Preclinical Dental Hygiene Exam 2

healthy gingiva

• pink firm no bleeding

• JE coronal to CEJ

• supragingival fibers intact alveolar bone intact pdl intact

Color – pink

Contour – pyramidal papilla, knife-edged margins, follows contours of roots

Consistency – firm, resilient

Texture – stippling

gingivitis

reversible damage

red swollen likley bleeding

JE at CEJ

supragingival fiber destruction

alveolar bone intact

pdl intact

beeding when brushing flossing and sulcualr bleeding 

Color:  Red (slight, moderate, or severe) (localized/generalized = greater than 30% or the dentition demonstrates signs of gingivitis)

Contour:  Rolled and Rounded Gingival Margins

Consistency:  Smooth and Shiny, Soft and Spongy Texture

5 tissue reactions to injury or disease

1. heat

2. redness

3. swelling

4. pain

5. loss of function bleeding is related to this

sulcular bleeding 

The most reliable clinical indicator of gingivitis – this shows slight, delayed bleeding upon probing

Note that otherwise the tissues look pretty good, don’t they?

No matter how healty the tissue appears, if there is bleeding upon provocation>there is inflammation

Where does this begin??? COL, can you see these changes…not always

What are factors that can contribute to the color of the gingiva?

Factors are: Vascularity, Thickness of tissue, Kerantinzation, Pigmentation, Presence of disease

normal color

Begin your evaluation at the attached gingiva, then look to the margins and finally the papilla

This approach allows you to compare tissues

Also compare right side to left side; mandibular to maxillary

Notice all the blood vessels in the alveolar mucosa – this is NOT part of the gingival tissues or the gingival evaluation

normal pignemtation 

Normal pigmentation – melanin

This is common in people of color/dark-skinned people (people of African, Mediterranean, & Eastern Indian descent)

amalgam tattoo

Amalgam remnants get under tissue

This is to be noted and recorded as part of the intraoral examination – remember our purpose for conducting a gingival evaluation is to determine healthy or “inflammed” gingiva 

An amalgam tattoo has nothing to do with inflammation!

A piece of amalgam is lodged in the tissue area

cyanotic gingiva

When tissues take on a magenta OR bluish hue, they are termed cyanotic, due to oxygen deficiency – compare maxillary to mandibular

This happens when there is a chronic, long standing inflammation of the tissues  Mod/severe

Crown Margins, Metals, Crown curvature,

lighter than normal 

When tissues are lighter than normal, this usually indicates the REPAIR PHASE of inflammation: 

Or a result of repeated, limited injury over time (excessive toothbrushing)

Associated with hyperkeratinization (excessive keratin in the epithelium)– gives the surface a white tone

Associated with hyperplasia – increased thickness of the gingiva (increased number of cells)

red papilla

Color change often occurs in the papilla first

Redness = erythema

Col area > non keratinized tissue has increased susceptabilty to bacterial toxins

red gingival margins

As gingivitis progresses, the redness extends to include the free gingival tissues – marginal gingivitis

This is the most common form of gingivitis – marginal gingivitis

examine throughout 

Must look at all tissues – notice here that the buccally the tissues look pretty good but when you view the lingual, it’s a whole different story

Thorough examination is critical

Typically have greater problems with lower linguals

linear gingival erythema

Gingivitis associated with HIV infection

diffuse redness

As gingivitis progresses even further – the signs of inflammation can be seen throughout all the gingiva – papilla, margins, and  the attached gingiva as seen here in the mandibular area (compare the color on the mandible with that of the maxilla)

When the entire gingival apparatus is involved – we call it simply gingivitis (vs. marginal gingivitis)

normal contour 

Papilla are pyramidal (triangular) in shape – coming to a peak at the contact area – filling the gingival embrasure

Margins are sharp and knife-edged

You can see the natural contours of the gingiva as it lies over the root eminences

Anterior= pointed pyramidial, Posterior more flat looking

normal variation in papilla

Notice the flattened look to the papilla between #22 – 23

This is a normal variation due to the diastema – teeth do not contact, therefore the papilla cannot assume the normal shape to fill the gingival embrasure

Think about it – where would the peak be?

blunted papilla

This would be termed blunted papilla because they should have a pyramidal in shape and they do NOT – there are no peaks to these pyramids! The peaks are flattened.

