Abstract
OSMF is a precancerous condition of the oral cavity. Cons umption of Areca nut in quid has been proved to be the most consistent factor. To assess middle ear function in OSMF patients by audiometry and tympanometry. Two Hundred patients of < 40 years of age with OSMF were examined and followed by PTA and impedance audiometry. Impaired mobility was seen in 20(10%) ears, and retraction of tympanic membrane was found in 36(18%) ears. Clinical staging was done in four stages. Majority of the patients were males (58%) in the age group of 21–30 years belonging to stage III (38%) and IV (26%) respectively. PTA showed varying degrees of hearing loss in 73 (36.5%) ears. In Grade I, mild hearing loss was seen in 10 (35.71%) ears and moderately severe hearing loss was in 5 (11.36%) ears whereas in Grade II mild hearing loss in 11(25%) ears. Grade III and IV showed mild hearing loss in 11(14.47%) and 12 (23.07%) respectively. Tympanometry revealed type A curve in 126 (63%) ears followed by C curve in 50 (25%) and B curve in 24 (12%) ears. In patients of OSMF, there is involvement of palatal/paratubal muscles in the fibrosis process, which causes eustachian tube malfunction leading to disturbed middle ear functions and negative middle ear pressure. Most patients of oral submucous fibrosis showed direct association with grade of hearing impairment and eustachian tube dysfunction. Higher clinical grades, both clinically and histologically showed similar findings thereby we concluded that if the disease is treated early, preventing patients from having higher grades of disease, involvement of ear can be avoided, and patients can be saved from hearing impairment.
Keywords: Oral submucous fibrosis, Middle ear function, Palatal muscles, Paratubal muscles
Introduction
Oral submucous fibrosis has been defined as an insidious, chronic, progressive, scarring, precancerous condition affecting the oral cavity and extending up to the pharynx and oesophagus. OSMF has been well established in Indian medical literature since the time of Sushruta– a renowned Indian physician who lived in the era of 600 B.C and was termed as “Vidari”. In modern literature it was first described by Schwartz [1], who coined the term atrophica idiopathica mucosa oris to describe an oral fibrosing disease, he discovered in 5 Indian women from Kenya. In India, first case was reported by Joshi [2], and he named it “Submucous fibrosis of the palate and pillars.” This condition has also been referred as idiopathica scleroderma of the mouth [3], and idiopathic palatal fibrosis [4] In India, the prevalence increased over the past four decades from 0.03% to 6 0.42%. Data published in a study [5] reported an estimate of 5 million OSMF patients in India (0.5 percent of the Indian population). The rate varies from 0.2 to 2.3% in males and 1.2 to 4.57% in females in Indian communities as studied [6]. Oral submucous fibrosis is widely prevalent in all age groups and across all socioeconomic strata in India. The occurrence of this condition in children is extremely rare. Youngest case reported was a 4- year- old girl [7].
Shear et al. [8] evaluated correlations between betel nut chewing and the onset of oral submucous fibrosis. Other described other etiological factors like, autoimmune, genetic, environmental, vitamin B complex, iron deficiency and excessive chilly consumption. However, the most consistent factor identified through epidemiological studies is areca nut consumption in form of quid [9–11]. Quid is defined as ‘a substance, or mixture of substances, placed in the mouth or chewed and remaining in contact with the mucosa, usually containing one or both of the two basic ingredients, tobacco and/or areca nut, in raw or any manufactured or processed form [12] Excessive spicy food and chillies consumption is also said to play an important role in the oral submucous fibrosis. (Fig. 1).
Fig. 1.
