Association of Noncarious Cervical Lesions, Gingival Recession And Cervical Dentin Hypersensitivity: A Narrative Review

Introduction

The prevalence of noncarious cervical lesions (NCCL) and gingival recession (GR) increases significantly with age.^1,2 The worldwide prevalence of NCCL is about 46.7%.1 Several endogenous and exogenous factors subject the tooth to pathodynamic mechanisms like friction, corrosion, and stress that are manifested as abrasion, biocorrosion, and abfraction respectively.³ They do not present with equal distribution within a given individual⁴ and usually occur at the cervical third of the tooth.⁵ Whereas, GR is a soft tissue condition involving the periodontal attachment apparatus exposing the root surface.⁶ It is caused by various anatomical, pathological, iatrogenic, oral hygiene, and behavioral factors.^6,7

Cervical dentin hypersensitivity (CDH) appears to be a pathognomonic sign of NCCL and GR and is localized to the cervical region of the tooth.⁸ The prevalence of CDH due to NCCL has been found to vary from 2% to 98%.8 Over 70% of the population with periodontal disease have experienced dentin hypersensitivity.⁹

NCCL and GR are often closely related in terms of etiologic and therapeutic aspects.¹⁰ Their combination is frequently manifested on the buccal aspect of the tooth, suggesting an etiological link between them.^8,10 GR exposing the root can further make the surface susceptible to NCCL.⁶ When NCCL and GR are not managed at the initial stage, their progression will lead to CDH. Previous literature is not clear about the definite role of NCCL and GR, in CDH and the explanation of why CDH is identified only in a few cases of NCCL and GR. Hence, the purpose of this review is to discuss NCCL, GR and CDH from an etiological perspective, the link between NCCL and GR, and their roles in the development and prevention of CDH.

Search strategy

Evidence for this narrative review was obtained by conducting a literature search in PubMed and Google Scholar. The search strategies in PubMed and Google Scholar included the following terms: (cervical dentin hypersensitivity) OR (dentinal hypersensitivity) OR (dentin sensitivity) OR (dentin hypersensitivity) OR (tooth hypersensitivity) AND (non-carious cervical lesions) OR (cervical tooth wear) OR (tooth abrasion) OR (dental abrasion) OR (tooth erosion) OR (dental erosion) OR (tooth abfraction) OR (dental abfractions) AND (gingival recession). The search was restricted to the English language, with no restrictions on time, study design, region, and publication type. About 1207 publications were identified though database search. Sixty-five publications were selected after screening for title and abstract, manual search for books, and back references. The most relevant thirty publications were used in this review.

Non-carious cervical lesions

Non-carious loss of hard tooth substance at the cervical region of the tooth is broadly termed non-carious cervical lesion.¹¹ Topographically, NCCL may involve only the tooth crown or the root surface, or both the crown and exposed root.¹² It is a regressive lesions⁵ with a multifactorial etiology, suggesting the complex interaction of three main mechanisms-friction, corrosion, and stress.³ Based on the mechanism involved, NCCL can be abrasion, erosion (biocorrosion), and abfraction. When these mechanisms overlap, combined lesions occur.⁵

Abrasion

Abrasion is derived from the Latin verbs abradere, abrasi, and abrasum meaning to scrape off.¹³ The abnormal wear of the tooth substances by an external mechanical process results in tooth abrasion. The enamel is the hardest calcified tissue followed by dentin and cementum. Hence, the effect of abrasion is greatest on the cementum.¹⁴ The rate of abrasion for cementum is 35 times higher than enamel while 25 times higher for dentin.¹⁵ Use of abrasive dentifrice, vigorous brushing technique, hard bristle, toothbrush, miswaks, toothpicks, and consumption of abrasive food are the common factors responsible for cervical tooth abrasion.^12,16 Other activities such as pipe smoking, pen, pin, and bag pipe chewing and professional activities such as playing wind instruments also result in tooth abrasion.¹⁷ Dentifrices in combination with toothbrushes with 0.20-mm filament diameter induce enamel losses greater than 0.15 to 0.25 mm.⁸ While the use of a soft bristle brush produces 0.5μm of dentinal wear per month and negligible wear upon enamel.⁸

