The effects of Inflammatory Bowel Disease (IBD) on the oral cavity
There is a paucity of large robust studies evaluating the effects of IBD on the oral cavity compared to its effects on other parts of the body. Orally related manifestations of IBD seem to be relatively common and might serve as indicators of potentially undiagnosed IBD, especially in children. The link between IBD and caries amongst IBD patients would seem to stem from their increased likelihood to eat little and often, snacking on high sugar content foods and avoiding 3 large meals a day. There would seem to be a link between IBD (especially Ulcerative Colitis) and periodontitis, although the nature of this association is unclear and research has far from proved a causal link. The treatment needs of patients with IBD are far reaching and the dental team and in particular the Dental Hygienist / Therapist have a key role to play – through both preventative and operative dentistry.
Aims and Objectives
To increase understanding of the effects of Inflammatory Bowel Disease (IBD) on the oral cavity
To describe IBD, and how it affects the body outside of the oral cavity
To examine the most common ways that IBD disease might present in the oral cavity
To examine the link (if any) between IBD and periodontitis, and IBD and caries
To highlight the role of the dental team and in particular that of the Dental Hygienist/ Therapist in caring for patients with IBD
To highlight potential areas of future research
Historical research background
Data on the frequency of extraintestinal manifestations (EIMs) in Crohn's Disease (CD) and Ulcerative Colitis (UC) and analyses of their risk factors are quite scarce despite oral manifestations being quite common. This is probably related to the difficulty associated with studying patients in a cross-sectional manner - only a few patients will suffer from EIM at the time of the study. This said, a few robust cohort studies do exist which shed invaluable light on the topic.
Further, research investigating the link between IBD and periodontitis, and IBD and caries does not often rank highly in the hierarchy of evidence e.g. cross sectional studies with small sample sizes. This is hardly surprising however given the relatively small amount of people per capita of the total population that suffer from IBD. Moreover, IBD’s often devastating effects on other parts of the body takes precedence over dental research. In spite of this, interest in the link between IBD and periodontitis, in particular, still remains in contemporary research.
Indriolo et al published a review paper in 2011 to try to explain the potential relationship between periodontitis and IBD. This research concluded that: ‘the two diseases (IBD and periodontitis) may be associated through sharing relevant pathogenic mechanisms and when both diseases co-exist, their progression could be accentuated and their treatment could improve both conditions’ (Indriolo et al., 2011).
Whilst it is difficult to draw definite conclusions from the research examined in this project, it is still possible to draw some tentative hypotheses and views and highlight some key areas for further research.
What is Inflammatory Bowel Disease?
The term Inflammatory Bowel Disease (IBD) is most often used to describe two separate illnesses: Ulcerative Colitis (UC) and Crohn’s Disease (CD). However, in around 5-15% of patients is not possible to distinguish between CD and UC through clinical, radiological, endoscopic and pathological investigations (Baxter, Sharma and Mann, 2011). When this is the case, the patient is diagnosed with ‘indeterminate colitis’ (Baxter, Sharma and Mann, 2011). The present project focuses largely on CD and UC.
Both Ulcerative Colitis and Crohn’s Disease can be described as chronic non-infectious inflammatory diseases of the gastrointestinal tract. The patient may have times of good health (remission), with few or no symptoms, and times of active disease (flare-ups). Both conditions are individual to the sufferer, with some people remaining well for long periods of time, and others having frequent flare-ups. At present there is no cure for IBD, with drug therapy and surgery focusing on reduction of inflammation and relief of symptoms.
What is the difference between CD and UC?
Crohn’s Disease causes inflammation of any part of the gastrointestinal tract from the mouth to the anus. Areas of ‘transmural granulomatous inflammation’ (Indriolo et al, 2011) are broken up by intermittent healthy parts. Inflamed patches can be small (1-2cms), or may extend along a large part the bowel. Patients with CD have a slightly shorter life expectancy than healthy people, with the severe chronic symptoms generally having significant impact on quality of life.
Ulcerative Colitis is a condition that causes inflammation and ulceration of the lining of the colon and rectum. Mucosal inflammations and sores develop on the surface of the lining, which may bleed and produce pus. Patients with UC have a normal life expectancy but the severe chronic symptoms can impact on quality of life.
CD and UC present somewhat differently (see Table 1), although differential diagnosis can be difficult.
What causes IBD?
