|Year : 2016 | Volume
| Issue : 4 | Page : 129-133
A comparative and observational assessment of gingival condition and il-1β level in vitiligo and nonvitiligo patients
Kharidhi Laxman Vandana, Halappa Sasvehalli Shalini, Roopa Patil
Department of Periodontics, College of Dental Sciences, Davangere, Karnataka, India
|Date of Web Publication||13-Feb-2017|
Kharidhi Laxman Vandana
Department of Periodontics, College of Dental Sciences, Davangere, Karnataka
Source of Support: None, Conflict of Interest: None
Introduction: Vitiligo is an autoimmune skin disorder that causes loss of skin pigment. Loss of skin pigment in oral mucosa may also become prominent and tend to be more noticeable in people with darker skin. There is much less information concerning this condition in gingiva. Therefore, an initial attempt has been made to compare clinical gingival status and biochemical assessment in vitiligo and nonvitiligo patients. Materials and Methods: This observational pilot study includes 45 patients of age group 20–40 years were divided as nonvitiligo pigmented gingivitis as observational 1 group, nonvitiligo nonpigmented gingivitis as control group, and vitiligo with gingivitis as observational 2 group. The clinical parameters assessed were plaque index, gingival index (GI), gingival bleeding index (GBI), dummett oral pigmentation index, and biochemical parameter such as gingival crevicular fluid (GCF) interleukin-1 beta (IL-1β) levels. Results: On intergroup examination using unpaired t -test and statistical analysis, vitiligo group showed highly significant results in GI (P < 0.001) and GBI (P < 0.001) than nonvitiligo group. Furthermore, the GCF IL-1β levels were found to be lesser (34.16 ng/ml) in vitiligo group as compared to nonvitiligo groups. Conclusion: At similar plaque level, higher gingival inflammation and bleeding were found in vitiligo patients. The loss of pigmentation of gingiva was evident in vitiligo patients. The possible defensive role of melanin is evident clinically.
Keywords: Gingivitis, interleukins, melanin, vitiligo
|How to cite this article:|
Vandana KL, Shalini HS, Patil R. A comparative and observational assessment of gingival condition and il-1β level in vitiligo and nonvitiligo patients. J Dent Res Rev 2016;3:129-33
|How to cite this URL:|
Vandana KL, Shalini HS, Patil R. A comparative and observational assessment of gingival condition and il-1β level in vitiligo and nonvitiligo patients. J Dent Res Rev [serial online] 2016 [cited 2022 Sep 28];3:129-33. Available from: https://www.jdrr.org/text.asp?2016/3/4/129/200018
| Introduction|| |
Vitiligo is an autoimmune skin disorder known as leukoderma that causes a loss of the skin pigment melanin (American Heritage Medical Dictionary 2002). Vitiligo is characterized by blanched or white dots, macules or patches of skin. The degree of pigmentation loss (depigmentation) in vitiligo varies in different individuals and may be mild (slight pigmentation) or severe (complete depigmentation). Although the skin is most likely to be affected, the hair, retina of the eyes, and mucous membrane of the mouth, nose, genital, and rectal tissue may also be affected. Like most autoimmune disorders, symptoms and the severity of the condition vary, changing over time.
Older theory is focused on the presence of melanocyte destroying autoantibodies contributing to vitiligo. Newer studies support the involvement of a cell-mediated autoimmune response related to an increase in suppressor T-cells (CD8 cells) and a decrease in helper T-cells (CD4 cells) in association with the presence of Type I cytokine. It has also been proposed that increased release of norepinephrine melanocytotoxin by the autonomic nerve endings near melanocytes causes their destruction. Approximately 2% of world populations (40–50 million people) have vitiligo. Vitiligo is more likely to occur in people with another autoimmune condition, particularly autoimmune thyroid disease, adrenal insufficiency, alopecia areata, which causes baldness and pernicious anemia. For instance, about 7% of people with Grave's disease develop vitiligo compared to a 1% rate among rate the general population. Studies show that 95% of those affected by vitiligo develop symptoms before the age 40, with most new patients between 10 and 30 years. Vitiligo occurs in all races, and it affects both the sexes equally.
Early symptoms of vitiligo include white or blanched patches of skin usually affecting the skin that exposed the sun. The white areas may blend into the skin and not be distinct, and the affected area may itch. Occasionally, the affected areas may have hypopigmented borders. Because vitiligo is often a progressive disorder, these patches tend to spread to other areas of the body. The rate at which the vitiligo spreads varies in different patients. Overall, most patients develop several areas of depigmentation on different areas of the skin. This is known as generalized vitiligo pattern. However, some patients develop a focal pattern of vitiligo, in which one or two areas of unpigmented skin persist for many years in the absence of other skin changes. Other patients may notice patches of vitiligo on only one side of the body, which is called a segmental pattern.
