Amalgam vs. Composite: Filling in the Blanks

By Michael Behnen, D.D.S.

Information concerning the molecular cold-sensing mechanism in teeth could lead to new advances in the management of cold sensitive teeth

Cold sensitivity is a chronic problem for many dental patients. Most dentists have tried multiple types of dentin desensitizing agents over the years, all with varying degrees of success. Persistent cold sensitivity can often result in dental patients seeking relief by having endodontic therapy, or even extractions of the offending teeth. A recent article in the New York Times highlighted research that is investigating proteins in the odontoblastic cells of teeth that specifically respond to cold stimuli.

Dentin Hypersensitivity

The widely accepted “hydrodynamic theory” of dental pain was introduced by Martin Brannstrom in the 1960s. It explains that fluid movement in the dentinal tubules is translated into electrical signals by sensory receptors in the tubules or the odontoblastic layer. The pulpodentinal complex is composed of A-delta nerve fibers in association with the odontoblastic cell layer and dentin. When the contents of the dentinal tubules are disturbed by a stimulus (like cold temperatures) enough to involve the odontoblastic layer, A-delta fibers are excited. This results in pulpal pain.

Current Management of Dentin Hypersensitivity

A review of desensitizing agents that are commonly available can be categorized based on their mechanism of action:

  • Nerve desensitization: potassium nitrate, potassium chloride, potassium citrate.

  • Protein precipitation in the dentinal tubules: glutaraldehyde, silver nitrate, zinc chloride.

  • Plugging dentinal tubules: sodium fluoride, stannous fluoride, strontium chloride, potassium oxalate, calcium phosphate, and calcium carbonate.

  • Dentin adhesive sealers: fluoride varnishes, oxalic acid and resin, glass ionomer cements, composites, and dentin bonding agents.

At-home desensitizing agents can include toothpastes, mouthwashes, and chewing gums. They typically work by reducing nerve excitability through the use of potassium salts, or by plugging the dentinal tubules through the use of fluorides. Resin-based dental adhesive systems or dentin-bonding agents are common in-office desensitizing agents. They typically seal the dentinal tubules by forming a dentin-resin hybrid layer. Newer dentin-bonding agents like “Gluma Desensitizer” causes a precipitation of proteins in the dentinal tubules and forms deep resin tags that occlude the tubules.

A New Understanding of Cold-Sensing Molecules in Teeth

Despite our understanding of the odontoblasts in the pulpodentinal complex acting as sensory receptor cells, evidence supporting their direct role in mediating thermal sensation is lacking. A series of studies in the field of neurophysiology has opened a great opportunity for understanding how specific protein molecules in our teeth respond to cold stimulation. A recent study published in “Science Advances” focused on understanding the molecular cold-sensing mechanism in teeth.

Cold sensing in the peripheral nervous system relies primarily on certain transient receptor potential (TRP) ion channels. These protein molecules are commonly found throughout the body. When these protein channels are opened, they can signal a response from the pain and thermosensory nerve endings. For example, TRPM8 and TRPA1 are the key sensors of decreasing temperature and pain to extreme cold in the skin and mucous membranes. In this study, the authors evaluated the role of TRPA1, TRPM8, and TRPC5 ion channels in cold sensing in teeth.


The authors in this study developed an intact mouse jaw nerve preparation to record electrical activity from intact teeth. They also studied healthy human teeth that were extracted for orthodontic or cosmetic reasons. Results of their testing identified:

  • The odontoblastic processes, predominantly via TRPC5, are the initiating site of cold transduction in the tooth.

  • TRPC5 along with TRPA1 are the main channels for cold sensing in healthy teeth. Less than 5 percent of genetically modified mice lacking TRPC5 responded to cold. The remaining responded by activation of TRPA1.

  • TRPC5 is required for inflammatory tooth pain. TRPC5 sensory nerve expression is increased in teeth with pulpitis, while TRPM8 decreased.


The findings in this study may lead to new methods and materials for treating cold sensitivity in teeth. It is interesting to note that eugenol inhibits TRPC5 currents, and it may help to explain why it has been an effective dental sedative medicament. While the majority of our current desensitizing treatments focus on blocking the dentinal tubules, new treatment modalities may focus on targeting TRPC5 to inhibit its activity and decrease cold sensitivity. This may lead to new and more effective methods for eliminating dentinal hypersensitivity.

Author: Michael Behnen, D.D.S. graduated from the Indiana University School of Dentistry in 1992. He was a member of the U.S. Army Dental Corps and completed residency training in endodontics at Fort Gordon, GA in 2000. He has been in private practice at Northwest Endodontic Specialists in Olympia, WA since 2003.

The information contained in this, or any case study post in Incisor, should never be considered a proper replacement for necessary training and/or education regarding adult oral conscious sedation. Regulations regarding sedation vary by state. This is an educational and informational piece. DOCS Education accepts no liability whatsoever for any damages resulting from any direct or indirect recipient's use of or failure to use any of the information contained herein. DOCS Education would be happy to answer any questions or concerns mailed to us at 3250 Airport Way S, Suite 701 | Seattle, WA 98134. Please print a copy of this posting and include it with your question or request.
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