305
Letters to the Editor TO THE EDITOR: Re: Anatomic Variation of the Position of the Nerve
Lingual
Injury to the lingual nerve is a potential complication of periodontal flap surgery in the mandibular arch.1 This postoperative injury may appear in the form of anesthesia, which is defined as the loss of feeling or sensation. It might also manifest itself as a paresthesia, or an altered sensation in the form of burning or tingling.2 Periodontal surgical procedures in the mandibular lingual posterior area commonly involve full thickness flaps, and some clinicians create lingual vertical releasing incisions in the molar area to obtain better access. While periodontists should know the anatomic course of the lingual nerve from the third molar region anteriorly, the path of the nerve exhibits some degree of variation.3 The purpose of this communication is to present a case report of an individual who presented with symptoms consistent with anatomic variation of the lingual nerve pathway, and to discuss the implications of such anomalies to
periodontal treatment. A 24 year-old healthy white male presented to the Chanute Air Force Base dental clinic for a routine periodontal exam. The patient had a full compliment of teeth, except that all 4 third molars were missing. Teeth #1 and 16 were congenitally missing. Upon probing the mid-distal aspect of #31, the patient immediately reported a sensation resembling an electric shock that traveled along the right side and to the tip of his tongue. Additionally, the patient experienced pain on the lingual-attached gingiva from #28 to 31, with the most pain around the attached gingiva of #31. When the distolingual line angle of #31 was probed, the patient felt a slight tingling at the tip of the tongue on the right side, with no other discomfort. The remainder of the periodontal exam was completed, and no pockets were found to be greater than 4 mm. A diagnosis of localized mild to moderate Periodontitis was made, the 4 mm pockets were scaled and root planed using local anesthesia, and following a re-evaluation, the patient was placed in periodontal main-
every 4 months. more detailed examination of the distal aspect of #31 was carried out, and a pertinent dental history was obtained. As previously noted teeth #1 and 16 were congenitally missing. Two years prior to the periodontal exam, the patient had #17 and 32 surgically removed. These teeth were mesioangularly impacted, according to past x-rays. When the patient brushes the lingual surface of #31, he experiences a tingling sensation in the attached gingiva of #29, 30, and 31. When he brushes the lingual aspect of #18, no discomfort is felt. The patient stated that before #32 was surgically extracted, he had no paresthesia in the right lingual gingiva when brushing his teeth. tenance
A
The soft tissue around #31 does not reveal any unusual anatomic surface variations, and radiographically the area appears normal. The patient is currently in periodontal maintenance, and the lingual gingiva of #31 is asymptomatic unless the "trigger areas" on the lingual gingiva are
probed. Although standard anatomy textbooks describe the lingual nerve as having a consistent pathway, variations in the course of the nerve may exist. Mozsary and Middleton gave an accurate description of the usual course of the lingual nerve; "After leaving the third division of the trigeminal nerve, the lingual nerve descends in the pterygomandibular
space almost on the surface of the mandible, anterior to the inferior alveolar and the mylohyoid nerves. It does not loop around the submandibular gland; instead it leaves the pterygomandibular space and runs superficially just under the mucosa and on the periosteum of the lingual plate of the alveolar process close to the gingival margin."3 Variations in the lingual nerve pathway occurring around the third molar area are important for the periodontist and oral surgeon. In rare instances the lingual nerve can be found in the retromolar pad on the top of the mandibular ridge.3 It is assumed that the right lingual nerve in this case report lies somewhat lingual to the retromolar pad. Kiesselbach and Chamberlain measured the position of the lingual nerve in the mandibular third molar region on 34 cadaver specimens and in 256 cases of third molar extractions. Since many of these specimens were bony impartions, there was considerable soft tissue present coronal to the lingual alveolar crest. In 62% of the dissections, the nerve was in actual contact with the lingual plate of bone. In one of the dissections (2.9%), the nerve passed through the retromolar pad 2.0 mm above the lingual plate, at the level of the occlusal surface of an impacted third molar. In 17.6% of the cases, the nerve was at the level of the alveolar crest or higher; 12 of the extraction cases (4.5%) showed the lingual nerve to be above the lingual plate of the lower third molar.4 It is