Periodontal pocket

What do we mean by periodontal pocket ? As you remember from the summer course that we have the gingival crevice or sulcus and the periodontal pocket , there is a clear difference that you shouldnt make any mistake about ! Gingival sulcus (crevice): is the healthy space between the gingiva and the tooth structure Healthy means that we dont have any attachment loss, depth of maximum 3 mm and no bleeding on probing . When this depth of the healthy normal sulcus increased under the effect of microorganisms i.e. pathology so we start calling it periodontal pocket

So basically periodontal pocket is just a deepening of the gingival sulcus as a result of pathology What happens for the periodontal pocket to take place or be a measurable with time? neutrophils which are subset of WBCs they release granules that hydrolyze/destroy the invading microorganisms and have the challenge of bacteria around teeth and gingival crevice so we have the first line defense that is the neutrophils around the teeth, these hydrolases degrade collagen which is the basic structure of PDL and connective tissue , it become abundant in numbers , as you know when we have infection there is increase influx of polymorphonuclear cells which are neutrophils to the site of infection.
We know that anybody has an infection if he does differential blood count will have higher number of WBC compare to the normal because they increase in response to infection and same happens with gingival infection

If the pocket depth is increased due to overgrowth of the gingival tissue so the distance between the gingival margin and the base of the pocket although it is all above the CEJ I mean no destruction or attachment loss this is called gingival pocket or pseudo pocket because its not pathology or due to PDL destruction, but if this attachment start to migrate apically in response to the accumulation of calculus we start having periodontal pocket, it might be due to partly apical migration and partly increased thickness of the gingival or may be just by migration apically of PDL tissue, in these cases its called true pocket , if the base of the pocket is above
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the alveolar bone we call it supra bony (above the bone) but if the destruction goes below the crest of the bone we call it infra bony.
*in the exam u will have a radiograph and u should be able to differentiate between infra and supra bony and you have to know the pattern of destruction, angular or horizontal.

Transseptal fibers which are the fibers that hold two teeth together, if the bone destruction is even at all level this is called horizontal bone destruction ,the direction of the the PDL will stay horizontal , but if the destruction is at one side more so we will have angular/vertical destruction and the direction of the trasseptal fibers will be oblique .

Vertical bone loss Horizontal bone loss

*P.S: In health, the crest of the alveolar bone is located approximately 2mm below the CEJ.

We said that the attachment of the gingival start at the CEJ, What is the first line of cells that attach the gingiva to the tooth and make like a seal to prevent invasion of bacteria ? Its the junctional epithelium 1mm and below there is C.T , so approximately 2 mm occupied by these two structures which we call them the biological width, the bone starts just below it.

Generally the clinical changes that take place whenever there is a pocket, even before examination you can suspect that pocket is there : 1. Color. Its very important marker, with time when the pocket is deepen the color of the gingiva transfer from pink to red then dark red then bluish type of color due to destruction of blood component at this site and the blood in the venules. 2. Bleeding 3. Puss formation 4. Bone destruction 5. Tooth mobility, some time teeth start migrating from their place under the effect of mastication forces. As you know the occlusion forces is distributed over teeth and when
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the tooth is in normal situation in terms of support even if its angulated it will stand these forces, but if the support is reduced some teeth will try to go away from the forces. 6. it may be associated with pain, not always !!

Pathogenesis : Bacteria will invade the area and some defense mechanisms which found in the connective tissue, so the inflammation will start at the level of C.T and after while also epithelial tissue will show signs . So what will happen is : The first step in inflammation is dilatation of vessels and increased permeability so more blood influx to the site of infection, inflammation which start within C.T will degrade the C.T itself and the major component of it which is collagen ,so the destruction of C.T cells apical to the junctional epithelium and some of it will start to proliferate around the root to replace the destroyed C.T , with this time the coronal part of junctional epithelium will detach from the tooth and move apically , this is how the pocket starts to form . With time you should know the key of bacteria that is found in PDL and responsible for periodontal destruction that we call them Periodonopathoginc cells such as P.G_ Porphyromonas gingivalis , A.A _ Aggregatibacter actinomycetemcomitans , prevotella intermedia which is very important when we talk about gingival disease in females . So we have destruction of collagen and the ability of bacteria to invade tissues, not only to reside at the surface of cementum some of the bacteria have the ability to penetrate into the epithelium, so even if you do root blading alone some of the bacteria will stay inside the tissue and if they are high in number then we have to add another component of treatment for example antibiotics to get rid of the bacteria that are within the gingival tissue. Periodontal pockets show some destruction and some healing ,as our body in general which is composed of dynamic tissues so despite destruction we have attempt for healing and repair to replace destruction but if the destruction exceed the ability of the body to restore net destruction tissue lost is seen! so when you look at the gingiva after bacterial invasion some of the signs will be edema and erythema of the gingiva.

Why edema is there? Is that found at all sites of gingival inflammation ? In fact No, it depends on the stage and the type of tissues of the patient, in the beginning as we said will be influx or plenty of fluid into the gingival epithelium so we will have the edematous type of clinical findings, but in some patients we find fibrotic gingiva which is harder and this means that the fibroblast within the periodontal ligaments is trying to replace the destroyed tissues so it produces plenty of fibrous tissue so you will have fibrotic gingiva.

