Role of female reproductive hormones estrogen and progesterone in temporomandibular disorder in female patients :Santosh R Patil, Nidhi Yadav, Mohammed Assayed Mousa, Abdalwhab Alzwiri, Mohamed Kassab, Rohit Sahu, Satish Chuggani, Journal of Oral Research and Review

ORIGINAL ARTICLE
Year : 2015 | Volume : 7 | Issue : 2 | Page : 41--43

Role of female reproductive hormones estrogen and progesterone in temporomandibular disorder in female patients

Santosh R Patil¹, Nidhi Yadav², Mohammed Assayed Mousa³, Abdalwhab Alzwiri¹, Mohamed Kassab⁴, Rohit Sahu⁵, Satish Chuggani⁵,
¹ Department of Oral Medicine and Radiology, College of Dentistry, AlJouf University, Sakakah, Aljouf, Saudi Arabia
² Department of Oral Medicine and Radiology, Jodhpur Dental College General Hospital, Jodhpur National University, Jodhpur, Rajasthan, India
³ Department of Prosthodontics, College of Dentistry, AlJouf University, Sakakah, Aljouf, Saudi Arabia
⁴ Department of Oral Surgery, College of Dentistry, AlJouf University, Sakakah, Aljouf, Saudi Arabia
⁵ CDCRI, Rajnandgaon, Chhattisgarh, India

Correspondence Address:
Santosh R Patil
Department of Oral Medicine and Radiology, College of Dentistry, AlJouf University, Sakakah, Aljouf
Saudi Arabia

Abstract

Aim: The aim of the present study is to investigate the role of female reproductive hormones estrogen and progesterone in temporomandibular disorder (TMD) in female patients. Materials and Methods: Serum estrogen and progesterone levels of 200 female participants who had varying grades of TMD were measured by enzyme immunoassay competition method in the luteal phase of menstrual cycle. Results: Mean serum concentration of estrogen was 302.1 ± 3.16 pg/mL, and the mean serum concentration of progesterone was 1.68 ± 38.3 ng/mL. Mean serum levels of estrogen and progesterone increased with increasing severity of TMD. Conclusion: Increased serum levels of estrogen and progesterone with increased grade of severity of TMD suggest role of these hormones as etiological factors for TMD.

How to cite this article:
Patil SR, Yadav N, Mousa MA, Alzwiri A, Kassab M, Sahu R, Chuggani S. Role of female reproductive hormones estrogen and progesterone in temporomandibular disorder in female patients.J Oral Res Rev 2015;7:41-43

How to cite this URL:
Patil SR, Yadav N, Mousa MA, Alzwiri A, Kassab M, Sahu R, Chuggani S. Role of female reproductive hormones estrogen and progesterone in temporomandibular disorder in female patients. J Oral Res Rev [serial online] 2015 [cited 2023 May 30 ];7:41-43
Available from: https://www.jorr.org/text.asp?2015/7/2/41/172492

Full Text

Introduction

Temporomandibular disorder (TMD) is a term that embraces a number of clinical conditions that involve the masticatory musculature or temporomandibular joint (TMJ), and associated structures. These clinical conditions are characterized by pain in the preauricular area, TMJ, or muscles of mastication, limitation or deviation in the mandibular range of motion, and TMJ sounds (clicking, popping, and crepitus) during mandibular movement, sometimes headache and facial pain. [1] Evidences suggest that this disorder is 1.5-2 times more prevalent in women than in men; 80% of patients treated for TMD are women. [2],[3],[4] It is also more prevalent in women of 20-40 years of age. This gender and age distribution of TMD raised questions about the link between its pathogenesis and the female hormonal axis. When extensive studies were carried out, it was found that endogenous reproductive hormones (especially estrogen) may play a pathophysiological role in TMD similar to many pain conditions (migraine headache) occurring predominantly in women. It was supported by the findings that:

The age of pain onset is almost always after pubertyPrevalence rates are higher in women than in menPrevalence is lower for women in the postmenopausal years than for those of reproductive age. [5],[6]

Later studies were done which focused on the role of exogenous hormone use (oral contraceptives, postmenopausal hormone replacement therapy) and the risk of TMD. [7] The results were that women with TMD reported higher use of exogenous hormones than controls. [8] In another study, it was found that the use of exogenous estrogen significantly increased the odds of having TMD. The odds of being a TMD case were approximately 30% higher among women receiving estrogen and 20% higher in those using oral contraceptives. [9] Certain points listed below will help in understanding the role of endogenous (especially estrogen) and/or exogenous female reproductive hormones (e.g., oral contraceptives, postmenopausal hormone replacement therapy) as an etiological factor for pain syndromes (migraines) and TMDs.