Current thinking points to the fact that IBD is caused by a complex interaction of multiple factors with genetics (Hampe et al., 2001; Hugot et al., 2001; Stoll et al., 2004), abnormal immunological function and environmental factors (e.g. bacteria) thought to play a part (Indriolo et al., 2011). It is worthy of note that CD is more common among smokers. In this regard, Cosnes et al. (1999) noted, that “Current smoking, particularly heavy smoking, markedly increases the risk of flare-up in Crohn’s disease…with a significantly increased risk of flare-up from a daily dose of 15 cigarettes’. Unlike Crohn’s, however, UC occurs more frequently in non-smokers.
How common is IBD and who is affected?
‘Approximately 1 in every 400 members of the UK population currently suffer from CD or UC, with 6000-12000 new cases of UC and 3000-6000 new cases of CD diagnosed annually in the UK’ (Crohn’s and Colitis UK, 2011). Both diseases are more common in urban populations in northern developed countries, but it is not understood why. They are also more common in white people of European descent, especially those descended from Ashkenazi Jews (Probert et al., 1993).
What are the extraintestinal manifestations of IBD?
Whilst it is outside of the remit of this project to examine all the extraintestinal manifestations of IBD, it is worthy of note that they can be classified into three major groups:
1. Reactive manifestations:
Associated with intestinal disease e.g. arthritis and erythema nodosum (painful red swellings, usually on the legs, which leave bruises).
Not associated with intestinal disease e.g. uveitis (soreness and inflammation of the white of the eye) and episcleritis (inflammation of the iris and can lead to blindness if not treated).
2. Non-IBD-specific autoimmune diseases: independent of IBD e.g. thyroid disease and hemolytic anaemia.
3. IBD-related complications: due to metabolic or anatomical abnormalities e.g. osteopathy and amyloidosis (abnormal deposition of amyloid proteins in various tissues of the body).
As already stated, data on the frequency of extraintestinal manifestations in large IBD populations is somewhat limited, however Vavricka et al (2011) identified them in 43% of CD and 31% of UC patients out of a total of 950 patients. These results are in accordance with studies from Greenstein et al (1976) who found manifestations in 36% in their IBD cohort of 700 patients and Veloso et al (1996) in a group of 792 IBD patients.
How is IBD treated?
Treatment for IBD depends on the extent and severity of the condition. For the majority of sufferers with symptomatic IBD, it is highly likely that medication will form a part of their treatment, either to reduce symptoms and to control a flare-up or to prevent a relapse
once the disease is under control. If the disease is very severe or does not respond to medicinal therapy, surgery to remove part or whole of the large bowel (UC)/ intestine (CD) may be required.
Oral manifestations of IBD
The mucocutaneous and cutaneous manifestations of IBD have been classified into the following categories according to pathogenesis (Danese et al., 2005; Trost and McDonnell, 2005; Passarini et al., 2007; Mnif et al., 2010; Levine and Burakoff, 2011):
Specific mucocutaneous / cutaneous manifestations or granulomatous lesions with the same histological features as the underlying bowel disease.
Reactive mucocutaneous / cutaneous manifestations of IBD with immunological mechanisms triggered by common antigens shared by gut bacteria and skin.
Mucocutaneous / cutaneous disorders or dermatosis associated with IBD.
Secondary mucocutaneous / cutaneous manifestations either due to complications of IBD or adverse effects of IBD treatments.
It is beyond the scope of this project to examine all manifestations from these categories. Examples from the first two categories have been selected because they demonstrate IBD’s direct effect on the mucosa of the oral cavity and have implications on the diagnosis and dental treatment of IBD patients. (Note: dental considerations are examined in a later section).
Specific mucocutaneous manifestations with the same histological features as the underlying bowel disease
1. Aphthous ulcers
Aphthous ulcers (Figure 4) are the most common complication of the oral mucosa associated with IBD (Rothfuss et al., 2006; Larsen et al., 2010). Whilst aphthous ulcers occur in about 20% of the general population, some studies have found a prevalence of oral aphthae of 40% amongst CD patients (out of 118 patients) and 33% (out of 234) with UC (Yüksel et al, 2009). Moreover Galbraith et al. (2005) highlighted that: ‘aphthae tend to be more extensive and persistent when associated with IBD’. Although a biopsy is rarely required, histology can reveal noncaseating granulomas similar to those seen in the colon. Treatment is most often symptomatic with topical anaesthetics such as viscous Xylocaine. Topical antibiotics can also be used for bacterial superinfection, although they are rarely required
2. Orofacial granulomatosis
The descriptive term “orofacial granulomatosis” encompasses any granulomatous process of unknown aetiology involving the oral cavity. Typically, orofacial granulomatosis presents as recurrent or persistent swelling of the lips, cheeks, gingivae, or oral mucosa. If the lips become very swollen, fissuring can occur in the midline or at the angles of the mouth (angular cheilitis). The swelling can even become severe enough to interfere with speech and eating. Histologically, the epithelium is intact but thickened, with epithelioid cells and giant cells surrounded by a lymphocytic infiltration (Wray et al, 1975). Swelling may also occur inside the mouth, with nodular granulomatous producing a ‘cobblestone’ appearance (Basu & Asquith, 1980).
