Young Adults' Experience of Appearance-Altering Orthognathic Surgery: A Longitudinal Interpretative Phenomenologic Analysis.

OBJECTIVE: To gain an experiential account of the processes of change associated specifically with orthognathic surgery. DESIGN: A qualitative design was used. Semistructured interviews were carried out with 7 participants approximately 1 week before and 6-8 weeks after surgery. The data were analyzed using interpretative phenomenologic analysis (IPA). SETTING: Participants were recruited from a NHS Dental Hospital. PARTICIPANTS: Patients aged 16 to 25 years scheduled to undergo orthognathic surgery on both the upper and lower jaws were purposively sought to participate. Seven participants aged between 18 and 25 years and who had undergone a bimaxillary osteotomy completed interviews (5 females and 2 males). RESULTS: Themes were identified in connection with the overall journey of treatment being a rite of passage; the treatment's role in raising awareness about the anomalies in appearance; the initial shock at the changes that followed surgery; the uncertainty about treatment; the impact of actual negative reactions of others; and the role of significant others in the decision-making process. CONCLUSIONS: Participants described undergoing a much more complex process of adjustment to change in appearance than has been identified elsewhere within the literature, and the study highlights the nuanced fashion in which both medical and parental communication influence patient expectation and experience of surgery. There is a need to improve communication between clinicians, families, and young adults seeking orthognathic surgery. Further studies are needed to investigate the processes associated with seeking to change facial appearance resulting from other forms of dentofacial condition.

Psychosocial Outcomes in Orthognathic Surgery: A Review of the Literature.

OBJECTIVE: To identify and critically appraise the literature on the psychosocial outcomes of orthognathic surgery, reflect on the clinical and theoretical implications, and suggest avenues for future research. DESIGN: A search of the literature was completed using the databases Web of Science, MEDLINE, and PsycINFO to identify English-language articles published since January 2001 that have reported a measure of psychosocial functioning posttreatment. RESULTS: A total of 38 articles were eligible for inclusion in the review. The studies reported improvements in areas such as satisfaction with facial appearance, self-confidence, self-esteem, anxiety, and social functioning. Small percentages of patients were left dissatisfied or had difficulty adjusting to appearance change despite the absence of treatment complications. Gains in psychosocial functioning were maintained over several years, and satisfaction increased over time. CONCLUSIONS: There are consistent positive outcomes reported as a result of orthognathic surgery, but conclusions are limited by methodological issues in study design such as small sample sizes, limited use of control groups, and measures that fail to tap into relevant areas of psychosocial functioning. In addition, further exploration is required of processes such as adjustment to facial change and the role of psychological support during treatment.

Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas.

BACKGROUND: Voltage-gated sodium channels Nav1.8 and Nav1.9 are expressed preferentially in small diameter sensory neurons, and are thought to play a role in the generation of ectopic activity in neuronal cell bodies and/or their axons following peripheral nerve injury. The expression of Nav1.8 and Nav1.9 has been quantified in human lingual nerves that have been previously injured inadvertently during lower third molar removal, and any correlation between the expression of these ion channels and the presence or absence of dysaesthesia investigated. RESULTS: Immunohistochemical processing and quantitative image analysis revealed that Nav1.8 and Nav1.9 were expressed in human lingual nerve neuromas from patients with or without symptoms of dysaesthesia. The level of Nav1.8 expression was significantly higher in patients reporting pain compared with no pain, and a significant positive correlation was observed between levels of Nav1.8 expression and VAS scores for the symptom of tingling. No significant differences were recorded in the level of expression of Nav1.9 between patients with or without pain. CONCLUSIONS: These results demonstrate that Nav1.8 and Nav1.9 are present in human lingual nerve neuromas, with significant correlations between the level of expression of Nav1.8 and symptoms of pain. These data provide further evidence that changes in expression of Nav1.8 are important in the development and/or maintenance of nerve injury-induced pain, and suggest that Nav1.8 may be a potential therapeutic target.