The synovial membrane, articular disk, and mandibular condyle harbor the presence of high-affinity estrogen receptors. Binding of estrogen to these receptors results in regulation of development and metabolism of the TMJ and associated structures such as bone, cartilage, and articular disk. [10] Estrogen increases joint laxity, at least during pregnancy, and this is thought to play a role in the development of some of these disorders. [11] Estrogen enhances inflammatory responses in the TMJ through interaction with various mediators of inflammation such as histamine, serotonin, substance P, platelet-activating factor, and nitric oxide. [12] These hormones may also act centrally to influence pain neurotransmission and not only TMJ but masticatory muscles are also the targets.Fluctuations of masticatory pain disorders, with pain nociceptive threshold variations across the hormonal cycle due to changes in the endogenous hormone levels, suggest their role in the modulation of pain levels. [1] Estrogen receptors are present on female's mast cell. When estrogen couples with its receptor, it causes degranulation to the cells. The substances released are nerve growth factor that stimulates production of substance P and vasoactive intestinal polypeptide that is the main neurotransmitters of the pain system.Estrogen and progesterone also increase secretions of prostaglandin, which inhibits central norepinephrine release (implicated in pain inhibitory system), sensitizes pain receptors (more pain receptors react to same stimulus), and increases neurogenic inflammation.

The aim of present study was to assess the role of serum estrogen and progesterone in female subjects with TMDs and to compare the serum level of estrogen and progesterone in mild, moderate, and severe cases of TMDs.

Materials and Methods

Two-hundred women in 20-40 years of age group participated in this study. Informed written consent was taken from all subjects after explanation of the aim of the study. Ethical clearance was obtained from the institutional committee. In the present study, only nonpregnant women, those already diagnosed with TMD, were included. Also women on oral contraceptives, diagnosed with any metabolic diseases (diabetes, hyperthyroidism), were excluded. Questionnaire proposed by Fonseca was used to evaluate the degree of TMD in the subjects. [13] The degree of disorder was graded as mild, moderate, and severe. A volume of 5 ml of blood was drawn from each participant during the luteal phase of menstrual cycle. The blood sample was put into plan tube without anticoagulant for serum separation. Serum separation was done by centrifuging the clotted blood samples at 3000 rpm for 10 min. Separated serum was stored in a deep freeze (−18°C) for further analysis. The assay principle combined an enzyme immunoassay competition method with final fluorescent detection. At the end of the assay, results were analyzed using pg/mL and ng/mL unit for estrogen and progesterone respectively.

Results

A total of 200 subjects were enrolled in the study; the patients' age was 14-40 years (mean ± standard deviation = 24 ± 8). Of the total subjects, 59 were grouped as severe, 66 as moderate, and 75 as mild cases of TMDs [Table 1]. The total mean serum estrogen concentration was 302.1 ± 3.16 pg/ml [Table 2]. The total mean serum progesterone concentration was 1.68 ± 38.3 ng/ml [Table 3]. The highest mean concentration of serum estrogen and progesterone was found in severe TMD cases (444.2 ± 3.57 pg/ml and 1.88 ± 41.9 ng/ml respectively). This finding was statistically significant for mean estrogen concentration with P = 0.02. It was not statistically significant for mean progesterone concentration with P = 0.84.{Table 1}{Table 2}{Table 3}

