda accounts for two types of palitya
i.e. Akalaja (premature grey hair)
Kalaja (senile grey hair)
Palitya i.e premature graying of hair is a burning cosmetic issue in
present era.
When graying begins before the usual age of onset, it is termed as
premature graying of hair.
The onset and progression of graying correlate very closely with
chronological aging and occur in varying degrees in all indivisuals
eventually, regardless of gender or race.
7. INCIDENCE & PREVALANCE
Palitya is common in young age between 20-30 years age group.
Even in children also the incidences are increasing day by day.
Hair is said to have grayed prematurely if it occurs before the age of
20 years in whites, before 25 years in Asians and before 30 years in
Africans.
The prevalence of premature greying of hair is found to be 1.2%
The prevalence was higher among female as compared to male.
8. NEED OF THE STUDY
Premature greying aids to embracement & social stigma. Current
treatment available are not much satisfactory to cure, check or
prevent this problem.
Treatment of Palitya as mentioned in Ayurveda includes sodhana
& samanachikitsa. Hence, aiming to derive a new treatment
modality for Palitya (Premature greying of hair) this research has
been proposed.
So in order to obtain an safe and cost effective remedy this
problem has been selected
9. PREVIOUS RESEARCH WORK DONE:-
1. Evaluation of Bhrungarajatailanasya with and without
Bhrungarajadirasayana in the management of Akala Palitya a
comparative study by Dr. Lokanath J Avadhani, Rajiv Gandhi University
of Health Science, Bengaluru 2011-12
2. Clinical management of Akala Palityam(Gray hair) with
Triphaladilepam with and without Nimbabeejataila Nasyam by Dr.
Lavudya Kamala Kumari, N.T.R. University of Health Science,
B.R.K.R.GOVT. Ayurvedic College & Hospital, Erragadda, Hyderabad
2005
3. Study of Khalitya&Palitya with special emphasis on etiopathogenesis
by Dr. Vishakha D Pathak, Tilak Maharastra University, Pune.
10. 4. A clinical study to assess the efficacy of pratimarshanasya in
prevention of Akala Palitya W.S.R. to premature greying of
hair by Dr. Sagar Sharma, Rajiv Gandhi University of Health
Sciences, Karnataka.
Sri Jagadguru Gavisiddheswar Ayurvedic Medical College &
Hospital, P.G. studies & Research centre, Gavinath Campus,
Koppal, Karnataka (2013-14)
11. AIM AND OBJECTIVE OF THE STUDY
AIM -
A clinical study on palitya w.s.r to Premature greying of hair
and its management with nimbabeeja taila nasya and
bhrungarajadi rasayana.
OBJECTIVE -
Review of literature of the disease both for ancient and modern
point of view and research of the drug.
To evaluate the efficacy of nimbabeeja taila & bhrungarajadi
rasayana in the management of Palitya.
To evaluate the efficacy of Nimbabeeja taila nasya in the
management of palitya
12. HYPOTHESIS
It is presumed that Nimababeeja taila & bhrungarajadi rasayana
described by Bhaisajyaratnavali can effectively control the clinical
symptoms of palitya .
(Ref- Nimababeej ataila– Bhaisajya Ratnavali, Kshudraroga 60/80
Bhrungarajadirasayana-BhaisajyaRatnavali, Rasanayanadhikara73/28-
29)
PURPOSE OF MEDICINE USE –
The need has already been felt to develop certain ayurvedic
treatment for the better management of palitya which could be safe,
effective, cost-effective readily available and without any side effect.
So, keeping all the fact in mind I have taken this formulation
Nimbabeeja taila and Bhrungarajadi rasayana.
13. MATERIAL AND METHODS-
DRUG REVIEW
The raw drugs will be purchased from local market .
The trial drug Nimbabeeja taila and Bhrungarajadi rasayana
will prepared in G.A.M,PURI pharmacy attached to Dept. of
R.S.B.K .
16. Ingredient
Bhrungaraj Chruna - 1PART
Krushna Tila Chruna -1/2 PART
Amalaki Churna -1/2 PART
Anupana: Sarkara or Guda
DOSAGE- 5gm b.i.d
Duration: 3 months
Follow up in every 1 month
19. DIAGNOSTIC CRITERIA-
Inclusion criteria
Patients having features of Akala Palitya.