Notice the open gingival embrasures

What do you think about the papilla between #25 – 26? Is that a slight diastema? 

If there is, then this would not be blunting due to an inflammatory process – it would be a normal variation in the shape of the papilla

bulbous papilla 

Notice that the papilla has taken on a very ROUND or bulb-like appearance. The papilla has enlarged to the point where it is pushing well out of the gingival embrasure space. It looks ready to burst.

This occurs with more mod-severe gingivitis – is NOT associated with mild forms of gingivitis

Jumping ahead, what do we call this kind of enlargement?

Edema – swelling (fluid in the tissues)

cratered papilla

Can you see that rather than a flat appearance (like with blunted papilla) we see an actual sunken appearance or a crater – our pyramid is really collapsing now!

“Punched Out” look

And often this cratering results in a separation of the facial and lingual halves of the papilla

Associated with necrotizing ulcerative gingivitis

rolled margins

Rolled Margins that give and appearance of a Life-saver shape to the margin

Sometimes simply referred to as “festooning”

clefts

These clefts in the gingival margins are due to extreme enlargement of the papilla

Clefts are very narrow and slit-like – like a slice, a sliver

stillmans clefts

Stillman’s clefts are associated with recession but it is the shape of the gingival margin that we are describing. Again notice the narrow, slit-like shape of the margin – fissure

Clefts of this shape can be from floss cuts due to inappropriate flossing….must eval patient’s flossing tech

Stillman’s clefts are often associated with frenum pulls

normal consistency and texture 

Consistency – firm, yet resilient

Texture – stippling (although not always present, even in health)Test for consistency lay side of probe against tissues

hyperplastic fibrotic

Notice first that the overall shape is different, too – the gingiva seems enlarged, bulky, thick

Notice that the texture is cobblestone vs orange peel – tough looking

This gingival response is usually related to a chronic, long-standing inflammation and the REPAIR PHASE of inflammation

The typical course of gingivitis is acute inflammation then healing following by more acute inflammation (breakdown and repair)

dialin hyperplasia

Gingival enlargement  due to the medication, Dilantin (for seizure disorder – Epilepsy)

Other medications can result in similar gingival enlargement

Calcium channel blockers – common HBP medications: nye fed i peen (Procardia)

Dilantin induced overgrowth may come from fibroblasts and osteoblasts depositing excesive extracellular matrix causing gingival overgrowth

Metciculus OH can help reduce this.

edematous 

This ROLLED MARGIN looks more spongy – can almost tell it would feel soft if you were to lay the probe against the tissue

A dent would remain when probe is removed= pitting edema

Do you see normal pigmentation?

embrassure classifications

• Normal

  • Interdental papilla fills space between contact and tooth

• Class I

  • Tip interdental papilla is apical to the contact point of adjacent teeth, but interproximal CEJ is not visible

• Class II

  • Tip of interdental papilla is at or apical to the interproximal CEJ, but coronal to the height of the facial CEJ

• Class III

  • Complete loss of the interdental papilla due to extensive gingival recession

diastema

A Diastema is NOT an embrasure.  An embrasure space requires that the teeth be contacting.  

white lesions leukoplakia

• Keratotic - cannot be wiped off

• Non - Keratotic - can be wiped off

• 5-25% of white lesions tend to be malignant

Leukoplakia is the clinical term for a WHITE LESION that CAN NOT be rubbed off and CAN NOT be diagnosed through clinical  characteristics alone.

white lesions leukoedema

Opalescence on the buccal mucosa, tends to become less prominent as you stretch the cheek tissue.  No treatment necessary.  

fordyce granules

• Small bumps on the inside of the Buccal mucosa and Lips

• Normal adipose tissue 

• Yellow in color

linea alba 

• White line extending anteroposteriorly on the buccal mucosa along the occlusal plane.

