Destruction of the Periodontal Tissues 

The process of periodontal destruction is of great interest as the direct action of the microorganisms is minimally responsible for the damage caused to the periodontium.

Instead, it is due to a poorly regulated inflammatory immune response to the dental plaque. This means that individuals who show a poorly regulated immune and inflammatory response are an increased risk. 

The Pathophysiology of Periodontal Disease

The pathophysiology of periodontal disease is a complex and progressive process. This lesson will take you through the various stages, from the initial plaque deposits, to gingivitis and eventually periodontitis. It is important to note that not all gingivitis progresses to periodontitis; a person’s risk factors, and susceptibility will influence their development. 

Initial Lesion 

• Within 24 hours of plaque accumulation, the gingivae become inflamed  
• Inflammation is facilitated by vasodilation of arterioles, capillaries and venules in the dento-gingival plexus; this leads to an increase in gingival crevicular fluid (GCF) 
• The Inflammatory cells move to the affected area through extravasation
  • Cellular components show mostly neutrophils present with few lymphocytes and macrophages present 

Early Gingival lesion 

• After one week of plaque accumulation, an early lesion will develop 
• This results in an increased inflammatory infiltrate
  • Dilation of the blood vessels continue, and more vessels will appear. 
    • This leads to the clinical appearance of red gingiva 
• Inflammatory cells continue to enter the area 
  • The number of lymphocytes and neutrophils will continue to increase
  • Plasma cells begin to enter however in a very small number
  • Fibroblasts show cell damage
• Gingival collagen fibers are lost in the infiltrating region, which provides more space for inflammatory cells 
• Basal cells in the junctional and sulcular epithelium proliferate; this acts as a mechanical barrier attempting to prevent the bacteria from entering the system
• Rete peg proliferation occurs which works as a mechanical barrier to maintain the epithelial barrier 
• Coronal epithelium is lost, allowing the plaque biofilm to extend sub-gingivally

This is called early gingivitis

Established Lesion 

The transition from early to established can take various timescales between individuals. However, has the following characteristics;

• Increase in the gingival crevicular fluid (GCF)
• Increase in the inflammatory infiltrate
  • Neutrophils predominate with an increased migration
  • Plasma cells makeup 10-30% of the cellular infiltrate 
  • Fibroblasts damage continues 
• The loss of gingival collagen continues apically and laterally, which allows further space for inflammatory cells 
• Rete pegs extend further into the connective tissue layer
• Junctional epithelium is no longer attached closely to the tooth and instead transforms into pocket epithelium, creating a false pocket
  • Pocket epithelium is leakier and can become ulcerated
•  Clinical evidence for established gingivitis is seen including redness, swelling and bleeding 
• There is no bone loss at this stage, only loss of collagen 

At this stage, it can stabilise, or progress to periodontitis

KEYNOTE:

For gingivitis to progress to periodontitis, it can take varied amounts of time and affect people in completely different ways. A person’s risk factors, and other elements can influence the immune and inflammatory response. In individuals with a well-rehearsed and organised immune response, there is a greater chance that the disease can stabelise. However, an unregulated and hyper-inflammatory host response against the plaque biofilm will lead to destruction of the periodontal tissues and the clinical signs of periodontitis (presence of pockets and bone loss). The risk factors and susceptibility are discussed in the 'The Risk Factors and Susceptibility' lesson.  

Advanced Lesion 

• This is where irreversible damage to the periodontium occurs, including true pocket formation due to the apical migration of the junctional epithelium and alveolar bone loss
• The gingival pocket continues to deepen, due to the apical movement of the epithelium as a result of the plaque extending sub-gingivally
• The inflammatory infiltrate continues to extend apically and laterally into the connective tissue
  • Plasma cells dominate in advanced stages, and make up over 50% of the infiltrate
• In the advanced lesion of periodontitis, the following characteristics are found;
  • Loss of connective tissue attachment
  • Apical migration of the junctional epithelium and formation of a true periodontal pocket 
  • Loss of alveolar bone 

Connective Tissue Changes during Lesion Progression

The inflammatory response to plaque begins to develop adjacent to the gingival margin. This leads to destruction of the connective tissue, with significant loss of collagen at the point of inflammation.