a Fibrotic bands over soft palate. b Dense fibrotic bands over retromolar trigone and buccal mucosa
The most frequently affected locations in oral submucous fibrosis are the buccal mucosa and the retromolar areas [13]. It also commonly involves the soft palate, palatal fauces, uvula, tongue, and labial mucosa. Fibrotic changes of the pharynx, esophagus and paratubal muscles of eustachian tubes have also been observed. It is generally believed that oral submucous fibrosis originates from the posterior part of the oral cavity and subsequently involves the anterior locations. A study on the regional variations of this condition pointed out that such an observation would depend on whether the areca nut juice and the quid are swallowed or spat out. The clinical picture of OSMF is varied and the early features include burning sensation, intolerance to hot and spicy food, hyper salivation/ xerostomia, and mucosal blanching with marble like appearance. Other features are vesiculations, ulcerations, pigmentation change and recurrent stomatitis. Histologically there is infiltration of inflammatory mediators. OSMF is associated with juxta-epithelial inflammatory reaction which is followed by changes in fibroelastic properties of lamina propria [14]. This early clinical presentation is because of fibrosis by deposition of fine fibrils of collagen, hypertrophic fibroblasts in the lamina propria and the submucosa along with loss of rete pegs resulting in increased loss in tissue mobility [15, 16]. With advancing pathology, the mucosa becomes leathery and inelastic with palpable fibrous bands by focal lysis and hyper-concentration of myofilaments along with fatty deposition between muscle bundles resulting in trismus and inability to open mouth [16, 17]. Eventually, OSMF leads to difficulty in swallowing, hyper nasality of voice, hearing defects and defective gustatory sensation [18]. There is very less information about effects of fibrosis of adjoining areas of oral cavity like oropharynx, pharynx, eustachian tube opening and esophagus or vocal cords [19]. It is one of the most important precancerous condition of oral cavity [15]. There is increased secretion of growth factors, deposition of fibroblasts and constriction of blood vessels along with tissue oedema and decreased activity of antifibrotic cytokines. OSMF is seen to cause degenerative changes in muscle fibers in the involved areas [16, 20].
The fibro-cartilaginous pharyngeal end of eustachian tube opens into the lateral wall of nasopharynx. This opening of the tube is functionally obstructed or collapsed at rest. When the eustachian tube functions normally, intermittent active dilatation (opening) of the tube maintains near- ambient pressures in the middle ear. Under physiologic conditions, the fluctuations in ambient pressure are bi-directional (i.e., either to or from the middle ear), relatively small in magnitude, and not readily appreciated [11]. Tensor veli palatini and levator veli palatine are the important muscles attached to the eustachian tube and soft palate. Eustachian tube musculature and its relation to the cartilaginous opening into the nasopharynx is a dynamic entity. In majority of OSMF patients, there is fibrosis of soft palate leading to its shortening and atrophy and involvement of the palatal muscles leads to impaired patency. This results in failure of eustachian tube to effectively regulate air pressure. If untreated, as this condition gradually worsens with time, air pressure in middle ear becomes more negative leading to hearing impairment.
This study has been planned to observe the effect of OSMF on middle ear function by pure tone audiometry and Tympanometry, taking into consideration the fibrosis of palatal and paratubal muscles because of OSMF and to comparatively evaluate middle ear function with different clinical and histological stages of OSMF (Fig. 2).
Fig. 2.
Various degree of reduced mouth opening
Material & Methods
This prospective study was carried out in Department of Otorhinolaryngology and Head Neck Surgery of a tertiary health care hospital in India after taking permission from Institutional ethical clearance committee. This study was carried out from October 2017 to March 2019. Patients of age less than 40 years who were clinically diagnosed as OSMF were included in the study. A written, informed consent was obtained after explaining the patients about the study. All the patients with limitation of mouth opening due to other causes like odontogenic infections and joint disorders along with patient with history of and/or evident hearing loss due to any other cause were excluded. Cases with tympanic membrane perforations, previous ear surgery, having mixed or sensorineural hearing loss, middle ear infections, nasal or oropharyngeal mass, patients with cleft palate were also excluded. In the form of a questionnaire, a detailed history and demographic data was recorded. A detailed history of each patient was taken including the duration, type & frequency of the chewing habit. The mouth opening was recorded using a graduated vernier caliper, to measure the distance between the upper and lower central incisors edges at maximal unaided mouth opening, taking the mean of three readings. Oral cavity was palpated to assess the extent of fibrosis. The clinical and functional staging was done as per protocol laid down by Haider et al. [21].
Clinical Staging: Stage I-Mouth opening ≥ 30 mm, Stage II-Mouth opening ≥ 20 mm, Stage III-Mouth opening 11–19, Stage IV-Mouth opening ≤ 10 m.
Procedure
All cases were examined in detail and relevant findings were recorded as per proforma annexed. Valsalva test was performed to inspect the mobility of tympanic membrane and to assess the patency of Eustachian tube. Patient was seated and asked to do Valsalva maneuver. The outward bulging of Tympanic membrane, if present, was noted with the help of Siegel’s speculum or otoscope. During compression, the triangular light reflex changes shape and the handle of malleus moves. If it does not change or move, there is evidence of complete loss of mobility of the tympanic membrane. The condition of the tympanic membrane and retraction, if any, was recorded.