• Can be bilateral 

• From occlusal trauma

• Common in clenchers

snuff dippers lesion

Can disappear after stopping snuff/smokeless tobacco

lichen planus

Wicham Striae on inside of buccal mucosa

Purple itchy skin lesions 

white hairy tongue 

Result of elongation of filiform papillae

black hairy tongue

Results from a specific irritant or chemical

necrotizing ulcerative gingivitis

Punched out papilla with grey matter along the gingival margins and in between the teeth.  Papillary tissue necrosis.  

thrush candidiasis

Is an opportunistic infection

Can be the result of antibiotic therapy

ulcers and fissures 

• Traumatic ulcer is the most common ulcer

• Ulcer is a deep crater that extends through the entire epithelium

apthous ulcer intraoral recurrent herpes simplex

• Apthous ulcers are painful but harmless

• Apthous ulcers are not caused by the herpes simplex virus

• RAU - usually on soft, non-keratinized tissue

• IRHS - usually on keratinized tissue

most common sites for squamous cell carcinoma 

• Lower lip

• Lateral border of the tongue

• Floor of the mouth

exophytic lesions

Pathologic growth projecting above the oral surface

• Hypertrophy: enlargement of the tissues caused by an increased in the number of normal cells

• Neoplasia: abnormal growth (proliferation) of cells

• Neoplasm: the abnormal growth or lesion

  • benign or malignant tumor

exostosis

Common exophytic lesion

Like Tori but on the buccal aspect rather than the lingual or palatal aspect.  

fibroma 

caused by chronic irritation 

pyogenic granuloma

• Related to calculus, restorations, chronic irritants, hormones in pregnancy

• Also called Pregnancy Tumor

brown blue and clack lesions

• Melanin - black

• Varicosities - bluish

• Amalgam Tattoo - dark bluish

• Hemangioma - blue

• Mucocele - blue

• Ranula - large mucocele - blue

• Oral Melanomas - either color

hemangioma 

Benign tumor - rare

mucocele

Blockage of minor salivary glands

ranula

Blockage of a sublingual salivary gland on the floor of the mouth.  Larger mucocele-like lesion that forms unilaterally on the floor of the mouth.  Ranulas may increase in size during meals.  The name “ranula” is derived from “rana” the Latin word for FROG.  Most times, Ranulas are treated by surgery, the cause of obstruction , often a salivary gland stone must be removed.

generalized red lesions 

• Ulcers

• Primary infections with Herpes Simplex

• Erosive Lichen Planus

• Geographic Tongue

• Dry Mouth

• Erythroplakic lesion

• Atrophic Candidiasis - burning mouth

• Angular Cheilitis

geographic tongue

Also known as Erythema Migrans

Patches of denuded areas on the dorsal surface of the tongue that can be aggravated by spicy foods and acidic foods.  The pattern on the tongue can come and go and change to different areas including the lateral border of the tongue.    

dry mouth

Mouthbreathing – observe the smooth and shiny appearance of the tissues, mouth breathers tend to have dry palatal tissues.  

eythroplakic lesion

Velvety red patch - often malignant

candidiasis 

Pseudomembraneous candidiasis – white lesions can be wiped off to reveal and erythematous surface underneath.  

