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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.
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
Sore knees due to arthritis.
Reflux for the last couple of months managed by diet modification.
Admitted to hospital in 2002 for chest congestion.
- Imdur 120mg/d
- Minax 100mg/d
- Triace 10mg/d
- Sozpren 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.
Dominique Abela SID: 200027582
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.

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:


Plaque scoring:

Periodontal Diagnosis:

Generalised moderate to severe chronic periodontitis.

Treatment Plan:

- Oral hygiene instruction.
- Removal supragingival and subgingival hard deposits.
- Prophylaxis
- Review Oral hygiene instruction and response of periodontium to
- Lower anterior tooth splinting or -/p for lower anteriors.
- Supportive Periodontal therapy every three months.

Treatment carried out:

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
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.

Integrated clinic Completed Worksheets:

Future treatment needs:

Splinting of the 42, 41, 31, 32 with composite resin.
Supportive periodontal therapy every three months.
Oral hygiene instruction.


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,

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)-, 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.,

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.,

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 didnt 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.


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