Audiometric assessment was performed using a clinical audiometer- Primus Auditdata calibrated according to ISO standard in a sound treated room. The frequencies selected for the purpose were 125–8000 Hz. The frequencies were tested in the following order- 1000, 2000, 4000, 500, 250, 125. The degree of hearing loss was based on the classification recommended by WHO. Impedance audiometry using Impedance audiometer INTERACOUSTICS AT235 was done to assess the patient`s ability to equalize pressure differences between the surroundings and the middle ear, which is called the ‘Tube function’. If the patient’s tympanic membrane is intact, this measurement is performed in AUTOTYMP mode. The audiometer can automatically give the patient a constant over or under pressure, of ± 200 daPa, in the auditory canal. The patient was made to swallow 8–10 times so that the over/under pressure which the tight tympanic membrane had caused in the middle ear was equalized. A compliance graph was recorded. The middle ear pressure now moved in the opposite direction of the static pressure which was present when the patient swallowed. Thus, the shifted compliance peak showed that the Eustachian tube function is normal. No shift in the compliance peak indicated poor Eustachian tube functions. If the patient was able to equalize the pressure, the Eustachian tube functions were normal and the inability to equalize the pressure were recorded as poor Eustachian tube function. In each patient a small surgical biopsy was taken from paratubal area with the help of flexible fiber-optic naso-endoscope. The biopsy was sent for histopathological examination and the patients were staged accordingly.
Histological Staging: Stage I-Only inflammatory infiltrates, Stage II-Few fibroblasts in lamina propria with normal muscle fibers, Stage III-Loss of rete pegs, Stage IV-Abundance of fibroblasts with only few muscle fibers. The collected data was recorded, tabulated, analyzed, and statistically evaluated using statistical package for social service (SPSS version 23, USA) software for Microsoft windows.
Observations and Results
A total of 100 patients were included in the study. Age ranged was from 14 to 40 years with a mean age of 29.34 ± 34 years The increase in number of the patients in the second and third decade probably is due to increase in the habits of chewing of betel nut, quid and gutkha and smoking among teenagers and young adults out of curiosity or influence from elders of the family. Fifty two (52%) male patients were in the age group of 21–30 years while 14 (14%) of female patients were in the 31–40 age group. Male preponderance in the study could be because of reluctance of female patients in attending the OPD/ clinics repeatedly and less prevalence of tobacco/ pan masala chewing in them (Table 1).
Table 1.
Age and sex incidence
| Age group (in years) | n = 100 | ||
|---|---|---|---|
| Male | Female | Total cases | |
| No. (%) | No. (%) | ||
| 11–20 | 08 (8%) | 04 (4%) | 12 (12%) |
| 21–30 | 52 (52%) | 08 (8%) | 60 (60%) |
| 31–40 | 14 (14%) | 14 (14%) | 28 (28%) |
Ninety four (94%) patients had trismus due to fibrosis of the musculature of the oral cavity and pharynx, while 86 (86%) patients had intolerance to chillies & spicy food, followed by difficulty in protruding out tongue in 80 (80%) and 76 (76%) patients had burning sensation in mouth and repeated vesicle or ulcer formation. Twelve (12%) patients complained of itching in ears while 23(23%) had ear fullness, and 16(16%) decreased hearing. These ear complaints were probably due to the fibrosis of soft palate including the palatal muscles, causing Eustachian tube dysfunction (Table 2).
Table 2.
Clinical symptoms of 100 patients with oral submucous fibrosis
| Clinical features | No. of patients |
|---|---|
| Inability to open mouth completely | 94 (94%) |
| Intolerance to chillies, spices, hot & cold food | 86 (86%) |
| Difficulty in fully protruding out tongue | 80 (80%) |
| Burning sensation in mouth | 76 (76%) |
| Repeated vesicle or ulcer formation in oral mucosa | 76 (76%) |
| Excessive salivation | 16 (16%) |
| Dryness of mouth | 04 (04%) |
| Pain in throat | 04 (04%) |
| Decreased hearing | 00(00%) |
Multiple sites were involved in all the patients of submucous fibrosis. It is because most of the patients showed up in the clinic in advanced stages. Most common site of involvement was palate in 88 (88%), followed by retromolar trigone in 86 (86%), buccal mucosa in 74 (74%) and floor of mouth in 72 (72%) (Table 3).
