Patient personal Details: Mr Perio Patient. DOB: January 22, 1943. Age: 66.
Sex: Male.
Marital status: Married. Country of Birth: Bangladesh. Language spoken: English. Religion: Muslim.
Pensioner.
Previous occupation: Engineer. Medical History:
Angina diagnosed in 2000. Managed with glycerol trinitrate sublingual spray and regular visits to cardiologist.
High Blood pressure. Managed with medications.
Non-insulin dependent diabetes. Managed by 3 daily BSL readings, regular 3 monthly blood tests and medication. But after questioning, patient sometimes skips daily BSL measurements and the blood tests are not done regularly, thus diabetes is poorly managed.
Sore knees due to arthritis.
Reflux for the last couple of months managed by diet modification. Admitted to hospital in 2002 for chest congestion.
Medications: - Imdur 120mg/d - Minax 100mg/d - Triace 10mg/d - Sozpren ½ tablet/d - Diaformin 1000mg/d - Diamicron 30mg/d - Zocor 40mg/d
Last HbA1c 9/3/09 7.7% and patient will be getting blood taken for this before fasting (for religious purposes) commences.
Social/Family History: Never consumes alcohol.
BDENT4 2009 PERIODONTOLOGY REPORT
Was previously a smoker 20 years ago for 15 years. Has been married for many years and has 2 children. Dental History:
Brushes in the morning before breakfast only. Nil flossing
Attends dental hospital at Westmead every couple of years for treatment. Previous treatment includes extraction of the 38 due to coronal fracture and
extraction of 47 due to mobility. Fully dentate except for 38 and 47. Nil restorations.
Patient has never been told he has periodontal disease or gum disease.
Patients gums bleed sometimes when brushing and this has occurred for a long time. But no bleeding occurs when eating or when the patient wakes up.
Patient has previously noticed pain and swelling of gums but does not have any pain or swelling at the present.
Patient has mobile lower anterior teeth and has noticed the gaps between these teeth have gotten bigger and teeth have moved out of alignment.
No bad taste noticed by patient.
Sometimes patient has bad breath with reflux. Reflux has only occurred recently. Chief Complaint:
1. Pain due to mobile lower anterior teeth. 2. Wants to preserve remaining teeth
3. Quadrant 3 molar region pain. But no pain at the present. History of Presenting Complaints:
Quadrant 3 molar region pain:
Since removal of the 38 that was carried out in September 2005 patient has felt pain. The pain is spontaneous, of short duration, localized to molar region, does not refer anywhere, nil sleep disruption. Has take paracetamol and get relief with this
analgesic. Warm salt water gargle also provides relief.
Lower anterior teeth have been mobile and drifting for some time. On examination:
Extra oral:
No swelling. No asymmetry.
Muscles (Temporalis, masseter) No abnormality detected (NAD). Lymph nodes (submandibular, submental, cervical) NAD
Temporomandibular joint NAD, 3 finger mouth opening. Intraoral:
Soft tissue exam: Lips, buccal mucosa, sulci, floor of mouth, soft palate, tongue NAD Hard tissue exam: hard palate, alveolar ridges NAD.
Teeth: No evident of caries, no previous restorations.
Gingiva: pale pink, blunt/rolled edge, soft/spongy, thick biotype. Plaque: generalised +++
Calculus: generalised supragingival +++; generalised subgingival +++. Periodontal charting:
Periodontal Diagnosis:
Generalised moderate to severe chronic periodontitis. Treatment Plan:
1. CAUSE RELATED THERAPY:
- Oral hygiene instruction.
- Removal supragingival and subgingival hard deposits. - Prophylaxis
- Review Oral hygiene instruction and response of periodontium to treatment.
2. CORRECTIVE AND RECONSTRUCTIVE:
- Lower anterior tooth splinting or -/p for lower anteriors. 3. MAINTENANCE:
- Supportive Periodontal therapy every three months. Treatment carried out:
DATE TREATMENT
4/03/08 Treatment Planning, Oral hygiene instruction (OHI). 1/04/08 Continued treatment planning, OHI.
15/04/08 OHI, scale and root plane lower anteriors.
20/05/08 OHI, scale and root plane quadrant 4 molar and premolars. 10/06/08 OHI, Scale and root plane quadrant 1 molar and premolars.
05/08/08 OHI, review previous treatment, scale and root plane quadrant 2 and 11,12,13.
26/08/08 OHI, scale and root plane quadrant 3.