Patients to age group of 20-30years
Patients yogya for nasya and rasayana.
Exclusion criteria
Patients with age below 20 years and above 30 years
Patients ayogya for nasya and rasayana.
Infection diseases of scalp like Alopecia areata.
Akala Palitya associated with the diseases of pigmentation like vitiligo,
leprosy and Albinism.
Any other systemic diseases.
Subjects with hormonal diseases and hereditary disorders.
20. PLAN OF PROTOCOL
Plan of study
Comparative clinical trial study will be undertaken to co-relate the clinical effect of
the trial drug.
In the present study 60 clinically diagnosed patient of either sex of palitya are
selected from OPD/IPD of G.A.M. & Hospital Puri.
A regular record of assessment of all the patient will be maintained according to the
format prepared for the purpose.
Group- A -30 Patients will be treated with both nimbabeeja taila nasya and
Bhrungarajadi rasayana internally.
Goup-B-30 patients will be treated with nimbabeeja taila nasya
Types of study –clinical study
22. DOUBLE GROUP DESIGN-
ASSESSMENT CRITERIA
Assessment will be made by assessment scale availing
subjective parameters & objective parameters.
23. Objective Parameters
Sphutita (absent or present)
Khara (absent or present)
Ruksha (absent or present)
Sukla (absent or present)
24. Hair Count
A new scoring system (Graying severity score, GSS) was devised
to evaluate the external of graying taking into account five
representative sites from the scalp by two independent
investigation and analysed for agreement GSS ranged from 0 to
15 that was further graded as mild, moderate and severe.
5zones- Frontal, vertex, right, left, occipital
A 1cm2 area was washed with a skin marker and the hair
within this square was cropped to approximately 1mm
above scalp surface. These five squares were then
photographical and projected on the computer screen to
count the numbers of white and black hair.
25. Based on the hair count, a score was assigned to each zone a/c to
the percentage of grey hair in each square. This was calculated and
scored as
Score-1-- 10% grey hair/cm2
Score-2 -- 10%-30% gray hair/cm2
Score-3-- more than 30% gray hair/cm2
The GSS was finally calculated for each patient by taking a sum of
the scores a the five represent sites. Thus the maximum attainable
score for a patient was 15 (3X5)
The objective scores were further graded as;
Mild (a score of 0-5)
Moderate (Score of 6-10)
Severe (Score of 11-15)
27. PRESENTATION OF RESEARCH WORK
The whole research work will be presented in the form of
binding thesis with suitable language by the following parts
and chapters.
Part-1
Introduction
Review of Literature
a) Ayurvedic Review of disease
b) Modern Review of disease
Part-2
Clinical Study
a) Materials and methods
b) Drug Review
c) Observation and Statistical evaluation
29. SUMMARY AND CONCLUSION
It has been hope that present study will bring out a new
standard, effective and successful treatment for Palitya.
30. PALITYA
pejmee kesÀMeeoew
MeewkeÀue³eced e
DecejkeÀes<e
Palitya means change of colour in hair or graying of hairs
At the age old, hair turned to be white in colour.
Palitya is a disease of rasadhatu drusti janya roga which is
described by acharya caraka and sushruta
INTRODUCTION
31. KESHA SWARUPA
keÀsMee: Meer<ex cegKes MceÞeg ves$es
He#ce Ye¦Jeew celeew e
leveew jesceeefCe pee³evless keÀjHeeoleues
efJevee e (meejbieOej)
Human body contains hair follicles in all area except palm & sole. It
is termed as different way in different area.
Sirsa – Kesa
Mukha – Smasru
Netra – Pakhma, Bhru
Rest of the body – Roma
32. KESHA UTPATI
According to Maharsi Caraka:- Kesha and Roma is the mala of Asthidhatu.
According to Maharsi Sarangadhar :- Kesha is the upadhatu of majjadhatu.
Roma is the mala of Asthidhatu.