Also known as Thrush

atrophic candidiasis

There are several different types of candidiasis and it can present differently, atrophic candidiasis appears as bright red and can often be found under partial dentures and full denture prosthesis.  Can cause Burning mouth

angular chelitis

Erythema or fissuring at the labial commissures.  May be caused by factors such as nutritional deficiency (Vitamin B) but most commonly results from Candida infection. (fungal)

sebacious cyst 

Slow growing bumps under skin, usually harmless.  Found in hair bearing areas, gland or duct gets blocked or damaged

oral cancer screenings

• Full Evaluation completed at the first appointment 

• Follow up at subsequent appointments for areas of concern

• NEVER dismiss the patient without having the EO/IO MYO evaluation checked.

periodontitis

• Inflammatory disease of the deeper supporting tissues of the periodontium

• Clinical features

  • Apical migration of the junctional epithelium

  • Loss of Clinical Attachment

  • Periodontal Pockets

  • Bone Loss

periodontal systemic disease connection

• Significant research on association between periodontal infections and various systemic diseases and conditions

• Not shown to cause systemic disease

• Mechanism for association not clear

• Association critical for early identification, treatment, and management of PD 

Cardiovascular disease.

• Adverse pregnancy outcomes, including premature low birth weight babies.

• Respiratory disease.

• Chronic kidney disease.

• Rheumatoid arthritis.

• Obesity.

• Cognitive impairment.

• Osteoporosis.

• Inflammatory bowel disease.

• Some cancers.

risk assessment 

 Etiologic factor: the actual cause of a disease or condition.

▶▶ Predisposing factor: renders a person susceptible to a disease or condition.

▶▶ Contributing factor: lends assistance to, supplements, or adds to a condition or disease.

▶▶ Risk factor: increases the probability that disease will occur.

▶▶ Etiologic, predisposing, and contributing factors may be local or systemic, defined as follows:

• Local factor: a factor in the immediate environment of the oral cavity or specifically in the environment of the teeth and periodontium.

• Systemic factor: a factor that results from or is influenced by a general physical or mental disease or condition.

etiology of perio disease

• MICROBIOMES

  • Made up of subgingival biofilms

  • Primary etiologic agents of periodontal disease

  • Complexity and diversity increases in periodontitis

  • Differ for gingivitis and periodontitis

  • Type of organisms shifts to gram-negative anaerobic species

Microorganisms in the form of subgingival biofilms forming communities called microbiomes are the primary etiologic agents of periodontal disease/infection.

• The microbiome complexity and diversity increases in periodontitis when compared to health.

• The microbiome of gingivitis is not the same as in periodontitis.

• The type of organisms shifts to gram-negative anaerobic species including Porphyromonas gingivalis and Tannerella forsythia (previously known as Bacteroides forsythus), Treponema denticola, and Fretibacterium species.

risk factors for periodontal disease modifiable

. Modifiable Risk Factors

▶▶ The common risk factors for periodontal disease and systemic disease include tobacco exposure, diabetes, metabolic syndrome (MetS), obesity, diet, and excess alcohol intake.

• These are all modifiable risk factors; however, most require a interprofessional collaboration with medical providers.

A. Tobacco Use

▶▶ The evidence provides strong that support smoking as an independent risk factor for periodontal disease (see Figure 19-2).

• Evidence is emerging to show that cannabis or marijuana use is associated with more severe periodontitis.

▶▶ The odds for developing periodontal disease in people who smoke range from three to seven times higher than in nonsmokers.

▶▶ More than 40% of cases of periodontitis are a result of cigarette smoking.

▶▶ Periodontal treatment may be less effective in smokers than in those who do not smoke.

▶▶ Users of smokeless tobacco products experience oral effects, including predisposition to oral cancer. Periodontal lesions with severe recession and clinical attachment loss (CAL) occur where the quid is held.

B. Diabetes Mellitus

▶▶ Periodontal disease and diabetes mellitus have a bidirectional relationship, meaning a patient who does not control blood  glucose is more likely to have more severe periodontal disease.

▶▶ Poor control of blood glucose (glycemic control) increases the risk of developing periodontal disease and results in poor outcomes to treatment.

▶▶ As a result of the increase in diabetes in the U.S. population, there is an increase in prevalence of periodontitis in children and adolescents with type 1 diabetes mellitus.

