VITAMIN B COMLEX
➢ Thiamine (vitamin B1) : it is available in a variety of diet such as peas ,
beans , pulses , yeast , green vegetables roots , fruits , meats , rice and
wheat brain. A few substances in the diet (strong tea , coffee) act as
anti-thiamines.
The main physiologic function of thiamine is carbohydrate metabolism in
addition , thiamine plays a role in peripheral nerve conduction by an unknown
mechanism.
Lesions in thiamine deficiency :- thiamine deficiency can occur in chronic
alcoholism being an important cause. The deficiency state leads to failure of
complete combustion of carbohydrate and accumulation of pyruvic acid. This
results in BERIBERI which produces lesions at 3 target tissues ( peripheral
nerves , heart and brain) . Accordingly BERIBERI is 3 types
● Dry beriberi (peripheral neuritis)
● Wet beriberi (cardiac manifestations)
● Cerebral berberi (wernicke-korsakoff’s syndrome)
1. Dry beriberi(peripheral neuritis) :- this is marked by neuromuscular
symptoms such as weakness , paresthesia and sensory loss. The nerves
show myelin degeneration and fragmentation of axons
2. Wet beriberi (cardiac manifestations):- Characterized by generalised
oedema & the heart in beriberi is flabby (due to thin and weak
myocardium), enlarged and globular in appearance due to 4-chamber
dilatation
3. Cerebral beriberi (Wernicke-Korsakoff’s syndrome) :- It consists of
the following features:
i) Wernicke’s encephalopathy occurs more often due to chronic
alcoholism. It is characterised by degeneration of ganglia cells & focal
demyelination.
ii) Korsakoff’s psychosis results from persistence of psychotic features
following brain haemorrhage in Wernicke’s encephalopathy
, ➢Riboflavin (Vitamin B2):- known as “cytochrome oxidase enzyme”
which is important in view of its role as cellular respiratory coenzyme.
The vitamin is usually distributed in plant and animal foods such as liver,
meat, eggs, milk and green vegetables.
DEFICIENCY:- Leads to ocular lesions , cheilosis, glossitis, and scaly skin
dermatitis
Oral manifestations of B1 and B2 deficiency
● Recurrent aphthous ulcers presents painful ulcers on the non-keratinized
oral mucosa, affecting speech and eating
● Angular cheilitis presents as redness and inflammation , particularly at
the corners of the mouth
● glossitis , characterized by inflammation and changes in the tongue’s
appearance and texture
● Impair postnatal amelogenesis, resulting in enamel hypomineralization
➢Niacin (B3) (Nicotinic acid):- widely distributed in plants, liver , kidney
, meat and cereals.
Physiologically…………niacin includes biologically active derivative called
nicotinamide, which is essential for the formation of NAD (Metabolism of fat
,carbohydrate and protein) & NADP (metabolism of glucose in HMP pathway)
Deficiency ……… causes roughness of skin known as pellagra, characterised
by 3D’s dermatitis , diarrhea and dementia (degeneration of neurons).
Without correction of niacin deficiency , the disease may evolve and presist
over a period of years eventually leading to death
Oral manifestations
● Stomatitis
● Glossitis with tongue appearing red, smooth and raw + enlarged
● Atrophy of papillae , papillae on tongue can disappear causing smooth
and bald appearance also described as “beet red” or “magenta” tongue
● Burning sensation in oral cavity