During Ahara poshana karna, Ahara rasa is processed by jatharagni and
dhatwagni to convert in to 2 part : (1) Prasada bhaga
(2) Kitta bhaga
During asthidhatwagni vyapara, the poshakamshas which nurish asthidhatu are
converted into 2 parts, its kittabhaga is processed by the action of malagni to
produce kasha.
33. NIDANA
¬eÀesOeMeeskeÀÞeceke=Àle: Meefjjes<cee
efMejeWiele: e
efHeÊeb ®e kesÀMeeved He®eefle Heefueleb
lesve pee³eles ee
(su.ni 13/36) Ma. Ni. 55/32)
It means heat of the body reaching the head due to anger, grief
and physical exertion, vitiating the local pitta makes the hairs
grey, palitya is thus produced.
¬eÀesOeMeeskeÀ Þeceke=Àle:Mejerjes<cee
efMejesiele: e
EfHeÊeáe kesÀMeeveHe®eefle Heeefueleb
lesve pee³eles ee (61/1)
Mejerjes<cee - osneeqive: efHeÊeáe
34. SkeÀ : ÒekegÀefHelees oes<e FlejeJeeefHe
keÀesHe³esod e
Fefle Je®eveeÜeleefHeÊeeY³eeb Mues<ceeb ®e
keÀesefHele:, me SJe kesÀMeeveeb MeewkeÀu³eb
keÀjesefle e SJeb $e³eesçefHe oes<ee:
Heeefuelem³e nsleJe:– kesÀMem³e MegkeÌuelee ee
(1) (61/1)
Increase of vayu especially due to excess of soka and shrama, at the same time
the pitta is being increased due to krodha in its ushma guna.
This provoked pitta circulates through out the body through rasayani (srota) by
the virtue of vikshepana guna of provoked vata to incease the sharira ushma.
This saririka ushma reaches to shira and vitiates sthanika vata and shlesma karya.
This tridoshas vitiated and graying of hair causes manifestation of palitya.
On the basis of samprapti, pitta prakopaka nidana (Ref. Su. Su. 21/21),
Rasadrushti (Ref. ca. su. 28/10) & (su. Su. 24/10) and asthidrusti (ca. ci. 15/18-
35. Pitta Prakopaka Nidana
Aharaja nidana
¬eÀesOeMeeskeÀ
Ye³ee³eemeesHeJeemeefJeoiOecew
LegveesHeieceve keÀìdJecueueJeCe
Leer#Ce G<Ce ueIegefJeoeefn
efleuelewue
efHeC³eekeÀkegÀuelLeme<e&Heel
e .....
Excess use of pungent (katu)
Sour (Amla)
Salt (Lavana)
39. TYPES OF PALITYA
According to According to According to
Vagvatta :- sarangadhara :- Yogaratnakar :-
1. Vataja (i) Kalajanita (i) vataja
2. Pittaja (ii) Akalajanita (ii) pittaja
3. Kaphaja (iii) kaphaja
4. Sananipatika (iv) sannipatika
5. Sirarujadbhaba
43. Premature greying of Hair
Hair is said to greying prematurly only if greying occurs before the age of
20 years in whites , before 25 years in Asians and before 30 years in
Africans.
According to W.H.O incidence of premature greying of hair is common in
age group of 20-30 years
SKIN
44. HAIR
Hair is a filamentous biomaterial that grows from follicles found
in the dermis.
Hair follicle :- the part beneath the skin.
Hair bulb :- the part when hair is pulled from the skin.
Hair follicle is located in the dermis and maintains stem cells
responsible for regrowth of hair and skin
50. HAIR CYCLE
From the time it is formed each hair follicle undergoes a
repetitive sequence of growth and rest known as the hair cycle.
52. HAIR PIGMENTATION
Hair pigmentation is a process, in which there is a precise
interaction in the hair follicle unit between follicular
melanocytes, keratinocytes and dermal papilla fibroblasts.
MELANIN :-
The colour of human hair is due to pigment melanin
produced by melanocytes.
Melanin is produced through a multistage chemical process
known as melanogenesis where the oxidation of amino acid
tyrosine is followed by polymerization.
54. Function
Protect underlying structure from the harmful
effects of sunlight.
