Dr Khalid 

I am of the opinion that theory of abfraction is more of myth than any reality. I have following arguments in favor of my statement.

1. Most affected teeth with Abfraction are canines and premolars. Buccal surfaces of these teeth are prone to abrasion due to tooth brushes and abrasive dentifrices. The same surfaces are worst affected by Abfraction. I therefore, think the lesion frequently involving these teeth are abrasive lesion rather than abfractive lesions.

2. Abfraction lesions involve buccal surfaces, while the lingual surfaces are found the least affected. Cause of Abfraction is stress concentration in cervical area due to repeated flexing of tooth during occlusal loading. Had it been true, bucaal and lingual surfaces would have been affected equally.

3. Occlusal loading in patients with habit of bruxism is very high. It means all bruxist must clinically show Abfraction lesions but this is not a common finding in bruxists.

4. Skulls of 2-3 hundred years show such lesions while prehistoric skulls dont have such lesions. The probable reason might be the use of abrasive  powders  for teeth cleaning in this era.

Dental abfraction is real! You see it on those teeth with the highest occlusal loads, functional or parafunctional, in patients where the teeth have been in use for 30 years or more. As posterior support is lost, there is more abfraction in bicuspids.

Dental abfractions are caused by flexural forces, usually from cyclic loading. The enamel especially atthe cementoenamel junction, undergos this pattern of destruction by separating enamel rods.This theory of abfraction is disputed by some who think that these type of enamel lesions are due to over-zealous brushing.I think that dental abfraction is real.

Occlusal loading induces concentration of stresses at cervical area for being the center of the tooth. If this would have been the cause for abfraction lesion then why it occurs only on the buccal side of a totth and not on the lingual side.

A lecturer (from Kaiserwald, Germany as far I can recall) showed once a picture series of a tooth. There was a need of flap operation in this area. As the operator raised the buccal flap a clear cervical defect was exposed. This was in an area that was never in touch of tooth brush or abrasive paste. Could it be that sulcus fluid in some cases is able to demineralize dentin slowly especially when loading is unpropitious? - I also tend to think abfraction is real.

Abfraction is a term introduced by JO Grippo in 1991 to describe noncarious cervical lesions of stress origin (multifactorial). It is based on the hypothesis firstly introduced by McCoy in 1983 of cervical enamel loss due to tensile stress. The sites and the morphology of the cervical lesions can help the clinical diagnosis: wedge-shaped defects for abfraction vs cup-shaped lesions for tribo-biocorrosion.

Why it occurs only on the buccal side of a totth and not on the lingual side?.... As reported by Young & Khan in 2002 the architectural form of dental arches mitigates the forces lingually directed and the flexure of teeth, at the same time, permits facially directed forces to flex teeth and result in stress concentration at the cervices of the teeth. Moreover, as stated by Kleinberg in 2006 there is five times more saliva on the lingual surfaces than in the vestibule. ….Abfraction is a real injury in spread in Western countries.

Abfraction is real, but to make a definitive diagnosis and distinguish it from abrasion is difficult in some cases

If it is real and occurs due to occlusal stresses, the patients having bruxism put lot of stresses during clenching of their teeth. As a rule, therefore such patients should have abfraction lesions on their entire dentition. But it is a common observation that they have worn out occlusal surfaces causing reduction in vertical height of the face. Abfraction lesions are not so frequently found in these patients

In my clinical experience abfraction is absolutely real, and I agree with Dr. Alkhatib in the difficulty in distinguish it from erosion!

I cant explaine why occurs the abfraction only the bucall side, if would be true the tension stress teory, that it must occurs both side. For me the abfraction seems to be abrasion.This proved by localisation of abfraction: canine, premolars(cornen teth), sometimes incisors.

I too agree with my colleagues who say that abfraction is a real lesion and not a myth. 

1. There is no way any abrasion or erosion can occur in a subgingival location.

2. As for the reason why buccal surfaces are affected more...In my clinical experience, it is seen more on mandibular premolars than any other. The nature of occlusion of these teeth causes them to flex lingually so the tension is maximum on the buccal cervical area.  The tension-compression theory explains this adequately.

3. As for bruxists, their tooth movement is mostly in a grinding fashion, so more than shear stress directed cervically, the teeth are subjected to occlusal surface wear. So before any actual abfraction could develop, the occlusal table is modified. The flatter the occlusal surface, less chances of shear stresses, less chances of abfraction.

My clinical experience is little different than yours, Dr Priya. I notice maxillary canines and premolars. This is an area worst affected by vigorous brushing or abrasive dentifrices. Does your statement " The nature of occlusion of these teeth causes them to flex lingually so the tension is maximum on the buccal cervical area." hold good for the area I have mentioned??

I have been told that abfraction has been seen in chimps.  I doubt if they use toothbrushes.

This is a good discussion from all. Dr. Price in the early 1900's found abfractions in the isolated tribes of South America...no tooth brushes or even use of sticks were found. Ancient skulls and even pre-industrial skulls tend to not have abfractions - was this due to short longevity or something else? Industrialized nations have a higher incidence of abfractions...yet their diet is softer. Does this mean the toothbrush is the culprit? Studies have found that the tooth structure in an abfraction is lost faster with a harder brush. Is this because when the tooth structure is weakened the hard brush can abrade an otherwise hard surface? 