▶▶ Although diabetes is a chronic disease, research suggests management of periodontal infection results in improvement in control of blood glucose.

C. Metabolic Syndrome

▶▶ MetS is a group of risk factors for heart disease and diabetes that includes hypertension, hyperglycemia, excess abdominal fat, and high cholesterol/triglycerides.

▶▶ A systematic review and meta-analysis found individuals with MetS are 38% more likely to have periodontitis.

▶▶ MetS increases risk of periodontal disease.

D. Obesity

▶▶ Obesity prevalence is about 40% in the United States and continues to increase resulting in a major public health problem.

▶▶ Obesity, overweight, weight gain, and increased waist circumference are emerging as risk factors for periodontal disease in adults, adolescents, and children.

▶▶ The odds of having periodontal disease in obese and overweight individuals is doubled.

E. Alcohol Consumption

▶▶ Alcohol intake is associated with an increased risk for periodontal disease.

▶▶ The risk in women was doubled and for men the risk was 25% greater for periodontal disease with heavy alcohol (>30 grams/day or >2 standard drinks) consumption.

F. Diet

▶▶ Macronutrient and micronutrient intake may be modifying factors in periodontal disease.

• Macronutrient intake such as high carbohydrate intake impacts glycemic control and may be involved in initiation of the inflammatory state in periodontal disease.

• Micronutrient deficiencies, such as vitamin C, vitamin D or vitamin B12, may impact onset, healing, and progression of periodontal disease.

G. Psychosocial Factors

▶▶ Some research suggests individuals under psychological stress, anxiety, or depression are more likely to have periodontal disease.

• The association may be related to the impact on the immune response as well as behavior changes.

H. Medications

▶▶ Medications for specific systemic conditions can lead to gingival enlargement. The enlarged tissue encourages dental biofilm retention and complicate removal, thus increasing the potential for periodontal infections. These medications may or may not be modifiable in discussion with the medical provider.

• Phenytoin-induced gingival enlargement: Phenytoin is a drug used to control seizures (see Figure 19-3).

• Cyclosporine-induced gingival enlargement: Cyclosporine is an immunosuppressant drug used for patients with organ transplants to prevent rejection.

• Nifedipine-induced gingival enlargement: Nifedipine is a calcium-channel blocker used in the treatment of angina and ventricular arrhythmias.

▶▶ Oral contraceptives with high doses of estrogen, progestin, or both.

non modifiable perio risk factors

 Nonmodifiable Risk Factors

A. Genetic Predisposition

▶▶ From 33 to 39% of the risk for periodontal disease is related to genetic factors.

▶▶ Genetic testing is likely to become more cost effective and will benefit patients and dental providers in targeting those at risk for enhanced prevention.

B. Host Response

▶▶ Host response refers to the way an individual’s immune response interacts with bacteria to resolve inflammation.

▶▶ Bacteria initiate an inflammatory response in periodontal disease and in susceptible individuals the body’s immune response becomes chronic resulting in tissue destruction.

▶▶ In addition to chronic diseases that impair the immune response, such as diabetes, genetic disorders associated with deficiencies in the immune system, such as Down syndrome, also result in a higher prevalence and severity of periodontal disease.

C. Osteoporosis

▶▶ Research suggests an association between osteoporosis and periodontal disease with three times the risk of greater than 4 mm of CAL.

▶▶ There was a five times greater risk of CAL greater than or equal to 6 mm.

▶▶ In osteopenia, there was nearly a two times greater risk of greater than 4 mm of CAL.

D. Age

▶▶ Age also is factored into the 2017 Periodontal grading system to take into consideration more severe periodontal disease at an earlier age.

• The grading of periodontitis is related to the potential for disease progression and will be described later in this chapter.

local factors

 Gingival Factors

▶▶ Position

• Deviations from normal provide retentive areas for biofilm.

• Gingival recession: may expose root irregularities that serve as areas for biofilm retention.