Chlorhexidine gel reduces incidence of alveolar osteitis after extraction of the mandibular third molars.

DESIGN: A randomised, prospective clinical trial with parallel groups was carried out in a single centre. INTERVENTION: The experimental (gel) group (n=41) applied a bioadhesive 0.2% chlorhexidine gel to the wound during the first postoperative week and a control (rinse) group (n=32) used a 0.12% (v/v) chlorhexidine mouthrinse during the first week following third molar extraction. Patients were evaluated on the third and seventh postoperative day. OUTCOME MEASURE: Alveolar osteitis was evaluated according to Blum's criteria.. RESULTS: A 70% decrease in postoperative alveolar osteitis in the gel group (P 0.04) was observed. The rinse group had 25% incidence of postoperative alveolar osteitis, whereas the gel group had 7.5%. T equates to a number needed to treat of six (95% confidence interval, 3-144). CONCLUSIONS: It was concluded that the topical application of bioadhesive chlorhexidine gel to the surgical wound during the postoperative week may decrease the incidence of alveolar osteitis after extraction of the mandibular third molars.

Interleukin-10 reduces scarring and enhances regeneration at a site of sciatic nerve repair.

Axonal regeneration at a site of peripheral nerve repair can be impeded by the formation of scar tissue, which creates a mechanical barrier and initiates the development of multiple branched axonal sprouts that form a neuroma. We have investigated the hypothesis that the application of a scar-reducing agent to the nerve repair site would permit better axonal regeneration. In anaesthetised C57 Black-6 mice, the left sciatic nerve was sectioned and immediately re-approximated using four epineurial sutures. In five groups of eight mice, we injected transforming growth factor-beta3 (50 or 500 ng), interleukin-10 (IL-10) (125 or 500 ng), or saline into and around the repair site, both before and after the nerve section. Another group of eight animals acted as sham-operated controls. After 6 weeks, the outcome was assessed by recording compound action potentials (CAPs), measuring collagen levels using picrosirius red staining, and counting the number of myelinated axons proximal and distal to the repair. CAPs evoked by electrical stimulation distal to the repair were significantly smaller in all repair groups except for the low-dose IL-10 group, where they were not significantly different from that in controls. The area of staining for collagen had significantly increased in all repair groups except for the low-dose IL-10 group, which was not significantly different from that in controls. The myelinated fibre counts were always higher distal to the repair site, but there were no significant differences between groups. We conclude that administration of a low-dose of IL-10 to a site of sciatic nerve repair reduces scar formation and permits better regeneration of the damaged axons.

Inflammatory cell accumulation in traumatic neuromas of the human lingual nerve.

OBJECTIVE: To quantify the accumulation of inflammatory cells in traumatic neuromas of the human lingual nerve, and to establish any correlation with the patients' reported symptoms of dysaesthesia. DESIGN: Using fluorescence immunohistochemistry, the extent of any chronic inflammatory infiltrate was quantified in human lingual neuroma specimens removed from 24 patients at the time of microsurgical nerve repair. A pan-leucocyte marker (CD45) and a specific macrophage marker (CD68) were used, and comparisons made between neuromas-in-continuity (NICs) and nerve-end neuromas (NENs) in patients with or without symptoms of dysaesthesia. RESULTS: CD68 and CD45 labelling was significantly associated with areas of viable nerve tissue in neuromas and the CD68 labelling was significantly higher in NICs than NENs. CD68 labelling density tended to decrease with increasing time after the initial nerve injury, but this correlation was only significant for labelling associated with viable nerve tissue in NENs. No significant difference was found between the level of CD68 or CD45 labelling in patients with or without symptoms of dysaesthesia. CONCLUSION: This study has demonstrated the presence of inflammatory cells within traumatic neuromas of the human lingual nerve. These cells were found to be closely associated with regions of viable nerve tissue, but there was no correlation with the patients' clinical symptoms.