The root surface wall : With deepening of the pocket even if collagen fibers are destroyed (we know that the major component is the sharpeys fibers which are part of the PDL embedded in the cementum) and what will happens is like microporous appear on the cementum, this porous will be a road for bacteria to invade even within the cementum and some studies showed that it can reach up to the cementum dentine junction even within the dentinal tubules, sometime the net result will be cementum necrosis by the invasion of bacteria and part of the cementum will be separated so when we examine our patient we have to look if there is any soft cementum and remove it .

It was believed long time ago that periodontal disease is a slowly progressing destructive disease but now its not accepted, there are some patients with rapid destruction of bone followed by period of remission or quiescence, they are trying to speculate what is happen!

Quick review : If the attachment is at the level of CEJ and probing depth of 1 mm this is a state of health. If that probing depth is 1mm but below the CEJ , this is called attachment loss. If we have 1 mm depth of probing plus 1 mm of recession so the attachment loss is 2 mm .

Alveolar Bone loss

Some notes : - Health is a state of balance between host defense and external challenges. - Bone is a dynamic tissue which undergoes continuous apposition and resorption, in most of the cases we have balance between resorption and apposition if this balance is broken due to any reason a disease takes place ! - Normally the destruction of the bone is caused by inflammation . - Whenever you have bone loss you have periodontitis - Gingivitis its not always proceeded to become periodontitis .

Extension of gingival inflammation: Which is the progression of gingival inflammation into the periodontal tissue, this happens with increased number of microorganisms ( a key thing that demarcate the conversion of gingivitis into periodontitis is the change in the bacterial composition). We know that in health or mild gingivitis cases most of the bacteria is gram positive coccus type of bacteria , when it start to transform to gram negative which is anaerobe ( if you remember aerobic bacteria needs oxygen so they are the superficial part of gingiva but when you have pockets and the plaque becomes thicker so the bacteria will be away from oxygen so they become anaerobic bacteria) these patient will be susceptible for transform gingivitis into periodontitis due to a major change in bacterial is there . Spread of inflammation : You have either direct spread of inflammation from the gingiva into the bone and sometimes from the bone to the periodontal tissue which start destruction or directly from the gingiva into the periodontal tissue (this is between teeth). At the site of buccal or lingual it is either from the gingiva along the outer periosteum which is just covering the bone and from the periosteum into the bone or from the gingiva to the periodontal ligaments . So there are three main roots to spread inflammation into the periodontal ligament : 1. Inflammatory infiltrate extends from gingiva to bone along the course of blood vessels. 2. Less frequently, inflammation extends directly into PDL to the interdental septum. 3. Facially and lingually, inflammation spreads along the outer periosteal surface of the bone and penetrates the marrow spaces.
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P.s : bone destruction is not bone necrosis !! , necrosis is when any part of the tissue is isolated from its blood supply and this part of the tissue undergoes destruction and these are dead cells, while in the case of bone destruction takes place in a viable tissue !

There is an interesting finding of a study that showed that almost 8% of persons have rapid bone destruction and the majority have slow or moderate bone destruction while around 10% has minimal or no bone destruction disease .

What causes bone destruction ? Bacteria has a minor direct rule in destruction of bone but most of the destruction takes place due to indirect effect of the host response due to inflammatory mediators like interleukins, prostaglandins, tumor necrosis and so on ,factors that are produced by invading bacteria and the body cells that we call them cytokines (gingival infection). Occlusion trauma , it is when the occlusal force is more than normal, for patients who have habit of chewing all time, bruxism, clenching they have susceptibility for bone destruction. Another example is when the teeth are weaken by disease so even normal force will be more than what the teeth withstand so will cause bone destruction and migration of the teeth Systemic disorders such as hyperparathyroidism , osteoporosis, leukemia and some immune deficiency disorders.

We have normal variation of alveolar bone some patients have thicker bone at one site and thinner bone at one site , alignment of the teeth , position of the root trunk , the bifurcation location For example, lower incisor has thin bone labialy so if bone loss takes place there it has to be horizontal , we cant have vertical bone loss because the bone is very thin; d estruction become more and more when we have wide remnant bone the destruction can be vertical/ angular; because it has been found that there is a radius of effect, bacteria can cause bone destruction within a radius of 2.5mm so if the bone thicker than 2.5 the destruction wont reach the other end of the bone so the destruction will be at end of the bone so angular/vertical bone loss

takes place, but when the bone is thinner than 2.5 mm the effect will be a fairly even , overall reduction in high of bone (horizontal bone loss) . Sometimes the osseous tissue try to replace and withstand this challenge so deposition of bone takes place more than the normal morphology it is called lipping of bone which you can feel it when you examine your patient . How we classify the defect around teeth ? We depend on the remaining walls ! for example if we have the lingual and buccal and mesial walls are defect so we say three walls osseous defect , if the defect just in the mesial we say one wall osseous defect etc

We have what we call crater which is a pattern of bone loss , where the destruction of bone takes place in the middle of the bone ( the buccal and palatal bone are in their place) . Normally the level of the bone is higher between teeth interdentally than the buccal and palatal , when the buccal and the palatal bone is higher than interdentally we call it reverse architecture or reversed topography of the teeth (this area need treatment). Sometimes there are some ridges which is like plateau, a shelf between teeth, as a result of destruction of the thin part of the bone , as you move apically a wide area of bone thickness is there and this is an area of pocket formation.

Forgive me if there is any mistake Done by : Abeer Derawi