Thanks. I partially agree but the true facts appear more complicated. Sometimes anal fissure may occur without passing hard stool also and dietary factors are mostly related indirectly to stool consistency.

The main cause of recurrence of fissure in ano is increased tone of internal anal sphincter. Dilatation can help in reducing chances of recurrence.

Thanks. But why should the tone of IAS increase intermittently in some but not in others or why should this increase cause anal fissure in some but not in others. Does it run in family i.e. is there a genetic predisposition for it? Dilatation can definitely help in cure but I am doubtful about the feasibility of long term dilatation (to reduce chances of recurrence) as this can damage the IAS and cause fecal incontinence.

There is no familial association. As we all know, there are high and low pressure fissures; the latter found in mainly multiparous women. The most accepted theory of formation is localised hypoxia; hence the positioning of primary fissures at the 12 and 6 o'clock positions; the transition zones of vascularity.

Since the advent of the specialty of ano rectal physiology, none of us can advocate any form of physical dilatation anymore! I would never perform an LAS in a woman, and the last time I performed one in a male was over 15 years ago! There are enough alternative pharmacological agents available!

The complete defaecatory habit is important: hard and loose stools, tense us, excessive wiping, straining, etc. Changing such habits are not easy, especially if not asked about. Of course, from the first presentation, rule out secondary causes, especially when fissures are in different locations and the first presentation is above 50. Do not forget dermatoses.

Thanks Dr. Kamal, I agree especially your opinion on dilatation. I have found close association of haemorrhoids and fissures and a hereditary predisposition e.g. A person having haemorrhoids has two kids where one each develop problems of  haemorrhoids and anal fissure from very young age. Since haemorrhoids are a common occurrence, it is difficult to be certain whether it is truly familial. But the mechanisms may be partially similar

It is important to be clear on terminology. The simple presence of a condition in family members does not make a condition hereditary or even familial. Haemorrhoids do not have a hereditary component; dietary factors, however, are similar in families.

The problem is not only hard stool, but stool small in volume. That is why bulking agents such as psyllium add in stool volume nad thus make let's say physiologic dilation of anal sphincter. Therefore it is not the number of stools that is important but the stool volume. It helps in both hemorrhoids and anal fisure. The prove is that nitroglicerine and other pharmacologica dilators help not only for anal fissure but for hemorroids.

Thanks. I agree Dr.Goran and Dr. Heer. There has however not been any study to document scientifically the absence of genetic link. In fact not enough insight  has been achieved into the mechanism of piles which is the reason why there is absence of curative therapy apart from surgery even after which piles recur. Don't you believe that development of piles (dilatation of veins) has something to do with rectal pressure changes? Genetic link may lie in the neuromuscular development and hence the neurophysiology of the anorectal region involved in defecation. Are you aware of any rectal motility studies in piles which might throw light on the condition?

The absence of a very complex and vast negative study is no reason to believe there is a genetic disposition. Further, I disagree that surgery is the curative therapy - nowadays, it is exceedingly rare that formal haemorrhoidectomy is indicated; specially as a first line intervention. I would suggest a more detailed assessment of defaecatory habits and physiological contributory factors in patients. Though there is often a combination of pathologies, it is unclear why you are 

My intention of stating surgery as "curative" [i.e. complete ablation of a lesion] was only to stress the fact that there are other definite but unknown factors in pathogenesis since it recurs commonly after removal.

Haemorrhoids are engorged arteriolar-venous sinusoids. If the predisposing and causative factors remains, it is not unusual that further such channels open up. Again, I'm afraid, nothing here is pointing towards a genetic predisposition.

I reiterate that it is a belief without scientific proof. Like other vascular engorgements (telagiectasias, malformations etc) have genetic determinants, this is a possibility in case of haemorrhoids also. We tend to study genetics of uncommon disease but not common ones for whom the relationship may be complex.

Recently an early insight into pathogenesis of anal fissure by an incisive study on the mechanisms of tone control of internal anal sphincter [IAS] has been published where ICCs are found even within IAS along with involvement of its muscle related electroionic potentials and all can have individual differences based on individual genetics. [Control of Motility in the Internal Anal Sphincter. K D Keef and CA Cobine. J Neurogastroenterol Motil. 2019 April; 25(2): 189-204.