Cajal cells and Megaesophagus

[Guest guest]

im sure , loss of both nitrergic and vipergic neurons in achalasia is known by

all members of this group. This injury is sufficient to increase lower

esophageal sphincter pressure that hards to transit foods from esophagus to

stomach. But this injury is not last ultrastructural degeneration of esophagus.

We must know some information about Interstitial cells of Cajal (ICC) shortly

cajal cells.ICCserve as electrical pacemakers,

provide pathways for the active propagation of slow waves, are mediators of

enteric motor neurotransmission and play a role in afferent neural signalling.

Morphological studies have

provided evidence that motor neurotransmission in the GI tract does not occur

through poorly defined structures between nerves and smooth muscle, but rather

via specialized synapses that

exist between enteric nerve terminals and intramuscular ICC or ICC-IM. ICC-IM

are coupled to smooth muscle cells via gap junctions and post-junctional

responses elicited in ICC-IM are conducted to neighbouring smoothmuscle cells.

Cajal cells are capable to keep and continue peristaltic movements of esophagus

to transit bolus even in the abence of vagal stimulation or nitrergic

signalling. They have special properties that make them unique in their ability

to generate and propagate slow waves in gastrointestinal muscles. The electrical

slow wave activity determines the characteristic frequency of phasic

contractions of the stomach, intestine and colon. Slow waves also

determine the direction and velocity of propagation of peristaltic activity, in

concert with the enteric nervous system. Cajal cells stays between esophagus

muscles and nitrergic neurons. At early stages in achalasida due to loss of

nitergic neurons cajal cells stays without having any input signal to modulate

and control related muscles.But still cajal cells are capable to form

peristaltic movements. Some suties showed at early stages of acahalasida density

of cajal cells increased via mast cell migration.

http://farncombe.mcmaster.ca/documents/Zarateetal.NeurogastroenterolMotil2006187\

556-68.pdf

Due to mast cells are important part of immune system the role of them is

surviving cajal cells to balance loss of nitrergic neurons. At this stage mast

cells release stem cell factors (SCF) and il-9. Activated Mast cells could

provide a source ofSCF and IL-9 for ICC-IM (intramuscular) in achalasia

promoting theviability of ICC. So our immune system fights with the fate of

cajal cells.Now nobody knows the fate of cajals cells but we know our immune

system afford to resolve this situation via mast cell accumulation. although

this mast cell activation is not sufficient to stop fate of cajal cells but

delays. This relation gives some evidences about achalasia is not directly

related with an immune system disturbances.

Generally loss of cajal cells often occurs in chagasic achalasia. This results

as a megaesophagus and probably requires need for esophago ectomy operation.

http://www.ncbi.nlm.nih.gov/pubmed/18620994

in primary achalasia Loss of neuronal nitric oxide synthase (nNOS)

immunoreactivity was completed within 3 years of acquiring

achalasia. Thereafter, progressive ultrastructural injury

to remaining nerve structures was evident. Within

the first 2 years, the number of ICC-IM did not decline

although ultrastructural injury was already present.In

conclusion, injury to ICC-IM in achalasia is variable,

but not related to duration of disease and injury to

nitrergic nerves. MC are prominent and form close

functional contact with ICC-IM which may be

responsible for their relatively long survival.

i think loss of cajal cells is more important than loss of cajal cells. in the

absence of cajal cells muscular fibrosis is triggering and peristaltic movements

diasappears. it is shows that not only intraluminal pressure of esophagus or

longtime stasis of foods results as megaesophagus.

interstitial cells of Cajal in chagasic megaesophagus.

http://www.ncbi.nlm.nih.gov/pubmed/18620994

An immunohistochemical study of the myenteric plexus in idiopathic achalasia.

http://www.ncbi.nlm.nih.gov/pubmed/19834336

i think before total loss of cajal cells there is some supportive medical

choices to modulate mast cell activation to save cajal cells.

According to these studies an unknown allergen antigen induced neurotoxic model

is more reliable reason for achalasia. As notan said i claim antigen induced

eosinophilic cationic protein that has capable to kill myenteric neurons. We get

this antigen from foods or drinks still according to me one component from

chlorinated water may be a contributor. The most common food or drink all of us

takes a lot ,in the world is chlorinated water this is true:)

Banu