Treatment takes the form of pain and aesthetic management, with topical steroids often used to treat the cobblestoning and systemic steroidal therapy reserved for more advanced swelling.
Reactive mucocutaneous and cutaneous manifestations of IBD with immunological mechanisms triggered by common antigens:
1. Pyostomatitis vegetans
Pyostomatitis vegetans (PV) is relatively specific to IBD, particularly to UC (Storwick et al., 1994; Timani and Mutasin 2008; Femiano et al; 2009). Whilst the pathogenesis of Pyostomatitis vegetans is not yet known, this condition is included here because abnormal immunological responses and/or microbial factors have been suggested (Kethu, 2006; Femiano et al., 2009; Ficarra et al., 2010).
PV is characterised by multiple pustules, erosions, and ulcers on an erythematous background with vegetations or folding of the gingival and buccal mucosa. These erosions often cause pain on touch, or when eating acidic, spicy or hot foods. Management of PV is often based on treatment of the underlying gastrointestinal disease with systemic steroids. Often the oral lesions can be managed with topical steroids and chlorhexidine mouthwash.
Oral lesions in paediatric patients
One area of particular interest is the apparent increased prevalence of oral lesions amongst children with IBD and the associated implication for diagnosis. In their 3-year study of systematic dental examinations on children with IBD, Harty et al (2005) found that out of the 49 children examined, 20 had oral manifestations (Figure 8). Further, in their retrospective 5 year review to consider whether expert oral examination would be of benefit in the diagnosis of CD in paediatric patients, Pittock et al (2001) found that out of 45 paediatric patients with CD, just under half had oral signs, concluding that ‘when oral lesions are present, they may be helpful in establishing the diagnosis of CD, because granulomatous inflammation will frequently be detected’. Even though their sample sizes were small, these studies serve to indicate that even in the otherwise asymptomatic child, such oral signs warrant further investigation, including consideration of IBD (especially because oral disease is not common in non immunocompromised children).
IBD and caries
Little research has been conducted into the link between IBD and caries. In a few studies with small samples, it was reported that CD patients have a higher prevalence of caries than healthy control subjects: Sundh & Hulten (1982), 21 patients; Bevenius (1988), 15 patients; and Schutz et al (2003), 48 patients. For the purposes of this project, these studies will not be examined in depth due to their small sample sizes. They are, however, useful for comparing and contrasting the findings of other studies. In these aforementioned papers, a higher risk of dental caries was suggested to be a result of nutritional deficiencies (Bevenius, 1998); changes in salivary and microbiologic conditions in the oral cavity (Sundh & Emilson, 1989); and increased sugar intake (linked to reduced taste perception for sweet) combined with insufficient oral hygiene (Schutz et al, 2003).
The two research papers most often quoted when examining the link between caries and IBD are by Grossner-Schreiber et al (2006) and Brito et al (2008). Both papers looked at the association between IBD, caries and periodontitis.
Grossner-Schreiber et al (2006) conducted a dental examination in two quadrants on 62 patients with IBD, making no distinction between UC and CD patients, comparing the results with 59 matched healthy controls from a dental practice. Research involved a clinical examination of each patient and of the control, consisting of tissue alterations, DMFT index, dentine caries, plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD) and clinical attachment loss (CAL). For each individual, all periodontal measurements (PPD, BOP, CAL) were calculated from the individual measurements in the two quadrants examined. These were then regarded as the representative value for that subject. Additionally some qualitative feedback was obtained pertaining to diet. The study offered no definition of periodontitis.
Brito et al (2008) conducted a full mouth dental examination consisting of probing pocket depth (PPD), clinical attachment loss (CAL), bleeding on probing (BOP), plaque and DMFT index amongst a larger group: 99 people with CD, 80 with UC and 74 healthy controls. Dentine caries was not examined, nor were any qualitative dietary records taken. This study was however the first to assess caries in UC patients. Periodontitis was defined in the study as the presence of at least four sites in different teeth with CAL over 3 mm.