Influence the colour of epidermis.
The synthesis of melanin reaction is catalyzed by the
tyrosinase, Tyrosine is found in only one specialized
type of cell, the melanocyte, and in this cell melanin
is found membrane-bound bodies called
melanosomes.
56. NORMAL HAIR FOLLICULAR MELANIN
UNIT AND MELANOGENESIS
Each melanocyte is associated with five keratinocytes in the
hair bulb forming a hair follicle-melanin unit.
Melanogenesis in the hair is closely associated with stages of the
hair cycle.
Follicular menocytes are derived from immature melanoblasts
that migrate from the neural crest into the skin during
embryogenesis.
As the hair follicle develops, the progeny of melanoblasts which
proliferate in the epidermis, known as transient – amplifying
melanocytes, leave that compartment and move into the
developing hair follicle.
57. MELANOGENESIS :-
The colour of human hair depend melanogenesis, through a
process of synthesis of melanin and its subsequent distribution
from the melanocyte to keratinocyte.
There, menalocytes may become or remain DOPA-oxidase-positive
cells (i.e. express active tyrosinase) or remain DOPA-oxidase-
negative cells (i.e. either fail to express tyrosinase or express on
inactive tyrosinase) depending on the intrafollicular compartment
in which they reside.
Melanocytes in the hair bulb retract their melanocyte and shut
down melanogenesis towards the end of anagen.
Simultaneously there is a decline in the activity on three main
melanogenic enzymes :-
Tyrosinase, gp 75 and dopa chrome tautomerase
58. This occurs a few days before the cessation of keratinocyte proliferation resulting
in the pigment free proximal ends of shed telogen hair.
During catagen, hair apoptosis occurs and quiescent hair follicle much smaller size
is left telogen.
Melanogenic activity restarts during early anagen with the reconstruction of the
follicular melanin unit.
Tyrosinase activity becomes apparent during anagen III, pigment transfer from
hairbulb melanocytes to cortical keratinocytes is initiated during anagen IV and
active melanogenesis continues throughout anagen V and VI, ceasing with the
onset of catagen.
Melanocytes are presents in two compartment of the hair follicules in the anagen
hair bulb where they transfer pigment to cells that will form the hair cortex, and in
the outer root sheath
Grey hair follicles lack melanocytes in the hair bulb while retaining those in the
outer root sheath.
Hair bulb melanocytes are probably recruited from the outer root sheath
melanocytes population at the onset of anagen.
59. Migration and activation of these melanocytes is possibly under
unknown local signaling mechanisms like a – melanocyte stimulating
hormone ( - MSH) modulation of failure of which may result in
graying.
The hair bulb matrix is the principle site for the fully differentiated
follicular menalocyte subpopulation, these melanocytes are
distributed, in particular, within the matrix above and around the
upperdermalpapilla.
They transfer their melanin granules to keratinocytes of the hair
cortex and less so to the medulla and very rarely to the hair cuticle.
Under stimulation from radiation or cytokines, the outer root sheath
melanocytes may be stimulated to migrate and differentiate to
naturally repigment graying hair follicles.
61. Histopathology of greying of Hair
A line across the widest part of the bulb of the hair follicle divides it into
two regions.
Two region
I. A lower region of undifferentiated cells.
II. An upper region in which the cells become differentiated to form the
innersheath and the haBelow the critical level known as the line of Auber lie
the matrix or the germination center of the follicle, where every cell is
mitotically active and the dermal papilla.
The pigmentary unit is is a pear-shaped black structure at the tip of the dermal
papilla above the Auber’s line in pigmented hair where individual melanocytes
cannot be distinguished.
Only unpigmented and undifferentiated putative melanocyte stem cells, but not
pigmented differentiated melanocytes, are normally found in the hair bulb
below the line of Auber.
62. In gray hair, the pigmentary unit becomes fuzzy melanocytes are few and
rounded and lightly pigmented oligodendritric melanocytes become
detectable in the proximal hair bulb below Auber’s line.
The resultant pigment loss in graying hair follicle due to a marked reduction
in melanogenically active melanocytes in the hair bulb of grey anagen hair
follicles is central to the pathogenesis of graying.