The effect of antibodies to TGF-beta1 and TGF-beta2 at a site of sciatic nerve repair.

Scar formation at a site of nerve injury can cause a mechanical barrier to axonal regeneration and lead to the development of multiple axonal sprouts to form a neuroma. We have investigated the hypothesis that the application of a scar-preventing agent to a nerve repair site would enhance regeneration of the nerve and reduce neuroma formation. The left sciatic nerve was exposed under general anaesthesia in 18 adult Sprague-Dawley rats. In 12 animals, the nerve was sectioned and immediately re-approximated using four epineurial sutures, and in 6 of these animals neutralising antibodies to transforming growth factor (TGF)-beta1 and TGF-beta2 were injected into and around the repair site. The six other animals acted as controls. After 7 weeks, the outcome was assessed by recording compound action potential (CAP) ratios, measuring collagen levels using picrosirius red staining, and counting the number of myelinated axons proximal and distal to the repair. After repair alone, the mean percentage of area of staining (PAS) for collagen within the nerve had significantly increased. However, after repair with the administration of antibodies, the PAS was not significantly different from that in the sham controls. After administration of antibodies, the CAP ratios were significantly smaller than in controls but not after repair alone. In both nerve injury groups, the myelinated fibre counts were significantly increased distal to the injury site, but there was no difference between these two groups. We conclude that administration of antibodies to TGF-beta1 and TGF-beta2 reduced scar formation at the repair site but did not enhance regeneration of the nerve or reduce the development of multiple axonal sprouts.

Scarring impedes regeneration at sites of peripheral nerve repair.

We have investigated the effect of scarring at a site of peripheral nerve repair by comparing regeneration of the sciatic nerve in normal mice and two transgenic strains with an increased or decreased propensity for scarring. The outcome was assessed by quantifying collagen at the repair site, recording compound action potentials and counting myelinated nerve fibres on each side of the repair. We found that higher levels of collagen scar formation were associated with smaller compound action potentials, slower conduction velocities and a reduction in fibre numbers across the repair site. We conclude that scarring impedes regeneration at sites of nerve repair and suggest that this could be amenable to therapeutic manipulation.

The effect of carbamazepine on injury-induced ectopic discharge in the lingual nerve.

Previous studies have shown that the development of ectopic activity from damaged axons following nerve injury may contribute to the aetiology of sensory disturbances, including dysaesthesia. Pharmacological manipulation of this activity could provide a method of treatment for this intractable condition. In this study we have investigated the effect of carbamazepine, an anti-convulsant, as it is known to have membrane stabilising properties. In eight anaesthetised adult ferrets the left lingual nerve was sectioned and the animals allowed to recover for 3 days. Then, in terminal experiments under general anaesthesia, the nerve was re-exposed and electrophysiological recordings were made from spontaneously active units in fine filaments dissected from the nerve proximal to the injury site. Carbamazepine in a modified cyclodextrin (hydroxypropyl-beta-cyclodextrin) was administered intravenously in increments, in order to achieve a progressively increasing systemic concentration, and serum levels were determined at the point that activity ceased. Twenty-one spontaneously active units were studied, with conduction velocities of 2.1-28.9 m s(-1) and discharge frequencies of 0.25-15.3 Hz. Spontaneous activity ceased in 13 units with a serum concentration of carbamazepine ranging from 3.5 to 8.4 mg/l, which was within the normal therapeutic range (4-12 mg/l). Four units ceased activity with carbamazepine levels above the therapeutic range (15.4-17.2 mg/ml), but the remaining four continued to discharge throughout the recording period. These data suggest that systemic carbamazepine can reduce the level of spontaneous activity initiated in some axons following lingual nerve injury.

The effect of brain-derived neurotrophic factor on sensory and autonomic function after lingual nerve repair.

