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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 26  |  Issue : 1  |  Page : 30-33

Possible role of estrogen in temporomandibular disorders in female subjects: A research study


Department of Oral Medicine and Radiology, Government Dental College, Srinagar, Jammu and Kashmir, India

Date of Submission23-May-2014
Date of Acceptance03-Aug-2014
Date of Web Publication26-Sep-2014

Correspondence Address:
Mirzada Bilal Ahmad
Department of Oral Medicine and Radiology, Government Dental College, Srinagar, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-1363.141846

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   Abstract 

Introduction: Temporomandibular disorders (TMDs) are common pain conditions that have the highest prevalence among women of reproductive age. The high prevalence of TMD pain among women, pattern of onset after puberty, and lowered prevalence rates in the postmenopausal years suggest that female reproductive hormones play an etiological role in TMDs. Aims and Objectives: To assess the possible role of estrogen in female subjects with temporomandibular disorders. Materials and Methods: A total of 195 subjects were examined for the study and divided into two groups: TMD positive and TMD negative subjects, which were further divided into women of reproductive age (20-40 years) and postmenopausal women. The serum estrogen (β-estradiol) level was estimated in both the groups. In reproductive women, the serum estrogen level was estimated in the follicular phase. Conclusion: A statistically significant association was found between the female sex hormone estrogen (β-estradiol) level and temporomandibular disorders.

Keywords: Estrogen, temporomandibular disorder, women


How to cite this article:
Chalkoo AH, Ahmad MB. Possible role of estrogen in temporomandibular disorders in female subjects: A research study . J Indian Acad Oral Med Radiol 2014;26:30-3

How to cite this URL:
Chalkoo AH, Ahmad MB. Possible role of estrogen in temporomandibular disorders in female subjects: A research study . J Indian Acad Oral Med Radiol [serial online] 2014 [cited 2020 Jan 22];26:30-3. Available from: http://www.jiaomr.in/text.asp?2014/26/1/30/141846


   Introduction Top


Temporomandibular disorders (TMDs) are loosely defined as an assorted set of clinical conditions, characterized by pain and dysfunction of the masticatory system. Pain in the masticatory muscles, in the temporomandibular joint (TMJ), and in the associated hard and soft tissues, limitation in jaw function, and sounds in TMDs are common symptoms. The disorder is 1.5-2 times more prevalent in women than in men and 80% of the subjects treated for TMDs are women. Pain onset tends to occur after puberty and peaks in the reproductive years, with the highest prevalence occurring in women aged 20-40 years. The gender and age distribution of TMDs suggests a possible link between its pathogenesis and the female hormonal axis or the estrogen level. [1] Endogenous estrogen affects the remodeling processes within the TMJ [2],[3],[4] possibly by changing the extracellular matrix in the joint [4],[5] or by changing the bone volume. Such changes can result in internal derangement of the TMJ. Beta estradiol is the most potent and dominant form of estrogen in human females, having biological effects through binding of the estrogen receptor alpha (ERα) and beta (ERβ). ER α and ER β act via binding to the DNA [4],[6] or by having biological effects through interaction with various kinases. Also both receptors can interact with membrane-associated molecules such as ion channels and G-protein coupled receptors, to alter the physiology of the cell. [4],[7]

The wide distribution of the estrogen receptors, ERα and ERβ, in the thymus, [4],[8],[9] bone marrow, [4],[10] and spleen [4],[11] suggests that it plays a modulatory role in the immune system, such as, modulating, differentiation, activation, proliferation, and antibody production from the lymphoid cells. [4],[12] Immune responses are important in joint disorders and an alteration in ERα and ERβ expression would have an impact on how estrogen affects the immune response in the TMJ. In particular, ERα is found in the articular cartilage and subchondral bone of the TMJ, which implies that estrogen directly acts on the cells in the TMJ tissue, to alter the gene expression and cellular physiology. [4],[13]


   Aims and Objectives Top


a. To assess the role of estrogen in female subjects with temporomandibular disorders

b. Compare the serum level of estrogen (β estradiol) in TMD positive (TMD +ve) and TMD negative (TMD −ve) subjects

c. Compare the serum level of estrogen of TMD +ve women of reproductive age (20-40 years) with postmenopausal women


   Materials and Methods Top


The study subjects were selected from those attending the Outpatient Department of Oral Medicine and Radiology, Government Dental College and Hospital, Srinagar. In the present study, 195 subjects were examined and divided into the following groups:

  • Subjects with and without signs and symptoms of temporomandibular disorder
  • Women of reproductive age (20-40 years)
  • Postmenopausal women <60 years of age


Inclusion criteria

Normal menstrual cycle of women of reproductive age

Exclusion criteria

Women who were on oral contraceptives.