Segmental vitiligo usually occurs early in life and spreads rapidly. Nonsegmental vitiligo has a slower course. Often, early patches of vitiligo persist for life although there is no spreading.
Some patients with vitiligo may also develop premature graying or whitening of the hair, including scalp hair, eyelashes, eyebrows, axillary hair, pubic hair, and beard. Vitiligo often occurs around the body orifices such as the lips, genitals, areolas, nipples, and gingiva. Loss of pigment in the oral mucosa may also become prominent and tend to be more noticeable in people with the darker skin. Some patients report an exacerbation or worsening of symptoms in times of both physical and emotional stress, including the stress and sunburn.
Gingival involvement had earlier been reported in 1959 and 1998, respectively. Vitiligo generally is known to have no racial or sex preference, but it is considered to be more troublesome in dark skinned due to the marked contrast between normal and pigmented areas. Although in vitiligo loss of pigmentation of skin has been described, there is much less information concerning this condition in gingiva. Depigmentation of affected tissues occurs due to loss of melanocytes and while its precise etiology remains unknown. Stress, trauma, chemicals, hormonal changes, and ultraviolet rays have been implicated as potential precipitating factors. Vitiligo of oral tissues is very rare and literature (Medline) showed that 14 cases of oral cavity vitiligo or similar lesions have been reported till date.
It has been hypothesized that oral mucosa melanin provides a defense barrier by acting as a binder of toxic products such as free radicals and polycyclic compounds. Therefore, the oral melanocytes may act as scavenging antioxidants and prevent oxidative stress by literally scavenging radicals as they form.
Inflammatory mediators such as interleukin-1 (IL-1) are suggested to be a product of macrophages in the gingival tissues  and elevated in the inflamed gingival tissue. IL-1, like tumor necrosis factor-α, acts on endothelial cells to increase attachment of neutrophils, and monocytes  thereby aids in the recruitment of these cells into site of inflammation. For these reasons, a measurement of the levels of IL-1α and IL-1β produced in periodontal disease is important.
Based on the hypothesis of melanin defensive activity, the objective of this study aims to assess gingival status and cytokine IL-1β levels in vitiligo and nonvitiligo patients. The proposed null hypothesis states that the vitiligo will not influence the gingival inflammation.
| Materials and Methods|| |
In this observational pilot study, 45 patients of both the sexes between the age group of 20–40 years were selected from the Outpatient Department of College of Dental Sciences, Davangere, India. The study group were divided as nonvitiligo nonpigmented gingivitis as control group, nonvitiligo pigmented gingivitis as observational 1 group, and vitiligo with gingivitis as observational 2 group. Informed consent was taken from all the patients. The systemically healthy nonvitiligo and vitiligo patients were included in the study. The systemic conditions such as Addison's disease, Albright's syndrome, Peutz–Jeghers syndromes, and drug-induced reactions that are known to cause gingival melanin pigmentation; smokers, female pregnant patients, or lactating mother were excluded from the study.
Clinical assessment was carried out by single qualified clinician. Dummett's oral pigmentation was recorded for each patient to assess the degree of gingival melanin pigmentation. Assessment of plaque was done with plaque index (Silness and Loe) on the basis of plaque at the gingival area of the tooth. The presence or absence of gingival bleeding was determined by gentle probing of the gingival crevice with a UNC 15 periodontal probe (UNC 15 periodontal probe). Examinations were performed on four sites in each tooth (distofacial, facial margin, mesiofacial, and entire lingual margin). The presence of bleeding within 10 s indicated a positive score, which was expressed as a percentage of the total number of gingival margins examined (gingival bleeding index [GBI], Ainamo and Bay, 1975). Gingival index (GI) (Loe and Silness, 1963) was recorded (4 gingival scoring units per tooth) and subjects with mild to moderate degrees of gingivitis were included in the study. The same investigator carried out all clinical measurements.
Gingival crevicular fluid collection and analysis
The gingival crevicular fluid (GCF) samples were collected using microcapillary pipettes (Sigma-Aldrich Germany). The experimental area was isolated with cotton rolls and gently air-dried. The supragingival plaque was removed carefully without touching the gingiva, which might stimulate fluid flow, to minimize plaque contamination of the microcapillary pipettes. The micropipettes were placed just at the entrance of the gingival sulcus till 2.5 μl of the GCF was collected. The GCF was stored in 100 μl of phosphate-buffered saline at −20°C. Total amount of the pro-inflammatory cytokine IL-1β was analyzed by the enzyme-linked immunosorbent assay (ELISA) techniques following the manufacturer's instructions (Immunotech, France) by a qualified microbiologist who was blinded to the groups. IL-1β was expressed in nanograms.