Erosion (Biocorrosion)

Erosion is the progressive loss of hard tooth substance caused by the action of acids unrelated to bacterial action.¹¹ The definition of “erosion” fails to explain the proteolysis and piezoelectric effects that are also involved in the degradation of tooth substances. Hence, erosion is replaced by a more precise term ‘Biocorrosion’ which explains the chemical, biochemical, or electrochemical degradation of the tooth substance.³

The chemical factors causing biocorrosion are either intrinsic or extrinsic (endogenous or exogenous acids).³ The intrinsic chemical sources are from gastric juices which reach the oral cavity during the following conditions: alimentary tract disorders (duodenal or peptic ulcers, chronic gastritis, intestinal obstruction, oesophagitis, hiatus hernia, increased gastric pressure, neuromuscular diseases), neurologic disorders (migraine, diabetic polyneuropathy), metabolic and endocrine disorders (adrenal insufficiency, hyperthyroidism), psychosomatic disorders (nervous vomiting, anorexia nervosa, bulimia, habitual regurgitation, rumination¹⁶) and pregnancy.¹⁵

The extrinsic sources of chemicals includes occupational exposure - wine tasters, swimmers (constantly in contact with treated pool water), professional athletes (major consumers of energy and sports drinks), and factory workers (manufacturing acidic products);⁸ low pH medications (iron tonics, aspirin, hydrochloric acid replacements, vitamin C, mouthwashes)¹⁵; acidic food (fresh fruits, pickled food, vinegar, vinaigrette, sauces, crisps, flavored acid-based chewing gums) and beverages (fruit juices, carbonated drinks, energy drinks, alcoholic drinks, sugar-sweetened beverages).¹⁶

The biochemical factors causing biocorrosion are proteolytic enzymes such as proteases (pepsin and trypsin), acidogenic bacteria, and gingival crevicular fluid. Electrochemical factors such as the piezoelectric properties of dentin also cause biocorrosion.³

Abfraction (stress corrosion)

Abfraction, is also called stress corrosion¹⁸ refers to the pathologic loss of hard tooth substance in areas of stress concentration caused by eccentric occlusal loading forces.⁸ The term abfraction is derived from the Latin verb frangere, fregi, fractum meaning ‘to break away’¹³ represents the microfracture of the tooth substance in areas of stress concentration.³ The thin cervical enamel and low packing density of the Hunter- Schreger band predispose the tooth to abfraction lesions.¹⁹ The dental crown morphology and geometry may also influence the occlusal stress pattern of the teeth.⁸ The excessive occlusal load was proposed to cause abfraction, which was supported by the evidence from finite elemental analysis.²⁰ It has been suggested that when a tooth is hyperoccluded, the masticatory forces are transmitted to the teeth, which in turn transfers this energy to the cervical region.

McCoy proposed that bruxism could be the primary cause of abfraction, and that tooth flexure from tensile stresses leads to cervical tooth breakdown. Later, Lee and Eakle hypothesized that the primary etiological factor in cervical lesions was the impact of tensile stress from mastication and malocclusion.²¹ Several population-based studies and clinical trials have reported the association of abfractions with bruxism, occlusal factors, occlusal wear, facets, group function, and premature contact. This evidence did not confirm a causal relationship or progression of the lesion. Hence, the concept of abfraction is theoretical and not supported by clinical evidences.²⁰

Gingival recession

Gingival recession is a periodontal condition characterized by the migration of the marginal gingiva apical to the CEJ exposing the root surface.6 Identified on labial, lingual, and/or interproximal tooth surfaces.²² It is associated with healthy and diseased periodontium in individuals maintaining either good or poor oral hygiene standards.¹⁴

The possible causative factors for GR are: Anatomical factors such as thin alveolar cortex, dehiscence, fenestration, and high frenal attachment; pathological factors like periodontitis, trauma, and self-inflicted injury; iatrogenic factors such as periodontal, orthodontic and prosthodontics therapies; and other factors include traumatic tooth brushing, oral piercings, and tobacco use.^6,7,14