Table 3.
Sites of oral submucous fibrosis in oral cavity/oropharynx
| Sites | Number of patients (%) |
|---|---|
| Palate | 88 (88%) |
| Retro molar trigone | 86 (86%) |
| Buccal mucosa | 74 (74%) |
| Fauces | 68 (68%) |
| Floor of mouth | 34 (34%) |
| Tongue and lips | 36 (36%) |
| Uvula | 54 (54%) |
Clinically, majority of the patients were in stage III of OSMF, followed by stage II and IV. Histologically, the predominant grades were III followed by II. Majority of male cases were seen in age group 21–30 years whereas women of age group 31–40 constituted higher number of cases. Usually in young age group prevalence of OSMF is rare but we had 12 patients from age group of 11–20 years. No statistical correlation was seen between Grading and age groups of study group (Table 4).
Table 4.
Clinical and histological grading of OSMF patients
| Severity of OSMF | 11–20 Years |
21–30 Years |
31–40 Years |
Total | P value | ||||
|---|---|---|---|---|---|---|---|---|---|
| M | F | M | F | M | F | ||||
|
Clinical grading |
Grade I | 04 | – | 04 | 01 | 05 | 02 | 16(16%) | 0.35 |
| Grade II | 01 | 03 | 07 | 02 | 06 | 05 | 24(24%) | ||
| Grade III | 02 | 01 | 29 | 03 | 01 | 02 | 38(38%) | ||
| Grade IV | 01 | – | 12 | 02 | 02 | 05 | 22(22%) | ||
| Total | 08 | 04 | 52 | 08 | 14 | 14 | 100(100%) | ||
| Histo grading | Grade I | 03 | 01 | 06 | 02 | 06 | 03 | 21(21%) | 0.43 |
| Grade II | 03 | 02 | 17 | 02 | 03 | 04 | 31(31%) | ||
| Grade III | 01 | 01 | 24 | 03 | 04 | 04 | 37(37%) | ||
| Grade IV | 01 | – | 05 | 01 | 01 | 03 | 11(11%) | ||
| Total | 08 | 04 | 52 | 08 | 14 | 14 | 100(100%) | ||
Out of total of 200 ears of 100 patients 164 (82%) had normal tympanic membrane while in 36 (18%) tympanic membranes were retracted, indicative of eustachian tube dysfunction probably due to palatal and paratubal muscles fibrosis. Tympanic membrane was mobile in 180 (90%) ears and mobility was impaired in 20 (10%) ears.
When compared clinically, there was normal hearing in 93 (63.5%) ears, while varying degrees of conductive hearing loss was present in 107 (36.5%) ears. Similar levels of hearing loss were seen in different clinical grades and the difference was statistically insignificant. On the other hand, when histological grading was taken in account, statistically it was seen that there was significant difference between hearing loss in lower and higher histological grade OSMF (p < 0.05) (Table 5).
Table 5.
Correlation of pure tone audiometry findings with severity of OSMF (N = 200 ears)
| Conductive Hearing loss in dB |
Normal (< 25) |
Mild (26–40) |
Moderate (41–55) |
Mod. Severe (56–70) |
Severe (70–90) |
Profound (> 91) | Total | P value ANOVA | |
|---|---|---|---|---|---|---|---|---|---|
|
Clinical staging |
Grade I |
13 (6.5%) |
09 (4.5%) |
04 (02%) |
06 (03%) |
– | – |
32 (16%) |
0.01 |
| Grade II |
24 (12%) |
11 (5.5%) |
07 (3.5%) |
06 (03%) |
– | – |
48 (24%) |
||
| Grade III |
40 (20%) |
22 (11%) |
08 (04%) |
06 (03%) |
– | – |
76 (38%) |
||
| Grade IV |
16 (08%) |
16 (08%) |
08 (04%) |
04 (02%) |
– | – |
44 (22%) |
||
| Total |
93 (41.5%) |
58 (29%) |
27 (13.5%) |
22 (11%) |
– | – |
200 (100%) |
||
|
Histo grading |
Grade I |
22 (11%) |
14 (07%) |
06 (03%) |
– | – | – |
42 (21%) |
0.02 |
| Grade II |
37 (18.5%) |
13 (6.5%) |
09 (4.5%) |
03 (1.5%) |
– | – |
62 (31%) |
||
| Grade III |
30 (15%) |
23 (11.5%) |
11 (5.5%) |
10 (05%) |
– | – |
74 (37%) |
||
| Grade IV |
04 (02%) |
08 (04%) |
02 (01%) |
09 (4.5%) |
– | – |
22 (11%) |
||
| Total |
93 (41.5%) |
58 (29%) |
27 (13.5%) |
22 (11%) |
– | – |
200 (100%) |
Tympanometry showed Type A curve in 126 (63.0%) ears with compliance < 2.c.c in 27 ears and > 2.c.c. in 99 ears, followed by C curve in 50 (25.0%) with compliance < 2.c.c in 38 ears and > 2.c.c. in 12 ears, B curve in 24 (12.0%) with compliance < 2.c.c in 19 ears and > 2.c.c. in 5 ears (Table 6).