• Enlarged gingival margin or papillae: extended to or over the height of contour.

• Reduced height of interdental papilla creating an open interdental area.

• Operculum: Tissue flap over occlusal surface of an erupting tooth (Figure 19-8).

• Periodontal pocket: Depth and shape can make biofilm removal difficult.

• Calculus creating a rough retentive surface.

▶▶ Size and contour

• Deviation of shape of enlarged gingiva: rolled, bulbous, and cratered.

• Combination with presence of irregular restorations or dental prosthesis can result in marked biofilm retention.

▶▶ Effect of Mouth Breathing

• Dehydration of oral tissues in the anterior region leads to changes in size, shape, surface texture, and consistency.

Other Factors

A variety of factors may predispose or contribute to the progression of periodontal infections. Some of the items listed here may have an indirect effect, whereas others have a direct effect on the oral tissues.

▶▶ Personal oral self-care

• Neglect: This can lead to generalized dental biofilm accumulation and disease promotion.

• Inadequate biofilm control techniques: Incorrect use of brush and interdental cleaning aids.

• Awareness of oral cleanliness: Cleansing habits, including both self-cleansing mechanisms and mechanical biofilm removal, depend in part on an individual’s perception and feeling of debris through taste and tongue activity. This can become impaired in individuals with some conditions like poststroke.

▶▶ Diet and eating habits.

• Soft foods tend to be less nutrient dense and more retentive than fibrous, firm foods.

• Masticatory deficiencies limit diet selection. Missing teeth, ill-fitting partial dentures, and various occlusal deficiencies alter diet selection and eating habits.

pathogenisis of perio disease

• Process by which a disease develops and progresses.

• Primary etiology of periodontal disease is bacteria that initiate an inflammatory process

• Inflammatory process is very complex

  • Influenced by patient and environmental factors

  • Progression of disease is impacted by the individual’s response to the bacterial challenge

development of gingival and perio infection

The stages of development of gingivitis and periodontitis are divided into the initial lesion, early lesion, established lesion, and advanced lesion. With an accumulation of dental biofilm on the cervical tooth surface adjacent to the gingival margin, an  inflammatory reaction is initiated, and the immune system responds.

A. The Initial Lesion

▶▶ Inflammatory response to dental biofilm

• Occurs within 2–4 days in response to bacterial accumulation.

• Migration and infiltration of white blood cells (neutrophils) into the junctional epithelium and gingival sulcus result from the natural body response to infectious agents.

• Increased flow of gingival crevicular fluid.

• Early breakdown of collagen of the supporting gingival fiber groups (Chapter 18).

• Fluid fills the spaces in the connective tissue.

▶▶ Clinical appearance

• No clinical evidence of change may appear in the earliest phases.

• Marginal redness with enlargement due to the fluid collection follows as the infection develops.

B. The Early Lesion

▶▶ Increased inflammatory response

• Dental biofilm becomes older and thicker (7–14 days; time reflects individual differences).

• Infiltration of fluid, macrophages, T-cells, and neutrophils with a few plasma cells migrating into the connective tissue.

• Breakdown of collagen fiber support to the gingival margin.

• Epithelium proliferates: Epithelial extensions and rete ridges are formed.

▶▶ Clinical appearance

• Early signs of gingivitis become apparent with slight gingival enlargement; will become an established lesion if undisturbed.

• Early gingivitis is reversible when biofilm is controlled and inflammation is reduced. Healthy tissue may be restored.

• Susceptibility of individuals varies; time before lesion becomes established varies.

C. The Established Lesion

▶▶ Progression from the early lesion

• Migration of B-lymphocytes and plasma cells within connective tissue are characteristics of the established lesion.

• Formation of pocket epithelium.

1. Proliferation of the junctional and sulcular epithelium continues in an attempt to wall out the inflammation.

2. Pocket epithelium is more permeable; areas of ulceration of the lining epithelium develop.

3. Early pocket formation with bleeding on probing.

• Collagen destruction continues; connective tissue fiber support is lost.