Brain-derived neurotrophic factor (BDNF) is important in the response to peripheral nerve injury and may enhance regeneration. We have assessed its role in the functional recovery of sensory afferents and autonomic efferents after repair of the chorda tympani and lingual nerves in the cat. Six months after entubulation repair, with or without the incorporation of BDNF at the repair site, the recovery of secretomotor and vasomotor efferents was determined by recording salivary flow from the submandibular gland and temperature changes on the tongue surface, each evoked by stimulation of the repaired nerve. Electrophysiological recordings from the lingual and chorda tympani nerves proximal to the repair were undertaken to characterise mechanosensitive, thermosensitive, and gustatory afferents. When compared with data from uninjured control animals, both repair groups showed changes in receptor sensitivity and spontaneous discharge, and persistent reductions in conduction velocity, proportion of gustatory and thermosensitive units, rate of salivary secretion, and vasomotor responses. Comparisons between the outcome of repair with or without BDNF revealed few differences. In the BDNF group, fewer units in the chorda tympani responded to gustatory or thermal stimuli and the sensitivity of the gustatory units was lower. The conduction velocity of afferents in the lingual nerve was also lower, but the mechanoreceptive field size was higher. Thus, despite its known trophic role in the gustatory system, BDNF had not enhanced recovery of these or other fibre populations. We conclude that the application of BDNF to a site of lingual nerve repair has a negative effect on the long-term outcome.

The effect of triamcinolone hexacetonide on the spontaneous and mechanically-induced ectopic discharge following lingual nerve injury in the ferret.

Investigations into the aetiology of nerve injury-induced dysaesthesia have revealed the development of spontaneous and mechanically-induced activity from damaged axons. Pharmacological manipulation of this activity could provide a method of treatment for this intractable condition. This study has investigated the effect of a corticosteroid applied to the injury site, as these agents are known to reduce inflammation and scarring. In 24 anaesthetised adult ferrets the left lingual nerve was sectioned and the animals allowed to recover. In eight of these animals the nerve was re-exposed under anaesthesia after 1 month and 100 microl of corticosteroid (triamcinolone hexacetonide, 20 mg/ml) was injected into and around the injury site. In eight others, 100 microl of the steroid carrier was injected, and the eight remaining animals were used as controls. In terminal experiments under general anaesthesia, 3 months after the initial injury, electrophysiological recordings were made from axons in fine filaments dissected from the nerve central to both the injury site and junction with the chorda tympani nerve. Spontaneous activity (SA) was found in approximately 13% of units in control animals, 12% following the application of steroid, and 14% in the carrier group. Mechanically-induced activity at the injury site was found in approximately 13% of units in controls, significantly fewer after the application of steroid 4% (P<0.001) and 12% in the carrier group. These data suggest that local application of the corticosteroid triamcinolone hexacetonide could reduce the level of mechanically-induced, but not spontaneous, dysaesthesia following lingual nerve injury.

The effect of nerve growth factor on functional recovery after injury to the chorda tympani and lingual nerves.

Nerve growth factor (NGF) is known to ameliorate central changes and enhance the regeneration of damaged axons in the early stages after peripheral nerve injury. We have assessed the long-term outcome of placing NGF at a nerve repair site by determining the functional characteristics of several groups of sensory afferent and autonomic efferent fibres in the cat lingual nerve. Six months after entubulation repair, with or without the incorporation of NGF, the recovery of secretomotor and vasomotor efferents was determined by recording salivary flow from the submandibular gland and temperature changes on the tongue surface, each evoked by stimulation of the repaired nerve. Electrophysiological recordings from the lingual and chorda tympani nerves proximal to the repair allowed characterisation of mechanosensitive, thermosensitive and gustatory afferents. When compared with data from uninjured control animals, both repair groups showed changes in spontaneous discharge and persistent reductions in conduction velocity, receptor sensitivity, proportion of gustatory units, and rate of salivary secretion. Comparisons between the outcome of repair with or without NGF revealed few differences. In the NGF group the conduction velocity of afferents in the lingual nerve was lower, and the level of spontaneous activity was higher. However, NGF appeared to preferentially enhance the regeneration of thermosensitive afferents, suggesting that it may play a role in determining the phenotypic profile of the regenerating axonal population. This suggests that future therapeutic enhancement of regeneration after peripheral nerve injury may require a combination of factors to encourage regeneration of specific fibre groups.

