Glenn–

You did an EXCELLENT service.

I witnessed the very scene you described with Dr. McCarthy and his 2 year old granddaughter. No Versed, no anesthesia.

The kids scream because they are not in CONTROL,………NOT because they are in pain.

He was screaming so loud and had so much adrenaline from the screaming and the fussing and all the fighting, he probably felt nothing from the laser.

After you were through, did the crying stop? Did the kid start running around?

Bob

Lee,

Thanks for the kind words.

Dentin and/or root hypersensitivity may involve more than just pulpitis.  See the article below on some theories.

If you de-focus at a distance away from the tooth, you can get some thermal energy into the tubules and have a “biomodulating” effect on the action potentials of the OD processes and the unmylenated C fibers in the pulp–it seems.

Occluding the tubules alone give us mixed results….around 50%.

Defocusing and “biostimulating” the pulp/tubules gives us 90+%

The sensitivity typically stays at the level of chairside treatment, however the patient may become dissatisfied if only 75% versus 95%.  Some others may feel that is just fine……

One VERY common observation post-op to de-focused laser desensitization is that an ache or throb–usually mild–appears within a few hours post-op that can increase in intensity for a few days, then tapers off slowly over a week or two.  VERY common observation.

Hope that gives you a “jump”!!

Bob

Dentinal Sensation and Hypersensitivity A Review of Mechanisms and Treatment Alternatives  Louis H. Berman

In any dental procedure, in the absence of local anesthesia, manipulation of dentin surfaces may cause pain. When dentin is exposed to thermal, osmotic or electrical stimuli, or when air blasts or various drugs are applied to its surface, the host feels pain which may be termed a “dentinalgia.” A “pulpalgia” is a more prolonged, chronic pain to given stimuli and may result from a rise in the local intrapulpal edema subsequent to deep caries and pulpal inflammation.1,2 Although histochemical, autoradiographic and electron microscopic studies have vividly described the relationship between the odontoblast and the neural fibers of the pulp, the exact mechanism of transmission of the pain response from the dentin to the terminal nerve endings is only hypothesized. Four theories have been proposed: the transducer, modulation, gate control and hydrodynamic theories.3,4 Of these theories, the hydrodynamic theory is currently believed most responsible for the transmission of dentinal sensation. However, a brief description of the other mechanisms will also be presented.

Transducer Theory. This theory of dentinal sensation takes into consideration the “synaptic-like” relationship between the terminal, sensory nerve endings and the odontoblastic processes. If a true synapse were present between these two elements to facilitate the transmission of dentinal sensations, then a neural transmitting substance such as acetylcholine would be expected in this area of the odontoblastic process and the predentin. There is no direct evidence for the presence of acetylcholine activity in the neural transmission in the pulp.

Modulation Theory. Upon an irritating stimulus to the dentin, the odontoblasts may become injured and subsequently release a variety of neurotransmitting agents as well as vasoactive and pain producing amines and proteins.5 These substances may modulate associated nerve fiber action potentials by increasing neuronal cAMP levels through cell membrane adenylate cyclase receptors.6

Gate Control Theory and Vibration. When the dentin is irritated, for example, by cavity preparation, all of the pulpal nerves become activated from the vibrations. The larger myelinated fibers may accommodate to the sensations. The smaller C-fibers may tend to be maintained and not adjust to the stimulus. Thus, as the low-intensity “pain gates” from the larger fibers are closed, the high-intensity “pain gates” from the smaller fibers are enhanced.3

“Pain gates” may be opened by some stimuli, such as anxiety, and may be closed by distracting stimuli such as “audio-analgesia” or gingival stimulation. Van Hassel2 demonstrated in monkeys that cortical responses to pulpal stimulation can be diminished by concomitantly stimulating the gingiva.

However, the gate theory does little to explain how pain responses from the dentin are transmitted and perceived by the nerve endings of the pulp—only how they may be centrally interpreted.

