Microstomia Classification Essay

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1. Introduction

Scleroderma is a disorder of the connective tissue characterized by fibrosis of the skin, vascular abnormalities, and presence of auto-antibodies. It is a rare disease with a prevalence from 8 up to 30/100,000 inhabitants. Women are affected more frequently than men are, with a preponderance of 4:1 [1]. The etiological agent is still unknown, even if previous findings evidence that the fibrotic process could be activated by lesional fibroblast activation [2,3,4].

It can be divided into two major groups: localized scleroderma /morphea and systemic sclerosis (SSc). The former can be classified into four main subtypes (plaque, bullous, linear, and deep) according to morphological and clinical presentation and is traditionally considered as a skin-limited disease whose systemic involvement is rare. The latter is classified into three categories including limited cutaneous SSc, diffuse cutaneous SSc, and overlap syndrome. SSc differs from localized scleroderma because it is accompanied by Raynaud’s phenomenon, acrosclerosis, and internal organ involvement [5,6]. The extracutaneous manifestations include gastrointestinal tract, heart, lungs and kidneys: esophageal dysmotility, restrictive pulmonary disease, pulmonary hypertension, arthralgia, myopathy, myocardiopathy, and progressive renal insufficiency can be observed [7]. Raynaud’s phenomenon, i.e., vasospasm of fingers which results in change in color of fingertips as a response to cold or emotion, is often the initial presenting complaint occurring in more than 95% of SSc patients. Limited SSc is characterized by symmetric and progressive skin fibrosis of the distal upper extremities (fingers) whereas diffuse SSc patients often develop widespread, symmetrical fibrosis involving the proximal and distal extremities, trunk, and face [5,6,8].

Oral and facial tissues are often affected, presenting characteristic features. Most clinical manifestations begin with tongue rigidity and facial skin hardening, leading to a classic mask-like face, white thin lips, a sharp nose, and deep wrinkles [9,10]. Telangiectasia of facial skin and oral mucous membrane are produced from the vasospasm of the small vessels (Figure 1).

SSc patients also manifest periodontal involvement, demonstrated by increased pocket depths and gingival scores [11]. The study by Pischon et al. demonstrates higher periodontal clinical attachment loss in SSc patients if compared with healthy people, indicating a possible relationship between SSc and periodontitis [12]. The etiology of periodontal disease in SSc is unclear and several factors could contribute to periodontal involvement. An obliterative microvasculopathy was suggested [11]. Wood et al. [13] indicated a relation with the reduced vascularity, with resulting tissue ischemia in scleroderma individuals. An association of reduced mouth opening and presence of periodontal disease is supposed [13] but not confirmed by Chu et al. [14]. Xerostomia is a common finding with scleroderma patients, occurring as a result of fibrosis of the salivary glands. Dry-mouth symptoms can cause a high caries rate and an increased incidence of Candida infections [15]. Xerostomia could promote dental plaque accumulation and a reduced manual dexterity could be a cofactor in periodontal involvement in SSc patients.

The tongue can also become rigid so that speech and swallowing become difficult [16].

The main oral manifestation of SSc is microstomia (reduction of the oral opening), due to the sclerosis of perioral soft tissue (Figure 2). Clinically, it may impair social relationships, mastication, reduction of the mandibular movements, and proper oral hygiene. Consequently, a higher incidence of oral diseases such as caries, periodontal diseases or other type of oral infections is detected [17] and dental treatment could be more difficult or sometimes impracticable due to limited mouth opening [14,18].

Mandibular bone resorption is more often observed in patients with diffuse cutaneous SSc and causes marked facial sclerotic involvement and limitation in mouth opening [19,20]. Systematic radiographic screening of different groups of SSc patients showed a resorption incidence of the mandible of 20%–33% of the examined mandibles [19]. In 1959, Taveras noted radiographic evidence of bone resorption of the angles of the mandible and similar areas of resorption have been reported to affect the coronoid processes and the zygomatic arches at the sites of the muscle attachments. This was explained by muscle contracture secondary to fibrotic changes [21]. However, the current hypothesis suggests that bone resorption could be caused by a multifactorial process including microvasculopathy and pressure ischaemia, secondary to thickening skin and muscle atrophy. Moreover, atrophic and fibrotic modifications of the synovia may also influence the temporomandibular joint (TMJ) involvement in course of SSc [22].