An electrophysiological study into the effect of neurotrophin-3 on functional recovery after lingual nerve repair.

OBJECTIVE: Neurotrophin-3 (NT-3) is known to ameliorate central changes that result from peripheral nerve injury and may promote regeneration of myelinated axons. We have assessed its role in the functional recovery of sensory afferents and autonomic efferents after repair of the chorda tympani and lingual nerves in the cat. DESIGN: Six months after entubulation repair, with or without the incorporation of NT-3 at the repair site, the recovery of secretomotor and vasomotor efferents was determined by recording salivary flow from the submandibular gland and temperature changes on the tongue surface, each evoked by stimulation of the repaired nerve. Electrophysiological recordings from the lingual and chorda tympani nerves proximal to the repair allowed characterisation of mechanosensitive, thermosensitive and gustatory afferents. RESULTS: When compared with data from uninjured control animals, both repair groups showed persistent reductions in conduction velocity, receptor sensitivity, spontaneous discharge, proportion of gustatory and thermosensitive units, and rate of salivary secretion. Comparisons between the two repair groups revealed that in the NT-3 group, salivary secretion rate was lower and the activity evoked in the chorda tympani by gustatory or thermal stimuli was lower, but the spontaneous discharge rate was higher. Mechanosensitive units in the lingual nerve had slower conduction velocities but the mechanoreceptive field size, adaptation time and discharge frequency had increased. CONCLUSIONS: Despite its known trophic role in the lingual somatosensory system, NT-3 did not enhance functional recovery from injury and had a negative effect on the long-term outcome for sensory and autonomic fibres.

Current management of damage to the inferior alveolar and lingual nerves as a result of removal of third molars.

In this review we present algorithms to guide the clinical management of patients who sustain damage to the inferior alveolar or lingual nerves during the removal of lower third molars. Monitoring recovery using simple sensory testing allows those patients who may benefit from some form of intervention to be identified. There is good evidence that some surgical procedures produce worthwhile improvements in sensation but management of nerve injury-induced dysaesthesia remains problematic.

Peripheral mechanisms for the initiation of pain following trigeminal nerve injury.

Injury to a branch of the trigeminal nerve may lead to the development of chronic pain in the affected area. The etiology of this condition is not clear, but there is strong evidence to suggest that spontaneous and mechanically induced neural discharge from the injury site plays a crucial role. In laboratory studies, we have characterized this discharge following injury to the inferior alveolar or lingual nerves and have shown a temporal association with the accumulation of neuropeptides in the damaged axons. Substance P, calcitonin gene-related peptide, and vasoactive intestinal polypeptide were all found to be capable of increasing the discharge when applied systemically, and enkephalin caused a decrease. There were also changes in the expression of specific sodium channels and nitric oxide synthase, both at the injury site and in the trigeminal ganglion. Studies on lingual nerve neuromas taken from patients undergoing nerve repair also revealed accumulation of peptides, as well as inflammatory and structural changes, but the presence of these features did not correlate directly with the reported symptoms. The application of corticosteroids to an experimental injury site decreased the mechanically induced discharge, and the anticonvulsant carbamazepine reduced the spontaneous discharge in some axons. Some of the responses that result from damage to a branch of the trigeminal nerve appear to differ from those that follow damage to other peripheral nerves. These differences will need to be taken into account when developing new therapeutic approaches for the management of injury-induced trigeminal pain.