Cervical dentin hypersensitivity

Cervical dentin hypersensitivity is a relatively common clinical condition that poses a challenge to clinicians.²³ It is characterized by a short, sharp pain arising from exposed dentin in response to a thermal, evaporative, tactile, osmotic, or chemical stimuli that cannot be attributed to any other form of dental defect or pathology.²⁴ This condition remarkably impairs the oral health-related quality of life of dental patients.²⁵

Although several theories have attempted to explain the mechanism of dentinal hypersensitivity, the most accepted is the ‘Hydrodynamic theory’ proposed by Gysi.¹⁴ According to this theory, when the exposed dentin is subjected to thermal, tactile, osmotic, chemical, or evaporative stimuli, there is fluid movement within the dentinal tubules which triggers the pulpal nerve.²⁴ The A-β and the A-δ fibres located near the pulp-dentin junction respond to the fluid changes within the dentinal tubules, which is manifested as dentinal hypersensitivity.¹⁴

Several potential etiological factors predispose patients to CDH. Loss of tooth enamel, cementum, or both is a prerequisite for cervical dentin exposure.⁷ Enamel loss can be attributed mainly to NCCL (abrasion, erosion, abfraction, or their combination) while loss of cementum to GR and NCCL.⁷ It usually develops in two phases. ‘Lesion localization’ through the exposure of dentin induced by GR and NCCL¹⁴ and ‘lesion initiation’ with the opening of dentinal tubules with progression of NCCL, plaque and vital bleaching.¹⁴ Deeper lesions expose a larger number of dentinal tubules when compared to superficial. Newly exposed dentin exhibits greater hypersensitivity and is often observed in young adults. While in older individuals dentinal hypersensitivity is unusual due to reactionary and reparative dentin deposition.¹⁴

Cervical dentin hypersensitivity arising from noncarious cervical lesions

Combined lesions, which include the combination of abrasion with biocorrosion, is a strong factor in causing cervical dentin hypersensitivity.¹⁴ Abrasion of dentin by mechanical agents causes removal of the smear layer, dentinal tubules remain patent and result in dentinal hypersensitivity.¹⁴ While brushing with occluded toothpaste reduces dentinal hypersensitivity due to deposition of toothpaste ingredients occluding the tubules.¹⁴ Hence, abrasion when compared to other NCCL is usually less sensitive and is only revealed during a clinical examination.^14,16 When these lesions are exposed to an erosive environment, there is opening of dentinal tubules exacerbating dentinal hypersensitivity.¹⁴

Biocorrosion begins by softening the tooth surface, and when the thickness of the softened layer reaches 0.02 to 3 μm, then the dissolution of the hydroxyapatite crystals begins.¹⁶ The process of biocorrosion removes the smear layer and exposes the dentinal tubules resulting in dentinal hypersensitivity.²⁶ When biocorrosion develops slowly, dentinal hypersensitivity is minimal or nearly asymptomatic, while it becomes hypersensitive when it is active.¹⁶ Abfraction is a chronic lesion, with time the exposed dentin gets blocked due to dentinal sclerosis. Hence, cervical dentin hypersensitivity is manifested during the early stages of the lesion and is temporary.¹⁹

Cervical dentin hypersensitivity arising from gingival recession

In gingival recession, the exposed cementum is removed by various mechanical and chemical factors resulting in dentinal hypersensitivity.²⁴ In approximately 10% of teeth, there is no contact between enamel and cementum at the CEJ. Hence, GR will directly expose the dentin.⁸ Overzealous toothbrushing creates gingival scratches/ trauma leading to GR and consequently dentinal hypersensitivity.¹⁴ CDH following a periodontal procedure depends on the duration and the type of procedure involved.²⁷ The role of plaque-induced periodontal disease and periodontal therapy²⁷ in causing CDH is still controversial.^14,24

Role of noncarious cervical lesions and gingival recession in cervical dentin hypersensitivity

Non-carious cervical lesions and gingival recession manifest either alone or in combination. Epidemiological evidence suggests approximately 50% of GRs are associated with NCCL.²⁸ Traumatic toothbrushing, biofilm acidity, and occlusal disturbance were reported as predisposing factors for both NCCL and GR and their progression to CDH (Figure 1).⁶ GR accounts for greater chances of CDH when compared to NCCL.²⁴ Incorrect brushing technique²⁹ and frequent forceful brushing using hard bristle toothbrush³⁰ can result in NCCL and GR, while the gingiva seems to be relatively healthy and the root surface appears to be clean, smooth, and polished.^29,30