Previous studies investigated the difficulty in mandibular movements in SSc patients. Nagy observed that the interincisal distance was significantly decreased in systemic sclerosis patients when compared with healthy controls [23] (Figure 3).

Marmary found that the majority of SSc patients revealed limitation in mouth opening [24].

Only a few studies reported a complete analysis of signs and symptoms of temporomandibular disorders (TMD) [18,25].

The aim of this study was to investigate the prevalence of both oral symptoms and manifestations and TMD symptoms (TMDs) and signs in SSc patients compared with healthy people, thus giving a complete survey of facial involvement in course of scleroderma.

2. Results

2.1. Characteristics of SSc Patients and Controls

Patients’ age ranged between 24 and 80 years, 92.5% were female and 7.5% were male in both groups. The two groups, matched for age and sex, results were similar for sociodemographic aspects, except occupation (χ2 = 11.036 p = 0.026). Among SSc patients housewives were prominent, while among controls office workers were prominent (Table 1).

The prevalent form of disease was the diffuse one, found in the 82.5% of SSc patients, the age at diagnosis varied between 8 and 74 years (mean = 44 years, SD = 14.24) with a disease mean duration of 12 years (SD = 8.39); 60% of patients had the pathology for over 10 years (Table 2).

Clinical characteristics of SSc patients and controls are reported in Table 3.

The principal drugs for SSc patients and controls are reported in Table 4.

2.2. SSc Oral Symptoms

The assessment of referred SSc oral symptoms, obtained from written responses to the questionnaire, revealed that the patients with SSc complained more frequently than controls: 78.8% of the SSc patients complained of one or more symptoms compared to 28.7% of the controls (χ2 = 40.23 p < 0.001). Statistically significant differences were found between two groups for each oral symptom considered as listed in Table 5.

2.3. TMD Symptoms

The assessment of TMDs showed that 92.5% of the patients with SSc and 75.0% of the healthy controls complained of one or more symptoms. Statistically significant differences were found between the two groups (χ2 = 8.012 p = 0.005).

In the SSc group, muscle pain on chewing, the sensation of a stuck or locked jaw, and arthralgia were the most commonly reported symptoms. In the control group tenderness or stiffness in the neck and shoulders were the major complaints.

Myofascial pain (MP) evoked by palpation was detected in 91.2% SSc patients and 83.8% of controls, revealing no significant difference between the two groups (χ2 = 2.057 p = 0.151). Data collected for each muscle couple were reported in Table 6.

2.4. SSc Oral Signs

At the clinical examination, oral signs correlated with SSc were more frequent in the study group than in the control one; 98.8% of SSc patients have at least one oral sign compared with 45% of controls (χ2 = 54.54 p < 0.001). Statistically significant differences were observed for each sign except for fibrous tongue. Table 7 lists the main findings collected from the oral examination.

2.5. TMJ Signs

At the clinical examination, restricted movements (RM) were more frequent in the SSc group than in the healthy controls. In particular, 85% of SSc patients showed restricted opening versus 20.0% of controls (χ2 = 67.77 p < 0.001); 81.2% of SSc showed reduced right lateral excursion versus 50% of controls (χ2 = 17.316 p < 0.001); 73.8% of SSc showed limited left lateral excursion versus 53.8% of controls (χ2 = 6.924 p = 0.009); and 73.8% of SSc had narrow protrusion versus 56.2% of controls (χ2 = 5.385 p = 0.02).

Measurement data related to movements were reported in Table 8.

Evidence of bruxism was observed in 81.2% of patients with SSc and 75% of controls, with no significant difference between the two groups (χ2 = 0.914 p = 0.339).

The prevalence of opening derangement (OD) was higher in controls (53.8%) than in SSc patients (43.8%). although this difference was not statistically significant (χ2 = 1.6 p = 0.206). Finally, no differences were recorded for sounds of temporomandibular joint (TMJs) in the two groups: this sign was observed in 50% of SSc patients and 50% of controls (χ2 = 0 p = 1).

3. Discussion

To our knowledge, the present study is the only report that analyzed and evaluated the prevalence of sign and symptoms of both mucosal damage and temporomandibular dysfunction in SSc compared with healthy controls with a cohort size larger than other studies investigating TMD and SSc (80 SSc patients versus 35 patients in Ferreira et al. [18], 14 SSc patients in Aliko et al. [22], and 68 SSc patients in Matarese et al. [25]).