All results were subjected to statistical analysis. Results were presented as mean ± standard deviation for quantitative data and unpaired t-test was used.
| Results|| |
A total of forty-five patients of both sexes in the age group of 20–40 years were included, fifteen patients in each group, nonvitiligo pigmented gingivitis (control), nonpigmented gingivitis, and vitiligo with gingivitis [Table 1].
For Dummett oral pigmentation index (DOPI), out of 15 vitiligo gingivitis cases, ten patients showed score of zero (pink gingiva with no pigmentation), four patients showed score of 0.5 (very mild pigmentation), and one patient showed score of 1 (slight pigmentation). DOPI score of nonvitiligo pigmented gingivitis was 3 (completely pigmented dark brown gingiva) and non vitiligo nonpigmented gingivitis was 0.
The mean plaque index score was higher in the nonvitiligo pigmented gingivitis cases (0.84 ± 0.42) and least was found in nonvitiligo nonpigmented gingivitis cases (0.63 ± 0.42). On intergroup comparisons, all three groups showed similar plaque levels were statistically nonsignificant (P > 0.05) [Table 2].
|Table 2: Comparison of various clinical parameters within each group (mean±standard deviation)|
Click here to view
The mean GI score was maximum in vitiligo minimally pigmented gingivitis cases (1.64 ± 0.37) and least was found in nonvitiligo pigmented gingivitis cases (0.89 ± 0.17). On intergroup comparisons of GI, nonvitiligo nonpigmented gingivitis versus vitiligo minimally pigmented gingivitis and nonvitiligo pigmented versus vitiligo minimally pigmented gingivitis were highly significant (P < 0.001); however, nonvitiligo pigmented gingivitis versus nonvitiligo nonpigmented gingivitis was statistically nonsignificant (P > 0.005) [Table 2].
The mean GBI score was maximum in vitiligo minimally pigmented gingivitis (86.2 ± 14.8) and least was found in nonvitiligo pigmented gingivitis (44 ± 8.9). On intergroup comparison, the GBI, nonvitiligo, nonpigmented gingivitis versus vitiligo minimally pigmented gingivitis and nonvitiligo pigmented gingivitis versus vitiligo minimally pigmented gingivitis were highly significant (P < 0.001); however, nonvitiligo pigmented versus nonvitiligo nonpigmented gingivitis was statistically nonsignificant (P > 0.05) [Table 2].
The GCF IL-1β levels were maximum in nonvitiligo nonpigmented group (64.60–65.75) followed by nonvitiligo pigmented gingivitis (control group), and least IL-1β level was found in vitiligo gingivitis group (34.16–46.35 ng/ml) [Table 3].
| Discussion|| |
Vitiligo is an autoimmune skin disorder known as a leukoderma that causes a loss of the skin pigment melanin; approximately 2% of world populations (40–50 million people) have vitiligo. However, its incidence across India ranges from 0.1% to >8.8%. Vitiligo is more likely to occur in people with another autoimmune conditions, particularly autoimmune thyroid disease, adrenal insufficiency, alopecia areata, which causes baldness and pernicious anemia. For instance, about 7% of people with Grave's disease develop vitiligo compared to a 1% rate among the general population. Studies show that 95% of those affected by vitiligo develop symptoms before the age 40, with most new patients between 10 and 30 years. Vitiligo occurs in all races, and it affects both the sexes equally. Although the skin is most likely to be affected, the hair, retina of the eyes, and mucous membrane of the mouth, nose, genital, and rectal tissue may also be affected.
Depigmentation of affected tissues occurs due to loss of melanocytes and while its precise etiology remains unknown. Stress, trauma, chemicals, hormonal changes, and ultraviolet rays have all been implicated as potential precipitating factors. Although in vitiligo loss of pigmentation of skin has been described, there is much less information concerning this condition in gingiva. Vitiligo effecting the oral tissue is very rare, Dayakar et al. in 2016 reported a case of vitiligo affecting only gingiva, in which the patient was otherwise absolutely asymptomatic.
The main reasons for this study are based on the hypothesis that melanin acts as a defensive barrier by binding to toxic products such as free radicals and polycyclic compound so that oral melanocytes may act as antioxidant scavenger and prevent oxidative stress by literally scavenging radicals as they form  in the oral cavity such as gingiva and palatal mucosa which are pigmented. Thus, this study was initiated to assess the clinical nature of gingival inflammation of vitiligo patient as compared to nonvitiligo patients at similar plaque levels.