Incorrect brushing abrades the CEJ causing loss of cementum, periodontal attachment, and alveolar bone.³⁰ In cases where the cervical wear is wedge-shaped and deep, plaque control is difficult, resulting in gingival inflammation.³⁰ This set off the destructive cycle in the periodontium.³⁰

The biofilm acidity, which triggers GR, acts as an endogenous biocorrosive factor contributing to NCCL progression.³ The association of traumatic GR combined with the exposure of cementum and dentin to chemical activity, may develop an abrasive erosive lesion.¹⁰

Occlusal disturbance can be attributed to both GR and NCCL. It has the potential to increase gingival inflammation and cause GR because of enhanced osteoclastic activity and collagen matrix destruction. Similarly, it can produce NCCL as a result of breakage of the bond between hydroxyapatite crystals, microfracture, chipping, and loss of tooth structure.⁶

Prevention and management of cervical dentine hypersensitivity

Modification of lifestyle and behavioral factors at an early age will prevent the occurrence of NCCL and GR. This can be harnessed through oral health education programs targeting children and young adults. Therefore, they must be encouraged to adopt a healthy lifestyle and behavior. Enlightening the population on the role of various causative factors can bring about change in their unhealthy lifestyles and behaviours. Coordination of the oral health sector with other sectors of society is essential for enhancing the oral and general health of the population.

In the earlier stage of NCCL and GR, the clinician must primarily focus on identifying the etiological factors through a comprehensive patient interview, complete oral examination, and investigations to yield additional information.⁸ Essential steps must be taken to eliminate, reduce, or modify the causative and predisposing factors. This will include dietary advice, oral hygiene instructions, habit cessation, counselling, and correction of occlusal imbalance.²⁴

Local measures to prevent the progression of the initial lesion of the NCCL include topical fluoride applications¹⁵, use of remineralization agents¹⁵, and laser treatment16. Regular application of topical fluoride agents such as gels (sodium fluoride and acidulated phosphate fluoride) or varnishes will form a protective layer on the teeth.¹⁵ But the protective layer is not acid resistant, hence it can be used as an alternative remineralizing agent can be used.¹⁵ Some of the remineralizing agents that can be used are titanium tetrafluoride¹⁵, casein¹⁵, APF gels containing nano-hydroxyapatite¹⁶, casein-phosphopeptide amorphous calcium phosphate nanocomplexes (CPP-ACP)¹⁶ and bioglass¹⁶.

Once the lesions progress and CDH develop, the treatment modalities available for their management include chemical therapy, laser therapy, and a combined protocol. Chemical therapy includes the use of neural, tubule-occluding, and mixed agents. Neural agents (potassium nitrate and potassium oxalate) act on nerve impulse transmission by preventing repolarization. Tubule-occluding agents (oxalate, strontium salts, glutaraldehyde, varnishes, fluoride products, sealants, CPP-ACP, bioglass, and arginine containing toothpaste) act by blocking dentinal tubules. Mixed agents (potassium oxalate, potassium nitrate, and NaF) act by preventing impulse transmission and occluding dentinal tubules. Low-power lasers reduce CDH by blocking the transmission of painful stimuli, while high power lasers obliterate dentinal tubules by melting and resolidification of the dentin surface. High-power lasers should be used with caution because they can damage the pulp tissue. The combined protocol for managing CDH will include the combination of chemical and laser therapy.⁸ In cases where NCCL is associated with GR, a combination of restorative and periodontal surgical procedures is essential for the effective management of CDH.⁸

Conclusion

The identification of potential etiological factors is the primary requisite for prevention and treatment. NCCL, GR, and CDH have similar multifactorial etiologies. Most of these factors such as lifestyle and behavioral factors are modifiable. Early identification and control of potential etiological factors will essentially prevent and halt the progression of these lesions, which enhance the oral health and the quality of life of individuals.

Conflict of interest

None