possible that the lingual nerve in this case report was located on or near the retromolar pad before the third molar surgery was done. When the flaps were closed, the flap over #32 might have been sutured in such a way that the lingual nerve might have taken a new position at the distolingual line angle of tooth #31. This could explain the tingling sensation the patient felt when brushing the lingual of #31 following the third molar surgery, but not before the surgery. It should be made clear that the above is purely a speculation by the author. Injury to the lingual nerve as a result of oral surgery usually results in complete recovery. In a study of 1,400 surgical extractions of third molars by using the lingual split technique (i.e., extraction to the lingual by removing the lingual bony plate), 6.6% of the extractions resulted in
J Periodontol
306
LETTERS TO THE EDITOR
May 1990
damage to the lingual nerve, resulting in some degree of paresthesia. In 6 months, all of the nerve injuries had recovered.5 If a lingual nerve is partially or totally transsected during periodontal surgery, recovery should be expected. One possible sequela to third molar surgery is lingual nerve entrapment syndrome. Following surgical third molar extractions, if the lingual nerve is compressed against a spicule of projecting bone, a neuroma-like thickening may occur at the point of compression. This may result in persistent paresthesia of the tongue or other sensory disturbances. Surgical decompression is the treatment of choice.6 Although the above discussion relates mostly to third molar surgical techniques, several parallels to periodontal surgery can be drawn. When making full thickness flaps on the lingual aspect of the mandibular molar area, or when designing distal wedge incisions, the periodontist should be aware that the lingual nerve may lie in or lingual to the retromolar pad. The fact that the nerve lies close to the
distal aspect of the second molar should also be considered. When flaps are sutured following third molar extractions, it is possible that the lingual nerve may be iatrogenically placed in a new position distal to the second molars. Vertical releasing incisions should best be kept to a minimal length around the retromolar pad area, and the patient should be made aware of the potential for nerve damage. Fortunately in the case presented, the lingual nerve anomaly was discovered during the initial examination. Any necessary surgical treatment could be planned with consideration of the anatomic variation. Thomas C. Reinhart, Maj, USAF, DC, PSC Box 995, APO SF 96366. References
Safety aspects of mandibular lingual surgery. J Periodontol 1976;47:224. 2. Wofford DT, Miller RI. Prospective study of dysesthesia following 1. Hunt PR.
odontectomy
of
impacted
third molars. J Oral
Maxillofac Surg
1987;45:15. 3. Mozsary PG, Middleton RA. Microsurgical reconstruction of the lingual nerve. J Oral Maxillofac Surg 1984;42:415. 4. Kiesselbach JE, Chamberlain JG. Clinical and anatomic observations the relationship of the lingual nerve to the mandibular third molar region. / Oral Maxillofac Surg 1984;42:565. Rood JP. Lingual split technique: Damage to inferior alveolar and lingual nerves during removal of impacted mandibular third molars. on
5.
BrDentJ 1983;154:402. 6. Ho KH, Lloyd RE. The lingual J 1987;163:387.
nerve
entrapment syndrome. Br Dent
TO THE EDITOR: Re: A Clinical Comparison of Antibacterial Mouthrinses (J Periodontol 1989;60:435:440)
The above referenced paper by Grossman et al. once again demonstrates the ability of Chlorhexidine to reduce plaque and gingivitis. What is most impressive about this particular study is the fact that its effects were evident on a population
subjects with very mild gingivitis (Löe and Silness GI 0.53) and very clean mouths (Turesky plaque index 1.14). There are several pieces of information which were not
of =
=
included in the report which would have been useful in the results. Chlorhexidine effected a 38.8% reduction on gingival bleeding at 6 months, compared with baseline. We are told that the mean bleeding index for the Chlorhexidine group was 0.1273. What does this number mean? How many sites bleed per subject? The GI diminished by 31.1% at 6 months compared to baseline mea0.53 at baseline presumably dropped surements; ie, GI to 0.36. This difference was statistically significant at the < 0.05 level. Is a change of this magnitude of clinical significance? This question is particularly relevant in light of the authors' claim that the study population met the ADA guidelines for an antigingivitis mouthrinse study, in that they represented "typical product users." Are the authors of this paper advocating the use of Chlorhexidine for patients with extremely mild gingivitis? Norman H. Stoller, D.M.D., Division of Periodontology, Department of Surgical Dentistry, University of Colorado Health Science Center, Denver, CO.