Both of the aforementioned studies were case control studies, which, by their nature, feature lower down the hierarchy of evidence than randomised controlled studies undertaken over a longer period to time.
Grossner-Schreiber et al (2006) found that the prevalence of dentine caries was significantly higher in those with IDB versus non IDB controls (40% versus 22%), but at a large confidence interval. Qualitative feedback from the participants, however, further served to highlight that 44% (27/62) of the patients had to eat more frequently and take smaller amounts of food to avoid gastrointestinal problems. As plaque scores in the IBD group were significantly higher in the study compared with controls, the researchers tentatively concluded that eating habits might be the reason for the significantly higher prevalence of dentine caries in the IBD patient group. Moreover, the link between sugar consumption and higher prevalence of caries in CD patients is backed up by conclusions drawn from other research studies (Schutz et al., 2003).
Grossner-Schreiber et al’s findings (2006) showed a higher DMFT in IBD patients. After adjustments for race, gender, smoking habit, age and plaque, both groups (CD and UC patients) had a significantly higher DMFT index than controls. This finding concurs not only with observations from the Bevenius pilot study (1988) suggesting a higher frequency of dental decay in patients with CD compared with healthy control subjects, but also the Sundh & Hulten study (1982) which suggested both the DMFT index and the risk of baseline caries were increased in CD patients. However it should be mentioned, this research postulated that the higher risk for dental caries was attributable to salivary and microbiologic conditions in the oral cavity, a finding that is yet to be substantiated by other research. It should also not be forgotten that this study did not specifically examine dentine caries present in the mouth.
Brito et al (2008) found that only UC patients have a significantly higher DMFT. This is interesting, especially if the link between DMFT index and increased sugar intake is believed. It is normally CD patients in particular, (and not UC patients), who tend to rely on refined carbohydrate intake at times of relapse. Whilst more research as a whole is needed on the subject of IBD and caries, this area in particular would seem of interest. Moreover, Brito et al., (2008) found CD patients had significantly less plaque than controls and there was no difference regarding plaque between UC patients and controls. Whilst this finding is in direct contrast to that of the Grossner-Schreiber et al. (2006) study, the researchers of the aforementioned study still surmised that diet was the cause of the higher DMFT index.
IBD and periodontitis
In a similar fashion to the link between IBD and caries, little research into the link between IBD and periodontitis has been conducted. Again, many studies are cross sectional with small sample sizes. This noted, all but one of the most noteworthy papers point to a link between IBD and periodontitis.
Grossner-Schreiber et al (2006) showed no distinct differences between cases and controls. However, compared with controls, patients with IBD had a higher (but not significantly different) amount of sites with CAL (81% versus 64% in controls = at least 4mm, and 63% versus 46% = at least 5mm). Interestingly the researchers linked the significantly higher plaque scores in the IBD group to prevalence of dentine caries, presumably because they failed to find any more clinical signs of gingival inflammation in the IBD group to that in the control. In the light of other evidence, it is tempting to conclude that examination of only four sites of all teeth in two quadrants (upper right and lower right or upper left and lower left quadrant alternating from one patient to the other) might have skewed the findings.
Flemming, Shanahan and Miyasaki (1991), found that periodontitis was more prevalent in those with IBD but they failed to find a link between IBD and severity of periodontitis. Whilst this research proved an interesting ‘pilot study’ into the field of IBD and periodontitis, it needs to be viewed with particular caution. Firstly, the research examined 46 CD patients and 61 UC patients with no non-IDB sufferer control group. Secondly, the periodontal examination was carried out at only two sites (mid- and mesiobuccal) of all teeth present in two quadrants. Lastly, the results were compared with the assessment of Oral Health of United States Adults (a review document of various pieces of primary research).
In a Jordanian case–control study by Habashneh et al., (2011) 260 Jordanian adults (101 with UC, 59 with CD and 100 with no IBD) received a questionnaire (which also collected data regarding food avoidance and changes to eating habits and frequency) and a clinical examination. The clinical examination included a full-mouth periodontal assessment, probing pocket depth and clinical attachment level measured at six sites on each tooth. Periodontitis was deﬁned as the ‘presence of four or more teeth with one site or more having a probing pocket depth of 4mm or over and clinical attachment level over 3 mm. Furthermore, plaque index, gingival index and calculus index (presence or absence) were assessed.