7/10/08 OHI, Review all quadrants, scale and root plane sextant 07, SPT in 2009 23/03/09 SPT: History, exam, 6 point charting, treatment planning, scale and root
plane all quadrants, review OHI.
7/08/09 SPT: History, exam, 6 point charting, treatment planning, scale and root plane quadrant 1, review OHI.
31/08/09 OHI, scale and root plane quadrants 2 and 3. 3/09/09 OHI, scale and root plane quadrant 4.
18/09/09 Review all quadrants (patient going overseas for 2-3 months) and OHI, SPT in 3 months.
Future treatment needs:
Splinting of the 42, 41, 31, 32 with composite resin. Supportive periodontal therapy every three months. Oral hygiene instruction.
DISCUSSION:
Having assessed, reviewed and treated this patient over a two year period, it is evident that his poorly controlled diabetes and oral hygiene practices have had a detrimental effect on the periodontal treatment outcomes. Bearing this in mind, the following discussion will focus on the relationship between non-insulin dependent diabetes mellitus (previously classified as type II diabetes mellitus) and periodontal disease. In addition part of the discussion will also include treatment of mobile teeth in severe periodontal disease. What Is Diabetes Mellitis?
Diebetes Mellitis is a metabolic disorder characterized by hyperglycemia due to defective secretion or activity of insulin. A definitive diagnosis of diabetes mellitus is made by assessing glycated hemoglobin levels and in those people with diabetes, sequential fasting plasma glucose levels will be 7 mmol/L or more. Diabetes mellitus can be classified into 3 distinctly different types according to signs and symptoms. These different types of diabetes mellitus include: Type 1 diabetes Mellitis (insulin dependent diabetes); Type 2 Diabetes mellitus (non-insulin dependent diabetes mellitus); Gestational diabetes (Matthews D, 2002).
The causes of type 2 diabetes mellitus range from insulin resistance with relative insulin deficiency to a predominantly secretory defect accompanied by insulin resistance. The onset is generally more gradual than for type 1, and this condition is often associated with obesity. In addition, the risk of type 2 diabetes increases with age and lack of physical activity, and this form of diabetes is more prevalent among people with hypertension or dyslipidemia (Matthews D. 2002).
Type 2 diabetes has a strong genetic component, with the disease being more common in North Americans of African descent, Hispanics and Aboriginal people (Matthews D, 2002). The prevalence of type 2 diabetes mellitus is increasing in Australia because of various known factors such as: greater awareness of the condition leading to increased diagnosis and reporting; shifts in lifestyle patterns; and increase in the aging population and a higher prevalence in of diabetes in some immigrant groups. In addition, people with type 2
diabetes constitute 90% of the diabetic population with Aboriginal people and Torres Strait Islanders have the fourth highest prevalence rate in the world (Taylor B. 1999).
What is periodontitis?
Periodontal diseases are a group of inflammatory diseases that affect the periodontium (bone, periodontal ligament, gingival and cementum). The most common periodontal diseases include gingivitis and chronic periodontitis. Gingivitis is characterised as inflammation of the gingiva initiated and sustained by plaque and its products and its a reversible disease (L. Vilata- lecture). Periodontitis is characterised as inflammation of the periodontal tissues and loss of attachment that is initiated and sustained by plaque and its products (L.Vilata-lecture). Periodontits is a more severe disease that is characterised by the loss of boney support for the teeth. Research has shown the causative role of plaque
containing bacteria in periodontal disease and research has also shown the treatment of periodontal disease with scaling and root planing usually stabilises the disease resulting in improved periodontal health (Taylor B. 1999). Thus, periodontal management, with an emphasis on bacterial plaque control, is an evidence-based intervention with established health outcomes (Cronin A. Et al. 2008)
Diabetes and Periodontal disease
The complications of diabetes arise from prolonged elevated blood glucose concentrations where the hyperglycaemia is longstanding. This hyperglycaemia results in the production of advanced glycosylation end-products. These advanced glycosylation end-products impair polymorphonuclear leukocyte and endothelial cell function, collagen production and
metabolism. This results in dysfunctional chemotaxis, adhesion and phagocytosis (Cronin A. Et al., 2008). Non-enzymatic glycosylation of body proteins in the hyperglycaemic
environment leads to a hyper-responsive state with over-secretion of inflammatory mediators such as interleukin-1 (IL-1) and tumour necrosis-factor (TNF)-α, making the patient more susceptible to tissue destruction. These factors are thought to be the underlying cause predisposing diabetics to periodontal disease (Matthews D. 2002). Additionally, there is some speculation that AGE-enriched gingival tissue has greater vascular permeability, experiences greater breakdown of collagen fibres and shows
accelerated destruction of both nonmineralized connective tissue and bone (Lalla R. 2001). Diabetes mellitus is now widely accepted as a risk factor for periodontitis and there is a large evidence base to support this. Studies have found the prevalence of periodontal disease is higher among diabetic patients (Kaur G. 2009. Demmer R. Et al., 2008) and recent evidence suggests the prevalence of periodontitis is 10% higher in type 2 male and female diabetics when compared to non-diabetics (Wang T. Et al., 2009). Diabetic patients are more likely to have attachment loss compared with non-diabetics (Grossi S. 1994). Diabetics (type 1) have significantly more clinical attachment loss than controls (Firatli E. 1997). Diabetes affected all periodontal parameters, including bleeding scores, probing depths, loss of attachment and missing teeth (Bridges R. Et al., 1996) and people with type I and type 2
diabetes appear equally susceptible to periodontal disease and tooth loss (Moore P. Et al., 1998).
