A non-carious cervical lesion (NCCL), is defined as the loss of tooth structure at the cementoenamel junction (CEJ) under pathological conditions. These lesions are often called “abfractions,” but this term is a misnomer and I'll soon explain why. These lesions most frequently occur on the facial surfaces of teeth, but it's not entirely impossible to spot them on the lingual or interproximal surface. Epidemiology studies report this phenomenon most frequently occurs in premolars (1, 2). Patients will typically report hypersensitivity because of enamel rod corrosion and dentin tubule exposure.
It's important to note that the loss of tooth structure associated with NCCLs is not attributed to caries (hence non-carious cervical lesion). There is oftentimes speculation of the cause of NCCLs. Current advances from the last decade have helped to shed light on the etiology of NCCLs as well as provide management strategies. I would also like to propose that we, as a community, refrain from using the term “abfraction” to exclusively describe 'non-carious cervical lesions.Abfraction is one of the mechanisms that may cause an NCCL, but the lesion may occur from other forces.
How Abfraction theory ignores the Bigger Picture
Today there is extensive evidence that the cause of NCCLs is multifactorial and not necessarily caused by a single variable. NCCLS may be caused by the synergist action of erosion, friction (abrasion), and possibly occlusal stress (abfraction). Below I will delve into those different factors and define what they are.
While dietary acid is a source of erosion, it is certainly not the only one. Intrinsic acids (gastric acid) are a common source of erosion. Patients should be screened for a history of GERD, bulimia nervosa and hiatal hernias. Interestingly, proteolytic enzymes, which are known to degrade the dentinal organic matrix, can be released into the oral cavity during vomiting (3). These enzymes arise from the stomach and pancreas. They can also be found in gingival crevicular fluid (4).
Gingival recession can make teeth particularly vulnerable to the damaging effects of acid exposure. What's more, impaired salivary flow or poor-quality saliva may impair the body's natural ability to buffer and counteract the effects of acid. Calcium and phosphate ions in the saliva facilitate remineralization after an acid attack, but the absence of such ions prevent the saliva from playing a protective role. Variables that may predispose a patient to poor salivary flow are a history of head and neck radiation, salivary gland resection and the chronic use of SSRIs, antihistamines, stimulants, anti-hypertensives and other medications (5, 6).
Patients with poor salivary flow may be instructed by their physician or primary care provider to use sugar containing sialogogues such as lemon drops or hard candy, but this is precisely the opposite of what these patients should be using.
Chewing gums or sugar free candy containing xylitol may be the best remedy because xylitol has long since been known to play a role in combatting caries. And while 5 grams of xylitol is needed to achieve the ideal therapeutic effect, a quantity which will most likely cause GI distress before it prevents caries, this low-sugar alcohol will at least not promote caries in xerostomic patients in low doses (7, 8, 9).
Abrasion (or friction) occurs when teeth are introduced to a foreign object that introduces a destructive mechanical force. The greatest offenders are the application of excessive force when brushing teeth, abrasive toothpaste and a horizontal brushing technique. Individuals with a thin tissue phenotype (formerly called biotype) are particularly susceptible to recession, which will more easily give way to abrasion (11). Other risk factors include the frequency and duration of the applied force. Clinical and lab data contends that there is little evidence that NCCLs are solely caused by abrasion (10).
The traditional abfraction theory postulates that upon occlusal loading, the cervical area of the tooth becomes a fulcrum. This action leads to tensile stress which leads to disruption of the enamel's brittle crystalline structure. Repeated loading eventually causes enamel to break away from the margin (12).
While this theory is logical, it is controversial among dentists and researchers. Several finite element analysis (FEA) studies and clinical trials have supported this theory, while systematic reviews have not demonstrated a clear association (13-19). Some clinicians treatment plan patients for occlusal adjustments and full-mouth equilibration as a way to manage NCCLS. However, considering the controversial nature of the evidence, more information may be needed to support this irreversible treatment strategy. To date, the literature is lacking a high-quality prospective clinical study which may elucidate controversy surrounding the etiology of abfraction lesions.
In effect, NCCLs are often caused by the interplay between the aforementioned variables. Clinicians should do their best to educate patients on causes of these lesions to prevent their initiation.
Dr. Melissa N.R. Seibert is the creator and host of the dental podcast, Dental Digest. She is a board member for the Academy of Biomimetic Dentistry and Industry Thought Leader for Crest and Oral-B.
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