Subjects having metabolic diseases (e.g. diabetes, hyperthyroidism).

Neurological disorders (e.g. trigeminal neuralgia).

Recent facial or cervical trauma.

Methodology

A thorough history was taken from all the subjects. All the subjects were examined for temporomandibular disorder. Joint tenderness, clicking, popping, grating, deflection/deviation, assisted, and unassisted painless mouth opening were noted. The serum estrogen (β estradiol) level was obtained in all the subjects.

Statistical analysis

Categorical data was analyzed using the chi-square/Fisher's exact test. Quantitative data was analyzed using two sample independent 't' tests and simple regression analysis. P ≤ 0.05 was considered to be statistically significant. SPSS 16.0 was used to carry out the statistical analysis of the data.


   Results Top


Among a total of 195 subjects, 52 subjects were found to be TMD +ve. In the TMD +ve subjects, 75% were in the reproductive age (20-40 years) and 25% of the subjects were in the post menopausal age. The Chi-square test performed on the data [Table 1], [Figure 1] confirmed a statistically significant association (P = 0.031) between TMDs and the reproductive age.
Figure 1: Distribution of subjects with respect to age

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Table 1: Comparison of reproductive age with postmenopausal age in TMD positive and TMD negative patients

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On the basis of the estrogen (β estradiol) level the subjects were classified into three groups, low, normal, and high, and compared with the age of the TMD +ve and TMD −ve subjects. [Table 2] and [Figure 2] clearly show that none of the subjects were found to be in the low estrogen group from the reproductive age and high estrogen group from the postmenopausal age. A P-value of less than 0.001 confirmed the strong association of estrogen of TMD +ve subjects with age. However, no association (P-value = 0.186) [Table 3] was found between the age and estrogen level of TMD −ve subjects, which indirectly supported the results of having a significant association between age and estrogen in TMD subjects.
Figure 2: Distribution of subjects showing TMD +ve and TMD −ve

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Table 2: Estrogen level comparison of reproductive age and postmenopausal age in TMD positive patients

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Table 3: Estrogen level comparison of reproductive age and postmenopausal age in TMD negative patients

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The simple regression model (y = a + b1x) was fitted to the data with and without the outlier, to detect the influence of the outlier on the regression coefficients [Figure 3] and [Figure 4]. The negative sign of the regression coefficient b1 indicated the significant negative correlation between age and estradiol level, which meant that as the age increased, the estradiol level decreased significantly, P = 0.012 and P = 0.004, with and without outlier, respectively [Table 4] and [Table 5].
Figure 3: Obtained data fi tted into the regression model with outlier

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Figure 4: Obtained data fi tted into the regression model without outlier

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Table 4: Simple linear regression model (with outlier)

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Table 5: Simple linear regression model (without outlier)

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The mean difference between the estrogen level obtained for the reproductive group of TMD +ve was 39 subjects with mean ± SD of 122.22 ± 77.21 and that of 81 subjects of TMD −ve was with a mean ± SD of 93.94 ± 27.98, which was found to be statistically significant (P = 0.001). Similarly the mean difference of the estrogen level in postmenopausal women of TMD +ve and −ve subjects was found to be statistically significant (P = 0.021) [Table 6] and [Table 7].
Table 6: Mean + SD of estrogen (β-estradiol level) in TMD +ve and TMD −ve subjects

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Table 7: Mean + SD estrogen level of post-menopausal women

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   Discussion Top


The findings in the study presented here were consistent with other studies reported so far, indicating an increased risk of TMDs in reproductive women aged 20-40 years. A higher percentage of TMD +ve subjects were found among the reproductive age group (20-40 years) and the serum estrogen levels were found to be significantly higher in the reproductive age group than in the postmenopausal group of TMD +ve subjects, which was in conformity with Landi's study. [14] None of the subjects were found to have lower estrogen levels in the reproductive age group. No association was found between the age and estrogen level of TMD −ve patients, which supported the significant association between age and estrogen in TMD subjects.

Several studies have examined the exogenous hormone use and the risk of TMDs among postmenopausal women. A 1997 audit of the records of a large health maintenance organization found that the use of exogenous estrogen significantly increased the odds of having TMDs, a risk that increased with higher doses of estrogen. This study also reported that the odds of being a TMD case were approximately 30% higher among women receiving estrogen, compared to those not exposed to it, and concluded that the use of oral contraceptives was associated with an increased risk of approximately 20%. [15] Abubaker's study found that women with TMDs reported higher use of exogenous hormones than the controls. [16] It was proposed that excessive exogenous ovarian hormones can put a woman at risk for TMDs. Endogenous hormones are essential for remodeling of the TMJ.