There is some evidence that how well the diabetes is managed impacts on the periodontal disease status and how well the periodontitis is treated impacts upon the diabetic state. Studies have suggested that effective control of periodontitis reduces the levels of advanced glycosylated end products in serum (Grossi S. Et al., 1998). Other studies have found that the level of periodontal health in well controlled diabetics was similar to that of
non-diabetics. Those with poor control were shown to have more attachment loss and had more disease recurrence (Tervonen T. Et al., 1997), (Christgau M. Et al., 1998), (Stewart J. Et al., 2001).
The patient in question has poor diabetic control. This is evident from the results of blood tests where glycosylated haemaglobin levels have been 9% and 7.7%. In the past two years of treatment the patient has only had their glycaemic control measured twice, despite strong encouragement to have this done every three months and speaking with the patients general practitioner. The patient however, has always measured blood glucose levels three times daily and claims that they always fall between six and seven. At each appointment blood glucose levels have been measured and have all been between six and eight. It has been explained to the patient that even though their daily blood glucose levels have been within normal limits, their glycaemic control is not optimal and this has a detrimental effect on their periodontal treatment and response to treatment.
After the first phase of periodontal treatment was carried out, review at three months revealed a modest reduction in the percent of sites with bleeding on probing in all quadrants. Also probing pocket depths of greater than 4mm were decreased by 1-2mm. However after another cycle of supportive periodontal therapy five months after this last review, the percentage of sites with bleeding on probing had increased and some
periodontal pocket depths has increased by 1-2mm. This decline in periodontal disease status could have been due to the extended period between supportive periodontal therapy treatments. However other factors such as non-optimal oral hygiene or poor gylcaemic control could also be a cause. In all likelihood it is a combination of extended time between treatment, non-optimal oral hygiene and poor diabetic control that lead to this decline in periodontal health.
Four months after the last supportive periodontal therapy treatment was completed
another review was carried out and this showed all areas had about the same percentage of sites with bleeding on probing except the lingual of the mandibular teeth which exhibited an increase of 20%. After examination and consulting with the patient it was revealed that the oral hygiene especially in this region was lacking and needed improvement. The probing
pocket depths in some regions had also shown some advancement indicating lack of response to treatment in localized regions. As mentioned above, this lack of response to therapy in some regions and minimal response to therapy in other regions is most likely due to the interaction between poor diabetes management , non-optimal oral hygiene and a need for more frequent treatment.
With respect to oral hygiene, instruction is given at each appointment and usually about fifteen minutes is spent on addressing how to access areas where plaque control is not adequate. Even after advising the patient that he would most likely lose his teeth in the near future due periodontal disease he persisted in not using any type of interproximal cleaning aid. Recently the patient was advised that his periodontal treatment would not be
continued if he didn’t use an interdental brush and this prompted the patient to finally start using this device. It is hoped that at the next review the benefits of this will be evident. Mobile teeth, Occlusion and periodontal disease:
The occlusion and its relationship to periodontal disease is still an area of considerable controversy. For over a century clinicians have studied this relationship however few evidence based conclusions have been made. Fleszar and colleagues in a study looking at the response of mobile teeth to periodontal therapy found that mobile teeth do not respond as well to periodontal treatment as do those of firm teeth exhibiting the same initial disease severity, however mobile teeth could be successfully treated and maintained (Fleszar T. Et al., 1980). Rupprecht proposed that trauma from occlusion does not initiate or accelerate attachment loss due to inflammatory periodontal disease (Rupprecht R, 2004). Another more recent review concluded that the exact effect of occlusal
discrepancies/occlusal trauma on the progression of human periodontal disease remains unknown but all studies performed to date strongly indicate that occlusion is not a causative factor in periodontal disease (Harrel S. Et al., 2006). This study also states that research involving humans has shown that occlusal discrepancies may be a significant risk factor for the progression of existing periodontal disease and that the treatment of occlusal
discrepancies significantly improves the outcome achieved with periodontal treatment (Harrel S. Et al., 2006).