Table 6.
Correlation of impedence audiometry with severity of OSMF
| OSMF grade |
A curve |
B curve |
C curve |
As curve |
Ad curve |
Total | P value | |
|---|---|---|---|---|---|---|---|---|
|
Clinical staging |
Grade I |
12 (6%) |
4 (2%) |
12 (6%) |
– | – |
28 (14%) |
0.10 |
| Grade II |
30 (15%) |
10 (5%) |
4 (2%) |
– | – |
44 (22%) |
||
| Grade III |
60 (30%) |
8 (4%) |
8 (4%) |
– | – |
76 (38%) |
||
| Grade IV |
24 (12%) |
2 (1%) |
26 (13%) |
– | – |
52 (26%) |
||
| Total |
126 (63%) |
24 (12%) |
50 (25%) |
– | – |
200 (100%) |
||
|
Histo grading |
Grade I |
31 (15.5%) |
05 (2.5%) |
06 (3%) |
– | – |
42 (21%) |
0.01 |
| Grade II |
45 (22.5%) |
06 (3%) |
11 (5.5%) |
– | – |
62 (31%) |
||
| Grade III |
46 (23%) |
08 (4%) |
20 (10%) |
– | – |
74 (37%) |
||
| Grade IV |
04 (2%) |
05 (2.5%) |
13 (6.5%) |
– | – |
22 (11%) |
||
| Total |
126 (63%) |
24 (12%) |
50 (25%) |
– | – |
200 (100%) |
In Clinical Grade IV OSMF, type C curve was predominant 26(50%) followed by A curve 24(46.16%). In Grade II and III OSMF, A curve 30(68.18%) and 60(78.94%) was present in majority of patients respectively followed by B curve. In Grade I OSMF there was equal distribution 12(42.85%) of A and C curve. The tympanometry findings did not show any statistically significant difference between various clinical grades. In histological grade IV, 13 patients showed type C curve while 20 patients had type C curve in Grade III OSMF, We observed that C curve was more in grade III, IV whereas on clinical grading, C curve was seen mostly in Grade IV. This difference was statistically significant.
Discussion
Oral submucous fibrosis is classified as an oral, potentially malignant disease and was described for the first time by Joshi [2] in detail. It is a disorder in which normal tissue is altered by an external force and the changes may result into malignant transformation of the affected tissue.
Most of the patients in the present study diagnosed with oral submucous fibrosis were found to be in the second decade (60%) and in third decade (28%) of life. Our data correlates with the study of Gupta et al. [19], Saurabh Goel et al. [22] and Kalbande et al. [15] who reported that maximum number of patients were in second and third decade of life. Merchant et al. [23] found average age of 49 years, with the youngest patient being 22 years while the oldest was 80 years old. In the present study male to female ratio was 2.84:1 showing male predominance. Our findings were in accordance with Kalbande et al. [15] and Noor-ul-Wahab et al. [24] who also observed a male preponderance in their study. It was at variance with Joshi [2] and Sirsat & Khanolkar [25] who found a nearly equal distribution of cases among males and females and also with those of Pindborg et al. [26] and Robin Sabharwal et al. [27] as they reported a definite preponderance of females. Male preponderance in the present study, could be because of reluctance of female patients in attending the OPD / Clinics repeatedly and less prevalence of tobacco / Pan Masala chewing in them.