evaluating
=
Authors'
Response:
Dr. Stoller raises a number of questions concerning our publication "A Clinical Comparison of Antibacterial Mouthrinses: Effects of Chlorhexidine, Phenolics, and Sanguinarine on Dental Plaque and Gingivitis" that we would like to address. First, Dr. Stoller states that the subjects used in this study had extremely mild gingivitis. Given that two rinses were tested, it seemed appropriate that the study population not be selected for advanced disease. Importantly, our objective in this work was to demonstrate the relative effectiveness of Chlorhexidine, phenolics, and sanguinarine rinses, not advocate the use of Chlorhexidine in patients with mild gingivitis. Patient selection is appropriately handled by the professional who has full knowledge of patient history, motivation, concomitant medications, and any other extenuating circumstances. This work clearly demonstrates the greater therapeutic benefit one can expect from a Chlorhexidine rinse relative to sanguinarine and phenolic rinses. One misconception in Dr. Stoller's letter we would like to clear up concerns how reductions in gingival bleeding were assessed. In all cases, % reductions in gingival bleeding (as well as plaque and GI severity), were calculated relative to placebo, not baseline as stated in the letter. Thus, the 38.8% reduction of gingival bleeding observed in the Chlorhexidine group at 6 months is versus placebo at 6 months, not calculated back to the initial baseline score. In fact, using the data provided in Table 1 and the legend to Figure 3, Chlorhexidine, relative to baseline, reduced gingival bleeding by over 60%. However, since any number
Volume 61 Number 5
LETTERS TO THE EDITOR
of extraneous factors (change in brushing habits, compliance) may have contributed to this reduction, we choose to isolate the drug effect by comparing directly to placebo at each time point. An explanation of the mean bleeding values presented in Table 1 can be found in the Materials and Methods portion of the paper. Briefly, the mean bleeding values represented the proportion of sites bleeding on probing or bleeding spontaneously with each natural tooth receiving a total of six scores. As an example, if a patient 168 total sites) with 23 6 had a full dentition (28 identified bleeding sites, his individual bleeding score would 0.1369. For the group, the mean bleeding be 23/168 score would be the sum of the individual scores divided by the number of subjects. We thank Dr. Stoller for his comments and questions and trust this clarifies any uncertainties regarding this study. Michael D. Manhart, Ph.D., Associate Director, Product Development, Procter & Gamble Company, Cincinnati, OH. =
=
TO THE EDITOR: Re: Clinical and Laboratory Profiles of Periodontitis if Periodontol 1989;60:557-563) I was surprised to see my definition of periodontosis credited to Wannenmacher in the above cited article. I had always assumed that the definition of periodontosis pres-
307
ently in use originated with me. Paul N. Baer, D.D.S., Professor and Chairman, State University of New York at Stony Brook. Authors' Response: We hope that the wording of the introductory sentence in our paper has not confused readers. In the 1930's Dr. Wannenmacher did indeed describe the histopathology of periodontal inflammation in young individuals, but as indicated by Dr. Baer, the term "periodontosis" was not used until later. The further definition of early onset Periodontitis initiated by Dr. Baer in the early 1970's (as cited in the paper) has been very useful in further research. The extensive classification of these disorders continues, even in the absence of a clear understanding of etiologic factors. Unfortunately, further categorizations on the basis of nonspecific associations may cause undue confusion among investigators. It is our hope that all researchers will pursue the study of possible causal mechanisms in all groups of patients with early onset periodontal disease, with the understanding that premature separation into subgroups based on certain phenotypic manifestations may cloud recognition of etiologic factors involved in one or more clinically defined classes of disease. Reference: Wannenmacher E: Umshau-auf dem Gebeit der Paradentose. Zeitschr Zahn-MundKieferh 1938:3:81. Jacqueline A. Astemborski, Joann A. Boughman, and Jon B. Suzuki, School of Medicine, University of Maryland at Baltimore
Letters to the Editor TO THE EDITOR: Re: Anatomic Variation of the Position of the Nerve
Lingual