As this develops, destruction is able to expand more apically and laterally, affecting the periodontal ligament (PDL) and the alveolar bone. 

The PDL is damaged through a breakdown of the collagen fibres which insert between the alveolar bone and cementum. The damaged fibroblasts additionally mean a reduction in fibres and the ground substance resulting in the inability for PDL repair.

The alveolar bone is typically damaged due to the immune response to bacterial products such as Lipopolysaccharide (LPS). LPS is an endotoxin found almost exclusively on Gram -ve bacteria, which stimulates the immune system to release cytokines, leukotrienes and prostaglandins – all of which activate osteoclasts. These osteoclasts begin to break down bone. Inflammatory mediators are also secreted from neutrophils, macrophages and fibroblasts leading to further alveolar bone damage. Some bacteria are additionally capable of causing direct damage to the alveolar bone. 

As this process occurs, fibrosis and scarring develop at the point of inflammation. This can contain the inflammatory cells and prevent them from causing further destruction. 

However, if this is ineffective it results in the periodontitis progressing, resulting in additional destruction to the connective tissue, PDL and alveolar bone; all of which result in the migration of the junctional epithelium. Therefore, resulting in a greater pocket depth. 

Cytokines and Mediators 

• As discussed during the immunology lessons, inflammation and the immune response is mediated by cytokines which allow white blood cells to communicate with each other
• During periodontal destruction, there is an increase in IL-1, IFN gamma, TGF beta and prostaglandins; these are all pro-inflammatory cytokines which exacerbate the response 
• Matrix metalloproteinases (MMP) and reactive oxygen species have shown to be involved with the destruction of the extracellular matrix. 
  • MMPs are a type of enzyme which modify the ECM of the stroma, including collagen 
  • Their actions allow cells to move through the basement membrane 

What prevents Periodontitis from being contained? 

Various risk factors are associated with periodontitis as they create a more susceptible host. These include;

• Smoking 
• Immunocompromised 
• Diabetes 
• Pregnancy 
• Poor nutrition

All of the above are systemic factors which can lead to a person being at an increased risk of progression in periodontal diseases. Further information about risk factors and susceptibility for periodontal disease can be found in the ‘Risk Factors’ lesson.

Patterns of Bone Loss

Bone loss patterns associated with periodontitis are varied and the type of bone loss can be different in various areas in the same patient. 

Bone loss should be reported on dental radiographs based on its pattern of appearance. This includes:

• Horizontal bone loss: is the most common pattern of bone loss. The bone is reduced in height, but the bone margin remains approximately perpendicular to the tooth surface. The extent and severity of horizontal bone loss can be easily assessed on dental radiographs. 
• Vertical or angular bone loss: occurs in an oblique direction to the tooth surface. The base of the bony defect is located apical to the surrounding bone. Proximal vertical bone loss can be seen on dental radiographs. However vertical or angular bony defects also appear on the buccal and lingual/palatal surfaces, but these defects cannot be seen on a radiograph. In most instances angular defects have infrabony periodontal pockets. Vertical/ angular defects are classified on the basis of the number of osseous walls (one two or three wall defects). However, this is very difficult to be determined from conventional dental radiographs.
  • Three wall defects; there are three walls of cancellous bone around the defect
  • Two wall defects; there are two walls of cancellous bone around the defect 
  • One wall defect; one wall of cancellous bone.
• Furcation involvement: Furcation involvement refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease. Furcation involvement is classified as Grade I, II and III according to the amount of tissue destruction. Grade I is incipient bone loss, Grade II is partial bone loss and class III is total bone loss with through-and-through opening of the furcation (more information on how to grade furcations can be found in the Periodontal assessment lesson). The pattern of bone loss in a furcation involvement varies in different cases and with the degree of involvement. Bone loss around each individual root can be horizontal or angular, and frequently a crater develops in the interradicular area. Although the furcation involvement bone loss can be seen on radiographs, sometimes the lesions can be obscured by angulation of the beam and the radiopacity of neighbouring structures.