In the present study, out of 100 patients, 52 (52%) were in the habit of using gutkha only. This was followed by gutkha with betel quid, betel quid (with tobacco) only and pan masala with betel quid and smoking, by 26 (26%), 08 (08%), 14 (14%) patients respectively. We did not find a single patient who was not in the habit of taking tobacco in various forms. This study therefore supports the contention of Gupta et al. [17], Hazarey et al. [28], Saurabh Goel et al. [22] and Tak et al. [29], who pointed out that chewing of pan masala / gutkha was associated with earlier presentation of submucous fibrosis than betel quid use because of the difference in the tobacco content, the absence of betel leaves and much higher dry weight of pan masala / gutkha.
Jeng et al. [30] reported that areca nut ingredients are critical in the pathogenesis of OSMF and oral cancer via their stimulatory effects on the prostaglandins, cyclo-oxygenase-2(COX-2) production and associated inflammatory responses. Su [3], Caniff and Harvey [31], Murti [32], Babu et al. [6] concluded that chewing of betel nut and tobacco is most important factor in causation of oral submucous fibrosis. Sirsat and Khanolkar [25] demonstrated changes like oral submucous fibrosis patients after painting rat palate with 2% concentration of Capacin pepper which is an active ingredient of chillies. Most of the patients in our study presented with trismus (94%), intolerance to chillies, spices, hot and cold food (86%), difficulty in fully protruding out tongue (80%), burning sensation in mouth (76%), repeated vesicles or ulcers in oral mucosa (76%). Similar complaints were noted by Robin Sabharwal et al. [27] and Syeda Arshiya Ara et al. [33]. Wahi et al. [34] however reported dental problems to be the most common presenting complaint. Malignant transformation potential of OSMF was estimated to be 7.6% in India and 4–13% in other parts of world [35, 36] (Fig. 3).
Fig. 3.
Histopathology Of OSMF. a Deposition of fine fibrils of collagen, hypertrophic fibroblasts in the lamina propria and the submucosa along with loss of rete pegs b- Hypertrophic fibroblasts in the lamina propria and the submucosa c, d- Lysis and hyper-concentration of myofilaments along with fatty deposition between muscle bundles
The sites of involvement of oral submucous fibrosis have been differently reported in the literature. In our study buccal mucosa, retromolar trigone, palate, floor of the mouth, fauces, tongue, lips and uvula were found involved in descending order. Haider et al. [21] concluded that the bands are common at the back of the mouth in mild cases of OSMF and, as the disease increases in severity, are more likely to be found anteriorly as well. In this study, ear fullness (23%), itching in ears (12%) and impaired hearing was found in (16%) cases. These ear complaints were probably due to the fibrosis of soft palate including the palatal muscles causing Eustachian tube dysfunction. Excessive salivation (16%], dryness of mouth (04%) and pain in throat (04%) were present in our study population of OSMF.
Histological features seen in early cases of OSMF in our study were fine fibrils of collagen, edema, hypertrophic fibroblast, dilated and congested blood vessels and an infiltration of neutrophilic and eosinophilic granulocytes, which is followed by a down regulation of fibroblast, epithelial atrophy and loss of rete pegs and appearance of hyalinization with an infiltration of inflammatory cells in later stages which is in agreement of findings with similar studies [6] These pathological changes not only affect the mucosa and sub mucosa, but also the underlying muscles and deeper tissues. (Fig. 4).
Fig. 4.