Injury to the lingual nerve is a potential complication of periodontal flap surgery in the mandibular arch.1 This postoperative injury may appear in the form of anesthesia, which is defined as the loss of feeling or sensation. It might also manifest itself as a paresthesia, or an altered sensation in the form of burning or tingling.2 Periodontal surgical procedures in the mandibular lingual posterior area commonly involve full thickness flaps, and some clinicians create lingual vertical releasing incisions in the molar area to obtain better access. While periodontists should know the anatomic course of the lingual nerve from the third molar region anteriorly, the path of the nerve exhibits some degree of variation.3 The purpose of this communication is to present a case report of an individual who presented with symptoms consistent with anatomic variation of the lingual nerve pathway, and to discuss the implications of such anomalies to
periodontal treatment. A 24 year-old healthy white male presented to the Chanute Air Force Base dental clinic for a routine periodontal exam. The patient had a full compliment of teeth, except that all 4 third molars were missing. Teeth #1 and 16 were congenitally missing. Upon probing the mid-distal aspect of #31, the patient immediately reported a sensation resembling an electric shock that traveled along the right side and to the tip of his tongue. Additionally, the patient experienced pain on the lingual-attached gingiva from #28 to 31, with the most pain around the attached gingiva of #31. When the distolingual line angle of #31 was probed, the patient felt a slight tingling at the tip of the tongue on the right side, with no other discomfort. The remainder of the periodontal exam was completed, and no pockets were found to be greater than 4 mm. A diagnosis of localized mild to moderate Periodontitis was made, the 4 mm pockets were scaled and root planed using local anesthesia, and following a re-evaluation, the patient was placed in periodontal main-
every 4 months. more detailed examination of the distal aspect of #31 was carried out, and a pertinent dental history was obtained. As previously noted teeth #1 and 16 were congenitally missing. Two years prior to the periodontal exam, the patient had #17 and 32 surgically removed. These teeth were mesioangularly impacted, according to past x-rays. When the patient brushes the lingual surface of #31, he experiences a tingling sensation in the attached gingiva of #29, 30, and 31. When he brushes the lingual aspect of #18, no discomfort is felt. The patient stated that before #32 was surgically extracted, he had no paresthesia in the right lingual gingiva when brushing his teeth. tenance
A
The soft tissue around #31 does not reveal any unusual anatomic surface variations, and radiographically the area appears normal. The patient is currently in periodontal maintenance, and the lingual gingiva of #31 is asymptomatic unless the "trigger areas" on the lingual gingiva are
probed. Although standard anatomy textbooks describe the lingual nerve as having a consistent pathway, variations in the course of the nerve may exist. Mozsary and Middleton gave an accurate description of the usual course of the lingual nerve; "After leaving the third division of the trigeminal nerve, the lingual nerve descends in the pterygomandibular
space almost on the surface of the mandible, anterior to the inferior alveolar and the mylohyoid nerves. It does not loop around the submandibular gland; instead it leaves the pterygomandibular space and runs superficially just under the mucosa and on the periosteum of the lingual plate of the alveolar process close to the gingival margin."3 Variations in the lingual nerve pathway occurring around the third molar area are important for the periodontist and oral surgeon. In rare instances the lingual nerve can be found in the retromolar pad on the top of the mandibular ridge.3 It is assumed that the right lingual nerve in this case report lies somewhat lingual to the retromolar pad. Kiesselbach and Chamberlain measured the position of the lingual nerve in the mandibular third molar region on 34 cadaver specimens and in 256 cases of third molar extractions. Since many of these specimens were bony impartions, there was considerable soft tissue present coronal to the lingual alveolar crest. In 62% of the dissections, the nerve was in actual contact with the lingual plate of bone. In one of the dissections (2.9%), the nerve passed through the retromolar pad 2.0 mm above the lingual plate, at the level of the occlusal surface of an impacted third molar. In 17.6% of the cases, the nerve was at the level of the alveolar crest or higher; 12 of the extraction cases (4.5%) showed the lingual nerve to be above the lingual plate of the lower third molar.4 It is possible that the lingual nerve in this case report was located on or near the retromolar pad before the third molar surgery was done. When the flaps were closed, the flap over #32 might have been sutured in such a way that the lingual nerve might have taken a new position at the distolingual line angle of tooth #31. This could explain the tingling sensation the patient felt when brushing the lingual of #31 following the third molar surgery, but not before the surgery. It should be made clear that the above is purely a speculation by the author. Injury to the lingual nerve as a result of oral surgery usually results in complete recovery. In a study of 1,400 surgical extractions of third molars by using the lingual split technique (i.e., extraction to the lingual by removing the lingual bony plate), 6.6% of the extractions resulted in