In multivariate analysis, the severity of periodontitis was significantly higher amongst IBD patients and especially patients with UC when compared with those with no IBD. However, the researchers themselves highlighted: ‘one has to be cautious when interpreting the results because of the small sample size and especially the low number of patients with CD” Habashneh et al (2011).
The findings of Habashneh et al (2011) are in line with those of Brito et al (2008) who found that: ‘the prevalence of periodontitis was significantly higher in both patient groups compared with the controls’. Further, it was found that UC patients, both smokers and non-smokers, had a tendency for more CAL and more sites with CAL over 3mm compared with CD patients. This suggests a different response to plaque between the groups. Further, when comparing the two IBD groups, Habashneh et al., (2011) observed that the severity and extent of periodontitis were different, however, the two groups did not differ in average plaque index and gingival index. Further research would be required to establish if these findings were coincidental.
Dental implications of IBD
Since CD and UC are not seen as frequently as many other diseases, dental professionals are less likely to be highly informed about what oral signs and symptoms to look out for, or the complex problems associated with treating such patients. There is particular need to be vigilant during the extra/intraoral examination. As it has already been seen, oral manifestations can be the first signs of IBD. Further, careful questioning about the history of family illnesses whilst taking the medical history can also prove helpful if the patient has undiagnosed IBD, since CD especially is thought to have an inherited genetic link (Baxter, Sharma and Mann, 2011).
Collaborative approach both inside and outside the dental field
Close liaison with other healthcare professionals involved in the patient’s treatment is paramount e.g. Immunology and Gastroenterology specialists. Such an approach helps treatment planning, highlights any potential risk factors in treating the patient (e.g. drug interactions and adverse effects) and also helps the dentist and his/her team decide if the patient needs more specialist dental care in a hospital setting.
A full medical history should be taken regularly, including all medications that the patent is taking/ and has taken over the past two years.
One of the greatest concerns to the dental team is the IBD patient’s corticosteroid therapy. Even when the patient is not currently taking a corticosteroid or carrying a steroid card, he or she still can be at risk of adrenal insufficiency (Figure 10). The effects of corticosteroids on the immune system and adrenal glands go on long after corticosteroid therapy has ended. As a result of long-term corticosteroid use, a patient’s adrenal glands can become atrophied and less responsive to the pituitary gland’s stimulation, and unable to secrete an increased amount of cortisone on demand when the patient needs it. This can lead to adrenal crisis; a very rare, but fatal, emergency. Franch, Soriano and Pérez (2003) suggested “Evaluation of hypothalamic/pituitary/adrenal cortical function to determine the patient’s ability to undergo extensive dental procedures”.
Whilst it is beyond the scope of this project to provide an exhaustive list, other associated medications with implications for the dental team are:
Aspirin and non steroidal anti-inflammatory drugs (e.g. Ibuprofen) not to be prescribed for dental pain in CD patients due to the possibility of further gastrointestinal disturbance.
Immunosuppressant drugs (especially cyclosporine) can cause gingival overgrowth in 25% of patients taking the medication. (Neild – Gehrig and Willmann, 2003)
Anticoagulants - Thromboembolism is a common complication of IBD, often treated with anticoagulants e.g. Heparin. Such drugs affect the patient’s clotting and bleeding time, which is important for the dental team to know if conducting operative procedures.
Clear and comprehensive oral hygiene instruction
As it has been shown, IBD patients seem to be at increased risk of developing periodontitis and dental caries. Thus, for treatment to be most effective, clear explanations about these issues are necessary. The aim is for the patient to take ownership and resolve to play their part in their care. For treatment to be effective, good home care is essential. Here, the role of the Dental Hygienist / Therapist is paramount in educating the patient in excellent oral hygiene through brushing technique and use of interdental aids. Moreover the DHT has a role to play in educating the patient in oral hygiene maintenance even when their mouth is sore (e.g. with ulcers). Such oral hygiene advice might include rinsing with a soluble paracetamol mouthrinse or lidocaine mouthwash for pain relief before brushing, use of sponge sticks (Figure 11) and replacement of toothpaste with chlorhexidine gel.
Whilst an in depth investigation of the link between IBD and smoking is beyond the remit of this project, the apparent link between CD and smoking has been highlighted. Whatever the link between smoking and IBD, smoking remains a very important risk factor for the progression of periodontitis (and one of the few that the patient him/herself can control). The dental team and in particular the Dental Hygienist / Therapist have a key role to play in both encouraging and supporting a quit attempt.