Tympanograms of OSMF patients
Reports of muscle changes in OMSF using incisional biopsy sections using light microscopy are few. Gupta et al. [19] in their study planned to assess the histopathological changes in palatal and paratubal muscles by taking incisional biopsy from the soft palate in proven cases of OSMF and observed signs of chronic inflammation and fibrosis in most of cases. They also reported degenerative changes in 13.2% patients. El-Labban et al. [37] studied two groups of patients of OSMF and observed that patients with restricted mouth opening showed severe necrosis with muscle fibres showing complete loss of plasma membrane with intact basal lamina. This suggested that restricted mouth opening might depend on muscle degeneration and not only subepithelial fibrosis. Rooban et al. [38] in their study-stained tissue sections from OSMF patients with Masson’s Trichrome stain and observed a wide spectrum of findings ranging from fibrosis sub epithelially to most of fibres being replaced with fibrous tissue and only few muscle fibres remaining. Kumar et al. [39] in a hospital study of 75 patients correlated mouth opening with histopathological grading and concluded that there was no direct correlation between clinical stages and histopathological grading. Gupta et al. [19] who took biopsy specimens from soft palate reported degenerative changes in palatal and paratubal muscles in the form of atrophy, loss of cross striations and edema of myoepithelium [20]. Palatal and paratubal muscles [levator veil palatini, tensor veli palatine, tensor tympani and salphingopharyngeous], which regulate the patency and function of pharyngeal orifice, hence may get affected, resulting in impairment of function and patency of eustachian tube. This leads to pain in the ear along with mild to moderate conductive loss of hearing [32]. Binnie and Cawson [40] have reported a homogenous collagenous subepithelial zone along with degeneration of muscle fibers. Oliver et al. [41] reported the presence of dense collagen bundles that were randomly oriented and extended into the underlying striated muscles. El Labban and Caniff [37] in their study reported severe degenerative changes in high proportion of underlying submucosal muscle fibers exhibiting complete loss of plasma membrane with surrounding edematous fluid.
The mobility of the tympanic membrane, examined in 100 patients (200 ears), was found to be decreased in 20 (10%) ears. Tympanic membrane was found to be retracted in 36 (18%) ears. This finding of our study is like that of Gupta et al. [17] in the study of whom, 8% patients had retracted tympanic membrane. Retraction of the tympanic membrane may be contributed to Eustachian tube dysfunction. Eustachian tube dysfunction could be due to involvement of palatal and paratubal muscles in the process of fibrosis as described by Gupta et al. [19]. However, Schuknecht and Kerr [42] had postulated that the cartilaginous portion of the Eustachian tube can be involved due to chronic inflammation in nasopharynx causing partial or complete obstruction of the tube. Conductive deafness, in oral submucous fibrosis patients, is probably because of abnormal functioning of the eustachian tube, due to the involvement of paratubal muscles. Our findings are like that of Gupta et al. [19], Maulik Shah et al. [14], Chaudhary et al. [43] and Chandran et al. [44].
Impedance audiometry results show A-type curve in 156(78%) ears, B- type curve in 31 (15.5%) ears and C-type curve in 13 (6.5%) ears, while Gupta et al. [19] study recorded type-A curve in 80 (75.5%) ears with B-curve in 17 (16%) ears and C-type curve in 09 (8.5%) ears. Maulik Shah et al. [14] showed type-A curve in 42 (77.8%) ears, followed by type-C curve in 12 (22%) ears and type-B curve in none, unlike our study.
In our study we observed that degree of hearing loss is equally associated with clinical grading and histological grading. In We saw that more patients with grade II, III OSMF had mild to moderate hearing loss and Grade IV has patients showing moderately severe hearing loss. On analyzing tympanometry, graph C which showed retracted tympanic membrane retraction was associated more with histological grading. This study shows a direct relation between the progression of OSMF and hearing loss. Tensor veli palatini, levator veli palatini, tensor tymapni and salphingopharyngeous are known as palatal/ paratubal muscles. Involvement of these muscles in fibrotic process leads to shortening of the muscle fibers. Atrophic and degenerative changes in these muscle fibers impairs the patency and ventilatory function of the eustachian tube leading to middle ear dysfunction and decreased hearing.
Conclusion
Based on our study findings considering histology and clinical findings, it can be concluded that in patients of oral submucous fibrosis, there is involvement of palatal/paratubal muscles in the fibrosis process, which causes eustachian tube malfunction leading to disturbed middle ear functions and negative middle ear pressure. It is also to be emphasized that most patients of oral submucous fibrosis showed direct association with grade of hearing impairment and eustachian tube dysfunction. Higher clinical grades, both clinically and histologically showed similar findings thereby we concluded that even though no patient complained of hearing impairment, findings were otherwise, and the underling hearing issues would benefit from prompt early treatment in retarding or stopping the progression of the disease.
Funding
No funding was received by the authors for this study.
Declarations
Conflict of interest
The authors declare that they do not have any potential conflict of interest.
Ethical Approval
Ethical clearance was given by the institutional ethics committee for this study in accordance with the 1964 Helsinki Declaration.
Consent to Participant
A written informed consent was taken by all study participants taking permission for participation and publication of their data.
Footnotes
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Contributor Information
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Nidhi Johri, Email: johri.nidhi2712@gmail.com.
References
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