When investigating the relationship between occlusion and periodontal disease it is
important to recognise that the determining factor of whether an occlusal contact produces occlusal trauma is the presence of periodontal injury, not the physical manifestations of the teeth, temporomandibular joints or muscles of mastication (Carranza F. Et al., 2002). If the periodontium is reduced enough, even a normal occlusal contact may produce occlusal trauma. Additionally, it is also possible that even the most severe deflective contact or mediotrusive interference will not cause or be associated with a traumatic lesion (Carranza F. Et al., 2002).
The patient this report is based on has significant loss of attachment in region of the lower anterior teeth. There is no evidence of active chronic periodontitis but the periodontium is significantly reduced in this region. This area also has clinically mobile teeth and the teeth have migrated/drifted in a protrusive manner. The patient has never had pain associated with the mobile teeth, the mobility has not progressed, there is no thermal sensitivity, there is a normal amount of wear, there is no root resorption or widened periodontal ligament space but there is a significant amount of bone loss. As mobility has not changed in the past two years and there is no clear evidence of occlusal trauma apart from the mobility it is hard to justify the placement of a fixed splint. The patient in this case may benefit more from identification and reduction of occlusal discrepancies to reduce the occlusal forces placed on these mobile teeth.
There is evidence that reduction of occlusal discrepancies is of no benefit in periodontal treatment and there is limited evidence on the benefits of elimination of occlusal discrepancies. In a study of first maxillary molars it was found that teeth with occlusal contacts in centric relation and in laterotrusive, mediotrusive or protrusive positions had no more severe periodontitis than did teeth without these contacts (Pihlstrom B. Et al., 1986). Another study found no significant differences in pocket depths, attachment levels or alveolar bone height when comparing teeth with and without various abnormal occlusal contacts (Jin L. Et al., 1992). One study looking at occlusal adjustment and periodontal treatment outcomes found a minor gain in attachment (0.4mm) in the group receiving periodontal treatment and occlusal adjustment compared to the group that recieved
periodontal treatment only, however both groups show no difference in mobility (Burgett F. Et al., 1992). Another study on occlusion and periodontal treatment found increased
probing depths in sites with untreated occlusal problems, decreased probing depths in sites with no occlusal problems and the greatest decrease in probing depths in sites with treated occlusal problems (Harrel S. Et al., 2001).
In the most recent review of the relationship between occlusion and periodontal
destruction it was emphasised that the exact effect of occlusal discrepancies and occlusal trauma on the progression of periodontal disease still remains unknown (Harrel S. Et al., 2009). But it is emphasised in this review that occlusal discrepancies are a risk factor in the progression of periodontal disease. It is stated that removal of occlusal discrepancies by selective grinding alone or in combination with an occlusal appliance is associated with a significant change in the progression of the disease and improvement in the cause related phase of periodontal treatment and thus treatment of occlusal discrepancies should be considered an integral part of periodontal disease treatment. On this basis, the future treatment of my patient will include reduction of occlusal discrepancies on the mandibular incisor teeth.
REFERENCES:
1. Barbara Anne Taylor, Head, Department of Periodontics United Dental Hospital of Sydney, Surry Hills. Periodontal Diseases And Systemic Health: Associations, Directions, Implications. (1999). New South Wales Public Health Bulletin 10(3) 14 - 16).
2. Debora C. Matthews. The Relationship Between Diabetes and Periodontal Disease. (2002) Journal of the Canadian Dental Association. 68(3):161-4
3. Grossi SG, Zambon JJ, Ho AW, Koch G, Dunford RG, Machtei EE. Assessment of risk for periodontal disease. I. Risk indicators for attachment loss. (1994) Journal of Periodontology. 65(3):260-7.