   Conclusion Top


There is a significant association between the estrogen level and TMDs, as is evident from the statistical analysis. The maximum numbers of subjects who are TMD +ve are in the reproductive age group and have a high level of estrogen compared to TMD −ve subjects. The regression analysis shows that as age increases, there is significant reduction in the estrogen level. Therefore, we believe that this is a women's health issue demanding further exploration and explanation.

 
   References Top

1.Warren MP, Fried JL. Temporomandibular disorders and hormones in women. Cells Tissues Organs 2001;169:187-92.  Back to cited text no. 1
    
2.Okuda T, YasuokaT, Nakashima M, Oka N. The effect of ovariectomy on the temporomandibular joints of growing rats. J Oral Maxillofac Surg 1996;54:1201-11.  Back to cited text no. 2
    
3.Yasuoka T, Nakashima M, Okuda T, Tatematsu N. Effect of estrogen replacement on temporomandibular joint remodeling in ovariectomized rats. J Oral Maxillofac Surg 2000;58:189-97.  Back to cited text no. 3
    
4.Puri J, Hutchins B, Bellinger LL, Kramer PR. Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint. Reprod Biol Endocrinol 2009;7:155.  Back to cited text no. 4
    
5.Smith GN Jr. The role of collagenolytic matrix metalloproteinases in the loss of articular cartilage in osteoarthritis. Front Biosci 2006;11:3081-95.  Back to cited text no. 5
[PUBMED]    
6.Marino M, Galluzzo P, Ascenzi P. Estrogen signaling multiple pathways to impact gene transcription. Curr Genomics 2006;7:497-508.  Back to cited text no. 6
    
7.Nilsson S, Mäkelä S, Treuter E, Tujague M, Thomsen J, Andersson G, et al. Mechanisms of estrogen action. Physiol Rev 2001;81:1535-65.  Back to cited text no. 7
    
8.Kawashima I, Seiki K, Sakabe K, Ihara S, Akatsuka A, Katsumata Y. Localization of estrogen receptors and estrogen receptor-mRNA in female mouse thymus. Thymus 1992;20:115-21.  Back to cited text no. 8
    
9.Törnwall J, Carey AB, Fox RI, Fox HS. Estrogen in autoimmunity: Expression of estrogen receptors in thymic and autoimmune T cells. J Gend Specif Med 1999;2:33-40.  Back to cited text no. 9
    
10.Smithson G, Couse JF, Lubahn DB, Korach KS, Kincade PW. The role of estrogen receptors and androgen receptors in sex steroid regulation of B lymphopoiesis. J Immunol 1998;161:27-34.  Back to cited text no. 10
    
11.Samy TS, Zheng R, Matsutani T, Rue LW 3 rd , Bland KI, Chaudry IH. Mechanism for normal splenic T lymphocyte functions in proestrus females after trauma: Enhanced local synthesis of 17-beta-estradiol. Am J Physiol Cell Physiol 2003;285:C139-49.  Back to cited text no. 11
    
12.McMurray RW. Estrogen, prolactin, and autoimmunity: Actions and interactions. Int Immunopharmacol 2001;1:995-1008.  Back to cited text no. 12
[PUBMED]    
13.Yamada K, Nozawa-Inoue K, Kawano Y, Kohno S, Amizuka N, Iwanaga T, et al. Expression of estrogen receptor alpha (ER alpha) in the rat temporomandibular joint. Anat Rec A Discov Mol Cell Evol Biol 2003;274:934-41.  Back to cited text no. 13
    
14.Landi N, Manfredini D, Lombardi I, Casarosa E, Bosco M. 17-beta-estradiol and progesterone serum levels in temporomandibular disorders patients. Minerva Stomatol 2004;53:651-60.  Back to cited text no. 14
    
15.LeResche L, Saunders K, Von Korff MR, Barlow W, Dworkin SF. Use of exogenous hormones and risk of temporomandibular disorder pain. Pain 1997;69:153-60.  Back to cited text no. 15
    
16.Abubaker AO, Raslan WF, Sotereanos GC. Estrogen and progesterone receptors in temporomandibular joint discs of symptomatic and asymptomatic persons: A preliminary study. J Oral Maxillofac Surg 1993;51:1096-100.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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