About sociodemographic characteristics, unemployed and housewives were most represented in SSc patients, while office workers were most represented among controls (Table 1). These data could be explained with a progressive physical disability in SSc group, leading to a severe impairment of patients’ quality of life to varying degrees, with troubles in catching and even in writing. Also psychological aspects, such as self non-acceptance, can damage social life.

An interesting finding in patients’ history (Table 3) is osteoporosis, affecting 19 (23.8%) SSc patients versus 1 (1.2%) of control group. Consequently, a higher rate of SSc patients (17.1%) takes bisphosphonates (Table 4). However, a long-term antiresorptive therapy could cause, as a side effect, medication-related osteonecrosis of the jaws (MRONJ) after oral surgery. Therefore, in daily routine, dentists should consider SSc patients a high potential risk category.

The SSc group showed more symptoms and signs of mucosal and temporomandibular joint (TMJ) involvement compared with the control group.

Sicca symptoms are thought to be a frequent complaint associated with SSc, although little is known about how often they occur. Xerostomia was often complained by SSc patients recruited for the present study (42%), showing a higher prevalence if compared with findings by Bajraktari et al., who recorded this oral manifestation in 32% of SSc patients [26] and with findings by Weisman et al., who detected features of sicca syndrome in 12% of SSc patients [27]. Wood recorded xerostomia in 70% of the SSc patients and associated it with an increased frequency of dental caries [13].

According to Avouac et al. [28], the main cause of sicca syndrome in SSc appears to be glandular fibrosis, rather than lymphocytic sialadenitis associated with Sjögren’s syndrome: on 78 biopsy specimens obtained from patients with subjective symptoms of xerostomia, 23% of these cases were explained by Sjögren’s syndrome and 58% were explained by glandular fibrosis. According to Vincent et al., xerostomia was considered more discomforting (mean VAS = 3.8) than decreased mouth opening (mean VAS = 2.6) and was significantly associated with the limited cutaneous form [29].

Dysphagia was reported by 51.3% of SSc patients collected in this study and it was the most frequent otolaryngologic symptom complained by SSc patients compared with controls. As assessed in a study by Weisman et al., where 39% of SSc patients showed this symptom, radiographically detected esophageal abnormalities could be suggestive of dysphagia, though they did not always record this complaint even with an abnormal esophagram. It could be caused by a loss of contractile power of the esophagus, alterations of esophageal mucosa, abnormalities of the tongue and pharynx [27].

The present study, gathering information on both remote and recent anamnesis, detects a higher prevalence of TMDs in the SSc group (92.5%) compared to the respective outcomes in healthy patients (75.0%). These data differ from ones by Matarese et al. [25] that recorded TMDs in 74.1% of their 27 SSc patients.

An etiological hypothesis of the high prevalence of TMD in SSc could insist in the disease duration. In this work, in fact, in the 60% of SSc group the disease diagnosis dates back more than 10 years (Table 2).

MP evoked by palpation was reported by 92.5% of SSc patients in the present work, with a remarkably higher prevalence if compared with Matarese findings (55.6%) [25]. A mild, progressive myositis can lead to different degrees of atrophy and fibrotic muscle retraction when an inflammatory reaction occurs: this could explain the increased frequency of complaints in the SSc group [30].

TMJs were detected in the same proportion both in SSc group (45%) and controls (50%). Different findings were obtained by Matarese et al. [24], who recorded TMJs in 63% of SSc patients and 7.1% of their controls. Such a difference could be explained with a diverse selection of controls. In the present study, the sample was selected from people attending a dental clinic, who would report TMD more frequently than the general population.

The main expected finding was a more severe restriction on mandibular movements in SSc patients than in controls. In this work, RM were detected in 80% of SSc group, in accordance to Marmary’s results [18]. Jaw mobility score was recorded by Ferreira et al.: they observed that none of the SSc patients showed normal width in jaw movements and in particular 77.1% of SSc patients had a severe jaw mobility impairment (all measures were lower than mean values) [18]. On the other side, in a work by Weisman, only 28% of patients had altered kinematics [27]. In this last case, this parameter was recorded as a referred symptom and not as a sign detected by a clinician.


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