People with IBD often follow specific eating plans given to them by a dietician. Such plans aim to help sufferers maintain a healthy weight and also to ensure they are not deficient in minerals and vitamins. IBD sufferers (especially those with CD) can experience weight loss, either due to not eating intentionally to avoid pain and diarrhoea, or due to being unable to eat during a relapse. Further, it has already been shown that the diets of those with IBD (especially CD) tend to be higher in sugar. During ‘flare-ups’, the sufferer aims to remain hydrated and energised but unable to eat solids, forcing a reliance on high sugar content drinks (e.g. fruit juices and milkshakes). Jarnerot et al (1983) pointed out ‘patients with an exacerbation of CD eat sugary food because it is more digestible’, a finding upheld by Schutz et al. (2003) who evaluated the nutritional status of patients with CD and found an increased intake of refined carbohydrates relative to normal controls.
The problem of a high sugar diet and its implications on the patient’s caries risk status is further compounded because patients often find that it is easier to eat little and often, rather than overloading the digestive tract with 2 or 3 large meals a day.
Whilst diet advice should never contradict that given by other healthcare professionals, the Hygienist / Therapist has a role to play in encouraging the patient to eat as healthy and varied diet as possible. This is especially important in times of remission when a reliance on foods with a high sugar content should be discouraged.
Given that many IBD sufferers are high caries risk, Grossner-Schreiber et al. (2006) pointed out that ‘regular use of fluoride treatment for prevention of dental caries appears to be justified’. For those at particular risk, the dentist might prescribe a high fluoride toothpaste (e.g. 5000 ppm, Figure 14), mouth rinse and twice yearly fluoride varnish (2.2%F) applications carried out by the Dental Hygienist / Therapist.
Frequent /increased dental visits
Franch, Soriano and Pérez (2003) highlighted the importance of ‘frequent preventive and routine dental care to prevent destruction of hard and soft tissue’. The DHT has an important part to play here too; be it through palliative care of the patient’s oral IBD manifestations or through operative dentistry of carious lesions.
Scaling and debridement
Given the apparent link between periodontitis and IBD, scaling by the Dental Hygienist / Therapist plays two vital functions. Firstly, it removes calculus, to which periodontally damaging toxins can adhere. Secondly, debridement disrupts the subgingival biofilm, disturbing the bacterial community. The need to scale should be dependant, however, on the patient’s general and oral health. Patients with the oral manifestations highlighted in this project will often not be able to tolerate operative or invasive dental care.
There is a lack of robust studies evaluating the effects of IBD on the oral cavity and data on the frequency of extraintestinal manifestations in large IBD populations is also somewhat limited (especially evaluating EIM associated risk factors). From the research examined, aphthae appear to be the most common complication of the oral mucosa associated with IBD. Other manifestations are also relatively common and can sometimes serve as indicators of potentially undiagnosed IBD, especially in children.
Much of the research into the link between IBD, caries and periodontitis could be thought of as ‘pilot’ studies, which warrant targeted prospective investigation through follow-up studies. This makes it difficult to draw definite conclusions. This said, after examination of the research, the most obvious (and logical) link between IBD and caries would appear to be diet, with a high and frequent sugar intake. Further, there would seem to be a link between IBD (especially UC) and periodontitis; although the nature of this association is unclear and research has far from proved a causal link. In this regard, longitudinal studies would be valuable in establishing a temporal association between IBD and periodontitis: such studies could encompass immuno-inflammatory common risk factors and genetic markers between the IBD and periodontitis.
Future research is also warranted into the role played by IBD associated oral conditions on patients’ ability / willingness to practice good oral hygiene and the effect immunomodulators have on the oral cavity and the progress of periodontitis.
The fact that IBD remains a relatively uncommon condition (although the number of people affected is rising) highlights the need for the whole dental team to remain informed through continued professional learning. A thorough medical history, including past and present medications taken is essential, failure to do so could in extreme circumstances prove fatal. The dental team also has an important role in the overall holistic care of patients with IBD, both in preventative and operative care. They can also be key players in the diagnosis of IBD on the basis of oral manifestations. This might be especially relevant in paediatric cases (as already highlighted). The need for operative or invasive dental care (debridement and restorations) needs to be carefully assessed so as not to cause undue pain or distress to patients with IBD who have painful oral manifestations.
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Article by Nick Coller
Source: Dental Health | March 2014 Page 21 - 28