Hydrodynamic Theory. Fish in 19278 observed the interstitial fluid of the dentin and pulp, referring to it as the “dental lymph.” He postulated that the flow of this fluid could take place in either an outward or inward direction depending on the pressure variations in the surrounding tissue. Isokawa9 found no pulpal lymphatics in dog teeth, but suggested that the pulpal lymph flow was continuous with that of the dentinal tubule fluid. This idea of fluid movement within the dentinal tubules is the basis for the transmission of sensations according to the hydrodynamic theory.

Short-term stimulation of the dentin and the resulting pain, a “dentinalgia,” is not necessarily the result of local changes in the intrapulpal pressure. According to the hydrodynamic theory, as put forth by Brannstrom and Astrom,11 a dentinalgia results from a stimulus causing minute changes in the fluid movement within the dentinal tubules. This may subsequently deform the odontoblast or its process and hence cause an elicitation of pain via the intimately associated “mechano-receptor-like” nerve endings.

Mjor and Pindborg12 stated: “Pulp and dentin sensation is characterized by being limited to pain only, irrespective of the initiating factor.” There is no direct support for any type of specialized terminal nerve receptors for hot, cold, electrical, osmotic, dehydration or chemical stimuli in dentin. The interpretation of most of these stimuli can be explained by the hydrodynamic theory. Figure 1 will help to visualize this model, as explained below.

The dehydration of dentin (i.e., by air-blasts) is probably the clearest example for understanding dentin sensation. When Brannstrom applied absorbent paper to exposed dentin it caused pain; but no pain was elicited using wet paper.11,13 The outward movement of the dentinal fluid into the dehydrating source (i.e., air-blasts or absorbent paper) is thought to stimulate the “mechano-receptor” of the odontoblast, causing pain.

The perception of acute thermal stimulation can also be explained by the hydrodynamic theory. The coefficient of thermal expansion of the dentinal tubule fluid is about ten times that of the tubule wall. Therefore, heat applied to dentin will result in an expansion of the fluid, and, conversely, cold will result in a contraction of the fluid, with both creating an excitation of the “mechano-receptor.”14,21,25 This fluid-flow model is further reenforced by the finding that pain is felt before temperature changes can be measured on the pulpal side of the dentin.15
It is also a common clinical finding that pain is produced when sugar or salted solutions are placed in contact with exposed dentin. When the irritant is rinsed or brushed away, the discomfort subsides.10 This again can be explained by dentin tubule fluid movements. Fluids of a relatively low osmolarity (i.e., dentinal tubule fluid) will have a tendency to flow towards solutions of higher osmolarity (i.e., salt or sugar solutions). When iso-osmotic solutions are applied, no stimulus is felt.

Source: Journal of Periodontology on CD-ROM (Copyrights © 1998, AAP), 1985 Apr (216 – 222):

cerecdoc,
Are you ‘anesthetizing the tooth w/ the laser prior to cutting? Make sure you do spend adequate time doing so. This alone can eliminate lots of sensitivity problems.
If still sensitivity:
Here’s a few things to check
1. make sure once you break thru enamel you back off on your settings . I usually drop wattage and then air.
2. make sure your suction isn’t too close so adequate h20 can get to the prep
3. if still sensitivity back off and defocus and  ‘anesthetize’ the tooth for 60-90 seconds more before proceeding.
How were you taught?

Bob et al,
I followed your strategy today on desensitization of 12 teeth(two molars and a bi in each quad). I requested and recorded a baseline sensitivity from the patient on a scale of 1 to 10 and then asked about today.  I then explained that we were look for subjective improvement not total reduction of sensitivity.  She said she was a 4/5 today so I suggested we try for a 2/3.  All the areas were on the buccal either recession or recession and abfraction.  I defocused and moved in as possible stopping when she let me know she was feeling it.(Biolase – .25W no w or A for about 35 to 45 seconds per tooth surface).  I had to return to one molar a second time and included the lingual on the second pass.  The patient was very satisfied and accepting of a reduction above 0 following a drink of cold water.  The success was in the patient management.  Gracias!
Pat

Hi Pat,
Tell me about the patient. How old, male/female, previous restoration, any cracks/crazes, occlusion, bruxer, etc….I MIGHT have a suggestion/answer, I have idea’s. Hope I can help!
Mark