Defective melanosomal transfer to the cortical keratinocytes or melanin
incontinence due to melanocyte degenation is also believed to contribute to
graying.
There is autophagolysosomal degradation of melanosomes within the
melanocytes itself and is usually followed by the degeneration of the
melanocyte.
Eventually, no melanogenic melanocytes remain in the hair bulb.
True gray hair show reduced DOPA reaction (indicator of tyrosinase activity)
while white hair bulbs are negative for the same.
64. Neurotransmitters
Neurotransmitters is a chemical substance that act as the
mediator for the transmission of nerve impulse from one
neuron to another neuron.
Depending upon their chemical nature.
3 types
1. Amino acids – involved in fast synaptic transmission,
inhibitory and excitatory in action
2. Amine – involved in slow synaptic transmission, inhibitory and
excitatory in action.
66. Adrenal medularry hormones are the amine derived from catechol
and these hormones are called catecholamine.
3 catecholamine are secreted by medulla.
1) Adrenaline or epinephrine
2) Noradrenalin or nor epinephrine
3) Dopamine.
Hormones of Adrenal medulla
74. Thyroid Hormones – leading to premature graying
Both T4 & T3 – iodine containing derivatives of amino acid tyrosine.
Iodine & tyrosine – are essential for the formation of thyroid hormones.
Each thyroglobulin molecules contains 140 mollecules of amino acid tyrosine.
77. Genetics
Mainly 2 genes are responsible for graying hair i.e Bcl2 & Bcl-w.
Stem cells at the base of hair follicles produce melanocytes –
there are the cells that produce and store pigment in hair and
skin, the death of melanocyte stem cells causes the onset of
hair graying.
81. Mode of action of Nasya :
Ayurvedic
According to Acharya Charaka & Vagvatta Nasa is the portal (gateway) of
shiras.
“Nasa Hi shiraso dwaram”
According to Astanga Sangraha the drug administered through nostrils,
reachers shringataka by Nasasrota and spreads in the murdha (Brain) taking
route of Netra (eye), shrotra (ear), kantha (throat), Siramukhas (opening of
the vessels) etc.
Scrapes the morbid doshas in supraclavicular region and extract them from
the uttamanga.
Maharsi Sushruta has explained sringataka marma as a sira marma formed by
the union of siras (blood vessels) supplying to nose, ear, eye and tongue.
82. The pharmacodynamics of Nasyakarmacan be explained in light of
modern anatomical and physiological studies as follows
1.Vascular pathway
The nasal tissue is highly vascularized making it an attractive
site for rapid and efficient systemic absorption. Rich vascular plexus
permits topically administered drugs to rapidly achieve effective
blood levels while avoiding intravenous catheters. Vascular path
transportation is possible through the pooling of nasal venous blood
into the facial vein which occurs naturally. The facial vein has no
valves. It communicates freely with the intracranial
circulation.It communicates through pterygoidplexus with the
cavernous venous sinus
Modern View
83. 2.Neurological pathway
Olfactory nerve is chemoreceptor in nature. It is known that through olfactory
pathway this nerve is connected with limbic system and hypothalamus which
are having control over endocrine secretions.10Moreover, hypothalamus is
considered to be responsible for ntegrating the functions of the endocrine
system and the nervous system. Electrical stimulation of hypothalamus in
animals is capable of inducing secretions in the anterior pituitary. So the drugs
administratedhere stimulate the higher centers ofbrain which shows action on
regulation of endocrine and nervous system functions.
3.Diffusion through nasal mucosa
In the absorption of drug from the nasal cavity first step is passage through the
mucus. Large and charged particles may find it more difficult to cross. But
small and uncharged particles easily pass through this layer. Mechanisms
for absorption of drug through the nasal mucosa include 1. Paracellular
route is the first mechanism which isan aqueous route of transport. This is slow
and passive route. 2. Transcellular process is the second mechanism of
transport through a lipoidal route and is responsible for the transport of
lipophilic drugs that show a rate dependency on their lipophilicity. Drugs
also cross cell membranes by an active transport route via carrier mediated
means or transport through the opening of tight junctions