4. Firatli E. The relationship between clinical periodontal status and insulin-dependent diabetes mellitus. Results after 5 years. Journal of Periodontology 1997; 68(2):136-40.
5. Bridges RB, Anderson JW, Saxe SR, Gregory K, Bridges SR. (1996) Periodontal status of diabetic and non-diabetic men: effects of smoking, glycemic control, and
socioeconomic factors. Journal of Periodontology. 67(11):1185-92.
6. Moore PA, Weyant RJ, Mongelluzzo MB, Myers DE, Rossie K, Guggenheimer J. (1998). Type 1 diabetes mellitus and oral health: assessment of tooth loss and edentulism. Journal of Public Health Dentistry. 58(2):135-42.
7. A. J. Cronin,N. Claffeyand L. F. Stassen. (2008) Who is at risk? Periodontal disease risk analysis made accessible for the general dental practitioner. British Dental Journal 205(3)131-137.
8. Lalla RV, D’Ambrosio J. (2001). Dental management and considerations for the patient with diabetes mellitus. Journal of the American Dental Association. 132(10):1425-32.
9. Grossi SG, Skrepcinski FB, DeCaro T, Robertson DC, Ho AW, Dunford RG. (1997) Treatment of periodontal disease in diabetics reduces glycated hemoglobin. Journal of Periodontology. 68(8):713-9.
10. Tervonen T, Karjalainen K. (1997). Periodontal disease related to diabetic status. A pilot study of the response to periodontal therapy in type 1 diabetes. Journal of Clinical Periodontology 24(7):505-10.
11. Christgau M, Palitzsch KD, Schmalz G, Kreiner U, Frenzel S. (1998) Healing response to non-surgical periodontal therapy in patients with diabetes mellitus: clinical, microbiological, and immunologic results. Journal of Clinical Periodontoogy. 25(2):112-24.
12. Stewart JE, Wager KA, Friedlander AH, Zadeh HH. (2001) The effect of periodontal treatment on glycemic control in patients with type 2 diabetes mellitus. Journal of Clinical Periodontology. 28(4):306-10.
13. Wang T-T, Chen TH-H, Wang P-E, Lai H, Lo M-T, Chen PY-C, Chiu SY-H. (2009) A population-based study on the association between type 2 diabetes and periodontal disease in 12,123 middle-aged Taiwanese (KCIS No. 21). Journal of Clinical
Periodontology. 36:372–379.
14. Demmer R, Jacobs D, Desvarieux M. (2008) Periodontal Disease and Incident Type Diabetes: Results from the First National Health and Nutrition Examination Survey and its Epidemiologic Follow-Up Study. Diabetes Care 31:1373–1379.
15. Commander R. “Dave” Rupprecht, DC, USN. (2004).. Trauma from occlusion: a review. Naval Postgraduate Dental School National Naval Dental Center 8901 Wisconsin Ave Bethesda, Maryland 20889-5602. 26(1) 25-27.
16. Harrel S, Nunn ME, and Hallmon W. (2006). Is there an association between occlusion and periodontal destruction?: Yes—occlusal forces can contribute to periodontal destruction. Journal of the American Dental Association. 2006;137;1380-1392.
17. Fleszar T, Knowles J, Morrison E, Burgett F, Nissle R, Ramfjord S. (1980) Tooth mobility and periodontal therapy. Journal of Clinical Periodoniology, 7: 495-505. 18. Carranza FA, Camargo PM. Periodontal response to external forces. In: Newman MG,
Takei HH, Carranza FA. Carranza’s Clinical Periodontology. 9th ed. Philadelphia: Saunders; 2002:371-83.
19. Jin L, Cao C. (1992) Clinical diagnosis of trauma from occlusion and its relation with severity of periodontitis. Journal of Clinical Periodontology. 19(2):92-7.
20. Pihlstrom B, Anderson K, Aeppli D, Schaffer E. (1986) Association between signs of trauma from occlusion and periodontitis. Journal of Periodontology. 57(1):1-6. 21. Burgett F, Ramfjord S, Nissle R, Morrison E, Charbeneau T, Caffesse R. (1992). A
randomized trial of occlusal adjustment in the treatment of periodontitis patients. Journal of Clinical Periodontology. 19(6):381-7.
22. Harrel S, Nunn M.(2001). The effect of occlusal discrepancies on periodontitis, part II: relationship of occlusal treatment to the progression of periodontal disease. Journal of Periodontology. 72(4):495-505.