Discussion

Many studies have evaluated serum estrogen and progesterone levels in TMD subjects and compared them with control group of healthy subjects. Landi et al. found higher serum levels of 17β-estradiol (estrogen) in patients affected by TMD. Their finding of higher serum levels was also statistically significant when compared to healthy controls and findings in luteal phases of menstrual cycles in females. [14] Another study which evaluated estrogen (17β-estradiol) and progesterone serum levels in subjects affected by articular forms of TMD versus a control group of healthy subjects found significant differences in serum estrogen concentration of TMD subjects and healthy controls. [15] Both of these studies also reported that progesterone serum levels were not significantly different between cases and controls. [14],[15] These findings are similar to our study where we have found increased serum estrogen level in subjects with TMD and a statistically significant difference between estrogen levels of mild, moderate, and severe cases of TMDs. Similarly, we have found the progesterone levels to be not statistically significant in three grades of TMD. Our study has the drawback of not including a control group that other studies have included. Contradicting the findings of above mentioned studies, our study is a study conducted by Madani et al. who assessed the serum 17β-estradiol and progesterone levels in menstruating women affected by internal derangement of the TMJ and found the mean progesterone level was significantly higher in control group compared to women with TMD. They also found no significant difference in two groups regarding 17β-estradiol level, hence concluding, lower progesterone level may play a role in the development of TMD. [16]

Conclusion

Increasing serum levels of estrogen and progesterone with increasing grade of severity of TMD suggest a role of these hormones as etiological factors for TMD. Similar study with control group is required to strengthen this finding.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1	Dao TT, Knight K, Ton-That V. Modulation of myofascial pain by the reproductive hormones: A preliminary report. J Prosthet Dent 1998;79:663-70.
2	Locker D, Slade G. Prevalence of symptoms associated with temporomandibular disorders in a Canadian population. Community Dent Oral Epidemiol 1988;16:310-3.
3	Dworkin SF, Huggins KH, LeResche L, Von Korff M, Howard J, Truelove E, et al. Epidemiology of signs and symptoms in temporomandibular disorders: Clinical signs in cases and controls. J Am Dent Assoc 1990;120:273-81.
4	LeResche L. Epidemiology of temporomandibular disorders: Implications for the investigation of etiologic factors. Crit Rev Oral Biol Med 1997;8:291-305.
5	LeResche L, Dworkin SF, Saunders K, Von Korff M, Barlow W. Is postmenopausal hormone use a risk factor for TMD? J Dent Res 1994;73:186.
6	Von Korff M, Dworkin SF, Le Resche L, Kruger A. An epidemiologic comparison of pain complaints. Pain 1988;32:173-83.
7	LeResche L, Saunders K, Barlow W, Von Korff M, Dworkin SF. Does Oral Contraceptive Use Increase the Risk of Temporomandibular (TMD) Pain? 7 ^th World Congress on Pain; 1993. p. 294-5.
8	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.
9	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.
10	Wang J, Chao Y, Wan Q, Zhu Z. The possible role of estrogen in the incidence of temporomandibular disorders. Med Hypotheses 2008;71:564-7.
11	Westling L. Temporomandibular joint dysfunction and systemic joint laxity. Swed Dent J Suppl 1992;81:1-79.
12	Haskin CL, Milam SB, Cameron IL. Pathogenesis of degenerative joint disease in the human temporomandibular joint. Crit Rev Oral Biol Med 1995;6:248-77.
13	Fonseca DM. Craniomandibular dysfunction (CMD): Diagnostic By anamnesis [Master Dissertation]. Bauru School of Odontology of Bauru of the USP; 1992.
14	Landi N, Lombardi I, Manfredini D, Casarosa E, Biondi K, Gabbanini M, et al. Sexual hormone serum levels and temporomandibular disorders. A preliminary study. Gynecol Endocrinol 2005;20:99-103.
15	Landi N, Manfredini D, Lombardi I, Casarosa E, Bosco M. 17-beta-estradiol and progesterone serum levels in temporomandibular disorder patients. Minerva Stomatol 2004;53:651-60.
16	Madani AS, Shamsian AA, Hedayati-Moghaddam MR, Fathi-Moghadam F, Sabooni MR, Mirmortazavi A, et al. A cross-sectional study of the relationship between serum sexual hormone levels and internal derangement of temporomandibular joint. J Oral Rehabil 2013;40:569-73.