# The Nallan–Nickel Effect: A Mechanistic Perspective on Burning Sensations and Lichenoid Reactions in Long-Serving Porcelain-Fused-to-Metal Restorations

**Authors:** Nallan C. S. K. Chaitanya, Nada Tawfig Hashim, Vivek Padmanabhan, Md Sofiqul Islam, Rasha Babiker, Riham Mohammed, Muhammed Mustahsen Rahman

PMC · DOI: 10.3390/dj13110507 · 2025-11-03

## TL;DR

This paper proposes a new theory explaining why some long-lasting dental crowns cause burning sensations and lichenoid reactions in the mouth.

## Contribution

The Nallan–Nickel Effect is introduced as a novel theoretical model linking nickel ion release from dental crowns to neuro-immune reactions.

## Key findings

- Nickel ions from corroded crowns may trigger inflammation and burning through immune and nerve pathways.
- Factors like low saliva and acidic pH can lower the threshold for these reactions.
- Replacing nickel-containing crowns may alleviate symptoms by restoring tolerance.

## Abstract

Porcelain-fused-to-metal (PFM) crowns continue to serve as a cornerstone of restorative dentistry owing to their strength, affordability, and esthetics. However, late-onset complications such as oral burning and lichenoid reactions have been observed in long-serving PFMs, suggesting complex host–material interactions that extend beyond simple mechanical wear. This Perspective introduces the Nallan–Nickel Effect, a theoretical model proposing that a host- and environment-dependent threshold of bioavailable nickel ions (Ni2+), once exceeded, may trigger a neuro-immune cascade culminating in a burning phenotype. Within this framework, slow corrosion at exposed PFM interfaces releases Ni2+ into saliva and crevicular fluid, facilitating epithelial uptake and activation of innate immune sensors such as TLR4 and NLRP3. The resulting cytokine milieu (IL-1β, IL-6, TNF-α) drives NF-κB, mediated inflammation and T-cell activation, while neurogenic mediators—including nerve growth factor (NGF), substance P, and CGRP—sensitize TRPV1/TRPA1 nociceptors, establishing feedback loops of persistent burning and neurogenic inflammation. Modifying factors such as low salivary flow, acidic oral pH, mixed-metal galvanic coupling, and parafunctional stress can lower this threshold, whereas replacement with high-noble or all-ceramic materials may restore tolerance. The model generates testable predictions: elevated local free Ni2+ levels and increased expression of TLR4 and TRPV1 in symptomatic mucosa, along with clinical improvement following substitution of nickel-containing restorations. Conceptually, the Nallan–Nickel Effect reframes PFM-associated burning and lichenoid lesions as threshold-governed, neuro-immune phenomena rather than nonspecific irritations. By integrating corrosion chemistry, mucosal immunology, and sensory neurobiology, this hypothesis offers a coherent, testable framework for future translational research and patient-centered management of PFM-related complications.

## Linked entities

- **Proteins:** TLR4 (toll like receptor 4), NLRP3 (NLR family pyrin domain containing 3), IL1B (interleukin 1 beta), IL6 (interleukin 6), TNF (tumor necrosis factor), NFKB1 (nuclear factor kappa B subunit 1), NGF (nerve growth factor), CALCA (calcitonin related polypeptide alpha), TRPV1 (transient receptor potential cation channel subfamily V member 1), TRPA1 (transient receptor potential cation channel subfamily A member 1)
- **Chemicals:** nickel ions (PubChem CID 934), Ni2+ (PubChem CID 934)

## Full-text entities

- **Genes:** NGF (nerve growth factor) [NCBI Gene 4803] {aka Beta-NGF, HSAN5, NGFB}, TAC1 (tachykinin precursor 1) [NCBI Gene 6863] {aka Hs.2563, NK2, NKNA, NPK, TAC2}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TRPV1 (transient receptor potential cation channel subfamily V member 1) [NCBI Gene 7442] {aka VR1}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, TRPA1 (transient receptor potential cation channel subfamily A member 1) [NCBI Gene 8989] {aka ANKTM1, FEPS, FEPS1, p120}, CALCA (calcitonin related polypeptide alpha) [NCBI Gene 796] {aka CALC1, CGRP, CGRP-I, CGRP-alpha, CGRP1, CT}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** Lichenoid (MESH:D017512), inflammation (MESH:D007249)
- **Chemicals:** Nickel (MESH:D009532), PFMs (MESH:C044626), Nallan (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12651289/full.md

---
Source: https://tomesphere.com/paper/PMC12651289