So, in an industrialized country it seems there are more orthodontic problems from allergies, collapsed arches from mouth breathing/lack of nursing/sleep disorders/etc. Perhaps in an unbalanced dentition the occlusal forces are at pathological vectors of force? If the teeth are only straightened to "appear" cosmetically appropriate the vectors of force may still be pathological. Finding that appropriate physiological position for the teeth and their supporting structures may be the answer? 

There is no hard evidence that abfractions exist, therefore we should use the term NCCL. But......clinically there are some lesions that cannot be explained other than by the abfraction theory. 

Tooth wear is more and more considered to be multifactorial and I think NCCL's have probably also a complex etiology: increased occlusal forces, clenching, the tooth brush, erosive attaque, lack of protection by saliva, it probably all has a possible influence and explains why the etiology of these NCCL's is so hard to explain.

So occlusal forces as an etiological factor in cervical tooth wear probably play a role, but in what extend will differ among patients.

I would agree that it is a multifactorial problem. Occlusion and stress on teeth with "normal" occlusion present "abfractions" on buccal surfaces. Malocclusion (cross bite) should create abfractions on the lingual surfaces? Or should be called plain wear, erosion or lesions from wrong tooth brushing 

Dr Luis is very right. In teeth with normal occlusion, abfracton is produced on buccal surfaces. Teeth in malocclusion should have abfraction lesions on lingual surfaces. But such finding is not common.

Interestingly, I just finished restoring a case with a cervical tooth structure loss on tooth 44 (right mandibular first premolar). The lesion had a much rougher surface than one expects from constant surface wear ( as for abrasion). No other teeth were involved. The said tooth is in normal alignment within the arch. No contributory factors in the history either.. So in such cases, probably we should consider the abfraction theory to be in operation.

In reply to Dr. Asaad about maxillary canines and premolars, I would say abrasion is more likely to be the reason for tooth structure loss, than abfraction.

However, as Dr. Opdam suggested, NCCL would be a more clinically useful term, and we need to consider all contributing factors in the etiology, i.e. tooth-brushing, occlusion, diet and so forth.

Dr Priya

Here I don't agree with you. Romeed et al (2012) has shown in study the about the concentration at cervical area in canine teeth and their role in development of abfraction lesions. Therfore, Not necessarily, all canine cervical lesions are abrasive lesions.

The tooth brush even with the greatest abrasive "toothpaste"...sensodyne is not an answer for the wear caused at the cervical of predominately the bicuspids and cuspids but will also include the 1st molars and to a lesser extent the 2nd molars.  There is an occlusal component to all these lesions and then an abrasive wear component of the fractured surfaces.  You could only blame this type of cervical erosion to a decreased salivary content or chemical wear in terms of eating disorders but these sadly have a much broader erosive problem covering the lingual and not the buccal surfaces.  Looking then at the fracture under load and then the wearing away of fractured surface with dental abrasives would explain the progressing "v" shaped surface and the smooth surface of the underlying dentine.  The phenomenon involves the fracturing under tension due to the extraoral movement of the jaw in excessive lateral movements or excursions...:ie bruxism and clenching...and the DEJ which then provides for the interface of a very thinning enamel material that is subject to fracture under load and a softer less mineralized yet brittle surface of the underlying dentin/cemental material.  These mismatched materials when put into tension loads will cause a vertical fracture which will be in a series of fractures spanning the cervical margin and along the cervical margin, along the thinner buccal bone compared to the thicker lingual/palatal bone, ergo the "abfraction lesions" normally occur on the buccal surfaces and disappear as the bone thickens proximally and lingually or palatally.  As the fractures progress vertically and then horizontally because of a property of brittle materials known as crack propagation, the enamel dentin complex then can be separated from the underlying tooth material by abrasion either with a tooth brush or with an abrasive diet noting the food flow patterns in lateral movements.  These will generally follow the direction of the dentinal tubules in this area.  Additionally, you find these normally associated with "idiopathic boney exostosis" called tori which generally if formed will be located lingual to the teeth in question namely from lingual of first molars to the lingual of the 1st bicuspids, normally bilaterally in the mandible opposite the area of the mental foramen where the mandible first flexes in an occlusal manner and then twists under load increasing the torsional loading of the DEJ interface.  The maxillary tori are normally found the the ares of loading thinnest in the bone, the buccal plate opposite the bicuspids and the midpalatal suture line, both indicative to torsional forces developed in extraoral lateral excursions.  This is an interface problem in materials and a prime reason that cervical restorations will likely fail in these areas because of the mismatch of properties of the restorative materials to the underling dental structures and the torsional forces both twisting and tensile/compressive during the extraoral lateral excursions.  As for the cuspids there is an easy explaination that cuspids will either have early or later abfractions depending on if there is a greater likely hood of cuspid rise (earlier formation) or group function (later formation as the cuspids become more involved as wear of bicuspids increase the likely hood of cuspid interferences) as this is still an excursive problem outside of normal lateral function.  Additionally there can be a more predominately active side of abfraction development if there is an occlusal discrepancy of asymmetry. 

Dear colleagues thank you very much for the participation and answers to my question regarding the existing of dental abfraction. From my clinical experience I do agree with all of you. The important factor is to diagnose abfraction from abrasion so we focus on the causative factors to eliminate them. In the literature I found abfraction specifically characterized by sharp internal and external line angles (Owens and Gallien, 1995; Bernhardt et al., 2006). Can we use an inlay wax to confirm this? Which types of occlusal abnormalities are associated with abfraction?!