• Progression to early periodontal lesion may occur or the established lesion may remain stable for extended periods of time.

▶▶ Clinical appearance

• Clear evidence of inflammation is present with marginal redness, bleeding on probing, and spongy marginal gingiva.

• This is followed by chronic fibrosis development.

D. The Advanced Lesion

▶▶ Extension of inflammation

• The two hallmarks of the advanced lesion include: alveolar bone resorption and collagen breakdown. B-lymphocytes and plasma cells are thought to influence both these processes due to the cytokines released.

▶▶ Progressive destruction of connective tissue

• Connective tissue fibers below the junctional epithelium are destroyed; the epithelium migrates along the root surface.

• Coronal portion of junctional epithelium becomes detached.

• Exposed cementum where Sharpey’s fibers were attached becomes altered by the host response to the bacterial challenge.

• Diseased cementum contains a thin superficial layer of endotoxins from the bacterial breakdown.

• Without treatment, loss of attachment results with an increase in pocket depth.

▶▶ Characteristics of the advanced lesion

• Pocket formation, bleeding, inflammation, and bone loss are all signs of periodontitis.

• Persistence of the chronic inflammatory process; plasma cells predominate.

• Junctional epithelium continues to migrate; lesion extends through connective tissue.

• Periods of disease inactivity alternating with periods of activity.

gingival and perio pocket 

• Distinguished by presence or absence of infection

• Pockets:

  • Have inner and outer walls

    • Inner - tooth surface

    • outer - sulcular or pocket epithelium of free gingiva

  • Contain substances such as microorganisms, gingival crevicular fluid, and desquamated epithelial cells

  • Divided into gingival and periodontal types

• Gingival Pocket or Pseudopocket

• Periodontal Pocket

• Tooth Surface Irregularities

recession

• Gingival margin has migrated apically

• Root surface is exposed

• Bone has been lost

• Tissues may have healthy pocket depths but if there is recession there is bone loss

Is recession a manifestation of periodontitis? Yes and no

No matter the cause for the recession (e.g. bacterial infection, tooth brush abrasion, orthodontia, frenum pulls), the tissue response has left a periodontal condition we must take note of

Visible Recession

measuring recesssion

• Measure from the CEJ to the gingival margin

• Buccal/Facial and lingual measurements

• Three recordings per buccal/facial or lingual surface

clinical attachment level CAL 

CAL Clinical Attachment Level or Loss - measured from the CEJ to the base of the sulcus/pocket.  

SO - IF there is recession present, then you will need to add the probe depth and the recession reading to get the total amount of CAL - Clinical Attachment Loss.

Better Indicator of Severity of Periodontal Involvement than Probe Depth

• Distance from CEJ to Base of Pocket

• Dentrix tabulates the CAL 

• CAL = PD + recession

  • Probe depth 2mm + 2mm recession = 4mm of CAL

measuring cal

If there is NO recession and the gingival margin is AT the CEJ, then the CAL is equal to the probe depth.

If recession is present, then you will add the recession reading to the probe score to get your CAL.

recording cal measurements

• 3 readings per tooth aspect

  • 6 PER TOOTH

• Once recession is recorded, Dentrix calculates CAL

• Mark a zero “0” if no recession present

• Reverse calculation of CAL if tissue is CORONAL to fixed point (CEJ).

pseudopocket vs perio pocket 

Pseudo - means FALSE in latin and so a Pseudopocket means a “False” pocket or Not a true periodontal pocket.  

A gingival pocket or Pseudopocket is when the gums swell UP onto the crown of the tooth but there is no apical migration of the junctional epithelial attachment.  

For Pseudopockets, we measure the amount of gum tissue that is swollen up above the CEJ and enter it into Dentrix under the GM (where we enter recession readings) as a negative number to get the CAL.  