A lacuna exists in literature regarding the comparative study of vitiligo and nonvitiligo pigmented and nonpigmented patients. This study is the first of its kind; however, Nilima and Vandana reported a study on evaluation of gingivitis with and without melanin pigmentation and estimation of GCF IL-1β using ELISA a clinical and biochemical study. In nonpigmented healthy and gingivitis groups, there was a positive correlation between plaque index, GI, and bleeding index versus the IL-1β levels in the pigmented healthy group. However, the pigmented gingivitis groups showed a negative correlation between the plaque index, GI, and bleeding index. Their study concluded that despite similar plaque levels, the GI, bleeding index, and the IL-1β levels did not show significant difference in both nonpigmented and pigmented healthy gingivitis groups. However, the negative correlation of inflammatory markers of clinical inflammation with the IL-1β levels in pigmented gingiva is thought provoking.
In the present study, all three groups demonstrated similar plaque levels, this is suggestive of the fact that at similar plaque levels, the gingival and GBI were measured.
The gingival inflammation was significantly higher in vitiligo patients as compared to nonvitiligo group. However, the gingival inflammation was found to be similar between nonvitiligo groups. The gingival bleeding was also observed to be similar to GI assessment in vitiligo and nonvitiligo groups. No comparative data exist in literature.
The maximum of vitiligo patients demonstrated zero score (66%) followed by 0.5 score (26.6%) and score one (6%). This is suggestive of the presence of gingival pigmentation to a minimal extent in vitiligo patients. Selection criteria in nonvitiligo pigmented and nonpigmented gingivitis were zero (pink gingiva without pigmentation) and three (completely pigmented dark brown gingiva), respectively.
The patients were grouped into three groups considering the pigmentation and vitiligo status, the basic idea behind this grouping is based on the objective of the study, i.e., whether melanin pigmentation could demonstrate the defensive potential against plaque-induced inflammation at the clinical level. The results of this study confirm the defensive role of melanin pigmentation, clinically by assessing the inflammation status of gingiva.
The possible reasons for increased gingival inflammation in vitiligo patients in the current study could be attributed to the following based on the hypothesis that melanin provides a defensive barrier the vitiligo patients with scanty/absence of melanin pigmentation demonstrated increased gingival inflammation. Another reason could be the decreased cell-mediated immunity as stress is one of the precipitating factors for vitiligo. There is increased bone loss and increased severity of periodontal disease associated with emotional stress and stressful life events.
The study results have supported the defensive potential of melanin; however, further studies are required to enhance and provide better evidence by including histologic, biochemical, and immunological markers along with clinical markers.
| Conclusion|| |
At similar plaque level, higher gingival inflammation and bleeding were found in vitiligo patients. The loss of pigmentation of gingiva was evident in vitiligo patients. The possible defensive role of melanin is evident clinically.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
American Heritage Students Medical Dictionary. United States: Houghton Mifflin Company; 2002.
Namazi MR, Phenytoin as a novel anti-vitiligo weapon, J Autoimmune Dis 2005;2:11.
Dummett CO. The oral tissues in vitiligo. Oral Surg Oral Med Oral Pathol 1959;12:1073-9.
Regezi JA, Sciubba J. Oral pathology clinical -pathological correlations, 2nd
ed. Philadelphia: WB Saunders. 1993:204.
Lawoyin D, Brown R, Reid E, Sam F, Obayomi T. Concurrent presentation of cutaneous and oral soft tissue vitiligo: a case report and literature review. The Internet Journal of Dental Science. 2006;5:1-4.
Hedin CA, Larsson A.In vitro
activation of amphibian dermal melanocytes by nicotine. Scand J Dent Res 1986;94:57-65.
Reade PC. Oral pigmentation in a group of Australian aborigines. J Dent Res 1962;41:510.
Iwata K, Inui N, Takeuchi T. Induction of active melanocytes in mouse skin by carcinogens: A new method for detection of skin carcinogens. Carcinogenesis 1981;2:589-93.
Center JM, Mancini S, Baker GI, Mock D, Tenenbaum HC. Management of gingival vitiligo with the use of a tattoo technique. J Periodontol 1998;69:724-8.
Faizuddin M, Bharathi SH, Rohini NV. Estimation of interleukin-1beta levels in the gingival crevicular fluid in health and in inflammatory periodontal disease. J Periodontal Res 2003;38:111-4.
Sehgal VN, Vitiligo SG. Compendium of clinico-epidemiological features. Indian j dermatol 2007;73:149-56.
Dayakar MM, Kumar J, Pai GP, Srivastava S. Gingival vitiligo: A very rare clinical entity. SRM J Res Dent Sci 2015;6:211-3.
Nilima S, Vandana KL. Melanin: A scavenger in gingival inflammation. Indian J Dent Res 2011;22:38-43.
Green LW, Tryon WW, Marks B, Huryn J. Periodontal disease as a function of life events stress. J Human Stress 1986;12:32-6.
[Table 1], [Table 2], [Table 3]