J Periodontol
306
LETTERS TO THE EDITOR
May 1990
damage to the lingual nerve, resulting in some degree of paresthesia. In 6 months, all of the nerve injuries had recovered.5 If a lingual nerve is partially or totally transsected during periodontal surgery, recovery should be expected. One possible sequela to third molar surgery is lingual nerve entrapment syndrome. Following surgical third molar extractions, if the lingual nerve is compressed against a spicule of projecting bone, a neuroma-like thickening may occur at the point of compression. This may result in persistent paresthesia of the tongue or other sensory disturbances. Surgical decompression is the treatment of choice.6 Although the above discussion relates mostly to third molar surgical techniques, several parallels to periodontal surgery can be drawn. When making full thickness flaps on the lingual aspect of the mandibular molar area, or when designing distal wedge incisions, the periodontist should be aware that the lingual nerve may lie in or lingual to the retromolar pad. The fact that the nerve lies close to the
distal aspect of the second molar should also be considered. When flaps are sutured following third molar extractions, it is possible that the lingual nerve may be iatrogenically placed in a new position distal to the second molars. Vertical releasing incisions should best be kept to a minimal length around the retromolar pad area, and the patient should be made aware of the potential for nerve damage. Fortunately in the case presented, the lingual nerve anomaly was discovered during the initial examination. Any necessary surgical treatment could be planned with consideration of the anatomic variation. Thomas C. Reinhart, Maj, USAF, DC, PSC Box 995, APO SF 96366. References
Safety aspects of mandibular lingual surgery. J Periodontol 1976;47:224. 2. Wofford DT, Miller RI. Prospective study of dysesthesia following 1. Hunt PR.
odontectomy
of
impacted
third molars. J Oral
Maxillofac Surg
1987;45:15. 3. Mozsary PG, Middleton RA. Microsurgical reconstruction of the lingual nerve. J Oral Maxillofac Surg 1984;42:415. 4. Kiesselbach JE, Chamberlain JG. Clinical and anatomic observations the relationship of the lingual nerve to the mandibular third molar region. / Oral Maxillofac Surg 1984;42:565. Rood JP. Lingual split technique: Damage to inferior alveolar and lingual nerves during removal of impacted mandibular third molars. on
5.
BrDentJ 1983;154:402. 6. Ho KH, Lloyd RE. The lingual J 1987;163:387.
nerve
entrapment syndrome. Br Dent
TO THE EDITOR: Re: A Clinical Comparison of Antibacterial Mouthrinses (J Periodontol 1989;60:435:440)
The above referenced paper by Grossman et al. once again demonstrates the ability of Chlorhexidine to reduce plaque and gingivitis. What is most impressive about this particular study is the fact that its effects were evident on a population
subjects with very mild gingivitis (Löe and Silness GI 0.53) and very clean mouths (Turesky plaque index 1.14). There are several pieces of information which were not
of =
=
included in the report which would have been useful in the results. Chlorhexidine effected a 38.8% reduction on gingival bleeding at 6 months, compared with baseline. We are told that the mean bleeding index for the Chlorhexidine group was 0.1273. What does this number mean? How many sites bleed per subject? The GI diminished by 31.1% at 6 months compared to baseline mea0.53 at baseline presumably dropped surements; ie, GI to 0.36. This difference was statistically significant at the < 0.05 level. Is a change of this magnitude of clinical significance? This question is particularly relevant in light of the authors' claim that the study population met the ADA guidelines for an antigingivitis mouthrinse study, in that they represented "typical product users." Are the authors of this paper advocating the use of Chlorhexidine for patients with extremely mild gingivitis? Norman H. Stoller, D.M.D., Division of Periodontology, Department of Surgical Dentistry, University of Colorado Health Science Center, Denver, CO.