So, if a pseudopocket is present we subtract the amount of gums above the CEJ from the pocket depth to get the accurate CAL measurement.  

necrotizing perio

• Acute condition with rapid tissue destruction - may become chronic

• Characterized by a history of pain, ulceration of gingival margin, and punch out papillae

• Predisposing factor is a compromised host immune response

perio as manefestation of systemic disease

• Diabetes Mellitus, Obesity, Osteoporosis, Arthritis (rheumatoid and osteoarthritis), Emotional Stress, Depression, Smoking, Medications

• Genetic Disorders (rare)

• Neoplasms, Odontogenic tumors, Squamous cell carcinoma, Hyperparathyroidism, Scleroderma

classification of perio 

• Pristine Periodontal Health

• Healthy pink color

• Clinical Periodontal Health (Intact Periodontium)

• No bone loss

• Periodontal Disease Stability (Reduced Periodontium)

• Periodontal Disease Remission/Control (Reduced Periodontium)

• Scalloped knife-edged margins

• Stippling

• No bleeding upon probing

•  Severity relates to the periodontal attachment loss at diagnosis and affects the complexity of management and treatment.

▶▶ Complexity of management includes factors such as probing depths, type of bone loss (vertical vs. horizontal), furcation involvement, occlusal issues.

▶▶ Extent refers to the number of teeth and distribution of the periodontitis and uses the terminology localized (<30% of teeth affected), generalized (>30% of teeth affected), and molar–incisor involvement only.

▶▶ Rate of progression is primarily dependent on radiographic evidence over time of attachment loss, but other methods to assess progression are under investigation.

▶▶ Risk factors.

stage 1 mild perio

• Severity

  • 1-2 mm CAL

  • RBL - Coronal third (<15%)

  • Tooth Loss - no tooth loss due to periodontitis

• Complexity

  • Pocket depth - maximum pocket depth less than 4 mm

  • Type of bone loss - mostly horizontal bone loss

  • No furcation involvement

  • No occlusal issues

• Extent & Distribution

  • Generalized or Localized, Molar/Incisor, Papillary, Diffuse

stage II moderate perio

• Severity

  • 3-4 mm CAL

  • RBL - Coronal third (15%-33%)

  • Tooth Loss - no tooth loss due to periodontal disease

• Complexity

  • Pocket depth - ≤ 5 mm

  • Mostly horizontal bone loss

  • No furcation involvement

  • No occlusal issues

• Extent & Distribution

  • Generalized or Localized, Molar/Incisor, Papillary, Diffuse

stage III severe perio 

• Severity

  • > 5 mm CAL

  • RBL - Extends beyond mid-third of root apically

  • Tooth Loss due to periodontal disease ≤ 4 teeth

• Complexity

  • Pocket depth - ≥ 6 mm

  • Vertical bone loss ≥ 3 mm

  • Furcation involvement

    • Class II or III

  • Moderate ridge defect

• Extent & Distribution

  • Generalized or Localized, Molar/Incisor, Papillary, Diffuse

stage IV very severe or advanced perio

• Severity

  • > 5 mm CAL

  • RBL - Extends beyond mid-third of root apically

  • Tooth Loss due to periodontal disease ≥ 5 teeth

• Complexity

  • Pocket depth ≥ 6 mm

  • Vertical bone loss ≥ 3 mm

  • Furcation involvement

    • Class II or III

  • Masticatory dysfunction

  • Secondary occlusal trauma (tooth mobility ≥ 2)

  • Severe ridge defect

  • Bite collapse, drifting, bearing less than 2 remaining teeth (10 opposing pairs)

• Extent & Distribution

  • Generalized or Localized, Molar/Incisor, Papillary, Diffuse

refferal to periodontist

• See Clinic Policy & Procedures Manual

• Clients with moderate and advanced periodontitis will be referred to a periodontist

• Priority referral is back to dentist of record

• Give list of periodontists 

  • Do not recommend any specific periodontist