evaluating
=
Authors'
Response:
Dr. Stoller raises a number of questions concerning our publication "A Clinical Comparison of Antibacterial Mouthrinses: Effects of Chlorhexidine, Phenolics, and Sanguinarine on Dental Plaque and Gingivitis" that we would like to address. First, Dr. Stoller states that the subjects used in this study had extremely mild gingivitis. Given that two rinses were tested, it seemed appropriate that the study population not be selected for advanced disease. Importantly, our objective in this work was to demonstrate the relative effectiveness of Chlorhexidine, phenolics, and sanguinarine rinses, not advocate the use of Chlorhexidine in patients with mild gingivitis. Patient selection is appropriately handled by the professional who has full knowledge of patient history, motivation, concomitant medications, and any other extenuating circumstances. This work clearly demonstrates the greater therapeutic benefit one can expect from a Chlorhexidine rinse relative to sanguinarine and phenolic rinses. One misconception in Dr. Stoller's letter we would like to clear up concerns how reductions in gingival bleeding were assessed. In all cases, % reductions in gingival bleeding (as well as plaque and GI severity), were calculated relative to placebo, not baseline as stated in the letter. Thus, the 38.8% reduction of gingival bleeding observed in the Chlorhexidine group at 6 months is versus placebo at 6 months, not calculated back to the initial baseline score. In fact, using the data provided in Table 1 and the legend to Figure 3, Chlorhexidine, relative to baseline, reduced gingival bleeding by over 60%. However, since any number
Volume 61 Number 5
LETTERS TO THE EDITOR
of extraneous factors (change in brushing habits, compliance) may have contributed to this reduction, we choose to isolate the drug effect by comparing directly to placebo at each time point. An explanation of the mean bleeding values presented in Table 1 can be found in the Materials and Methods portion of the paper. Briefly, the mean bleeding values represented the proportion of sites bleeding on probing or bleeding spontaneously with each natural tooth receiving a total of six scores. As an example, if a patient 168 total sites) with 23 6 had a full dentition (28 identified bleeding sites, his individual bleeding score would 0.1369. For the group, the mean bleeding be 23/168 score would be the sum of the individual scores divided by the number of subjects. We thank Dr. Stoller for his comments and questions and trust this clarifies any uncertainties regarding this study. Michael D. Manhart, Ph.D., Associate Director, Product Development, Procter & Gamble Company, Cincinnati, OH. =
=
TO THE EDITOR: Re: Clinical and Laboratory Profiles of Periodontitis if Periodontol 1989;60:557-563) I was surprised to see my definition of periodontosis credited to Wannenmacher in the above cited article. I had always assumed that the definition of periodontosis pres-
307
ently in use originated with me. Paul N. Baer, D.D.S., Professor and Chairman, State University of New York at Stony Brook. Authors' Response: We hope that the wording of the introductory sentence in our paper has not confused readers. In the 1930's Dr. Wannenmacher did indeed describe the histopathology of periodontal inflammation in young individuals, but as indicated by Dr. Baer, the term "periodontosis" was not used until later. The further definition of early onset Periodontitis initiated by Dr. Baer in the early 1970's (as cited in the paper) has been very useful in further research. The extensive classification of these disorders continues, even in the absence of a clear understanding of etiologic factors. Unfortunately, further categorizations on the basis of nonspecific associations may cause undue confusion among investigators. It is our hope that all researchers will pursue the study of possible causal mechanisms in all groups of patients with early onset periodontal disease, with the understanding that premature separation into subgroups based on certain phenotypic manifestations may cloud recognition of etiologic factors involved in one or more clinically defined classes of disease. Reference: Wannenmacher E: Umshau-auf dem Gebeit der Paradentose. Zeitschr Zahn-MundKieferh 1938:3:81. Jacqueline A. Astemborski, Joann A. Boughman, and Jon B. Suzuki, School of Medicine, University of Maryland at Baltimore
