Periodontal bone defects: classification and diagnosis

Periodontal bone defects: classification and diagnosis

Bone destruction in periodontal disease is caused mainly by local factors including inflammation and occlusal trauma.

2. Reminder on the alveolar bone:

The bone alveolus or alveolar process is a specialization or extension of the maxillary bone (basal bone), that is to say, it is located in the extension of the latter, without precise anatomical or histological delimitation.

The bone socket only exists because of the presence of the teeth it surrounds; this means that the alveolar bone, unlike the maxillary bone, is born and dies with the tooth.

The alveolar bone is made up of:

• the cortices

→ external cortex (vestibular)

→ internal cortex (lingual or palatal)

• The alveolar wall: dura lamina, sieve plate.
• Interdental and interradicular septa
• alveolar ridge (marginal)

3. Mechanism of bone resorption during periodontal diseases:

The bacterial biofilm continuously releases antigenic bacterial components (lipopolysaccharides LPS, arabinomanans, fimbriae, etc.) which penetrate the periodontal tissues and cause their destruction: the best described, and probably the most pathogenic of these antigens, are LPS, components of the external wall of Gram-negative bacteria.

Among the effects of these toxins, the destruction of alveolar bone is particularly problematic due to its irreversibility.

There are two pathways of osteoclast activation by LPS present in periodontal pockets:

   Indirect pathway: results from the release of pro-inflammatory cytokines by the

cells present at the site of infection; these cytokines act on osteoblasts and Th1 lymphocytes and induce the expression of RANK-L on their surface: it is the interactions between RANK-L (RANK ligand) and RANK (receptor activator of NF-kB), located on the surface of preosteoclasts and inactive osteoclasts, which induce the

differentiation and activation of osteoclasts.

   Direct pathway : described more recently, is the consequence of a direct action of LPS on osteoblasts, osteoclasts and pre-osteoclasts; completely independent of pro-inflammatory cytokines, this pathway amplifies the previous one. The LPS receptor involved in periodontal diseases is made up of two proteins: CD14, a glycoprotein (free or membrane) to which LPS binds, and TLR4 (Toll-like receptor 4), a transmembrane protein which, in dimeric form, associates with CD14 and ensures the transduction of the message. In vivo, LBP (LPS binding protein) binds to LPS and potentiates their action; in the presence of LBP, the sensitivity of receptors to LPS is greatly increased.

Fig 1: mechanism of alveolar resorption

4. Classification of periodontal bone defects:

According to the classification of Goldman and Cohen 1958, there are two types of bone lesions: supraosseous or intraosseous. However, the location of the lesion can be specific

when it is located at the level of the inter-radicular space of a multi-rooted tooth; we then speak of an inter-radicular lesion.

Lesions can also be combined, i.e., associating supra- and intra-osseous defects with inter-radicular lesions.

In addition to this classification, there are also lesions of the marginal bone.

4-1- Suprabony lesion:

They are defined as periodontal lesions associated with alveolysis, or the bottom of the pocket is located coronal to the alveolar crest.

Fig 2: supra and infra bone lesion.

4-2- Infraosseous lesion:

Intraosseous lesions are defined as periodontal lesions whose pocket base is located below the level of the alveolar crest and they correspond to a bone defect whose base is located apically to the marginal edge of the alveolar crest. This is called vertical alveolysis.

The description of intraosseous lesions takes into account the number of residual walls and the angle that the lesion makes with the adjacent dental root.

   Number of walls:

Intraosseous lesions are divided into two categories:

• Intrabony defects initially affect only a single tooth. They are subdivided into three subcategories depending on the number of residual bone walls:

• 3-walled intrabony defect
• 2-walled intrabony defect
• Single-wall intrabony defect

In the same defect, the number of residual walls is often greater at the apical level than at the coronal level. This is called a combined intraosseous defect.

• Craters: correspond to a circumferential bone defect in the shape of a more or less pronounced arc of a circle with apical convexity, affecting two adjacent teeth with relatively symmetrical destruction mesially and distally. The vestibular and lingual walls are located more coronally compared to the proximal residual walls.

Fig 3: intraosseous lesion a) 3-wall lesion, b) 2-wall lesion, c) 1-wall lesion,

d) crater.

   Fault angle:

The angulation of the defect relative to the axis of the opposite tooth appears to be a second necessary component to identify in therapeutic decision-making. Many authors show that a defect presenting an angle less than approximately 25°

will present a better attachment gain than a defect with an angulation greater than 37°. It will generally be noted that a defect less than or equal to 35° has a good prognosis.

4-3- Lesion of the marginal bone:

   Fenestration and dehiscence:

• windows:

These are isolated parts where the root is exposed, and where its surface is covered only by the periosteum and the overlying gum.

• Dehiscence:

It is an isolated denudation of the alveolar bone opposite the dental roots which occurs

extends to the alveolar rim in the form of a notch. These defects are found in approximately 20% of cases. They affect the vestibular bone more frequently than the lingual bone. They are more common in anterior teeth than in posterior teeth. They are more numerous in the incisors and canines due to the thinness of the vestibular cortex.

Fig 4: a) dehiscence, b) fenestration.

   Irregular edges:

These are angular or U-shaped lesions that are caused by resorption of the buccal or lingual alveolar cortex, or by abrupt differences in height between the buccal or lingual marginal edges and the height of the interdental septa.

   Thick rim: Buttress bone

Inflammation causes bone destruction but also stimulates bone apposition.

   Exostosis:

These are bone growths of varying shape and volume. They are common on the vestibular surfaces.

5. Diagnosis:

The diagnosis of bone defects is made based on a clinical and radiographic examination.

   Clinic:

Clinically, the diagnosis is made by periodontal probing, measuring the degree of attachment and the depth of the periodontal pocket.

Transgingival or bone probing under local anesthesia also appears to have diagnostic value because it allows the complexity and depth of the bone defect to be assessed.

   Radiological:

X-rays allow the height of the alveolar bone and the contour of the bone crest to be analyzed. In the case of infrabony lesions, they allow the interproximal area to be analyzed.

as well as root morphology. Caution must be exercised when interpreting a photograph because the superposition of dental and bone structures resulting from the transposition of three-dimensional elements onto a two-dimensional image does not allow the lesion to be observed from all angles. Thus, it is difficult to assess bone involvement of the vestibular, lingual or palatal walls.

Furthermore, the indication of three-dimensional radiography in the diagnosis of intraosseous lesions is controversial due to its cost and the radiation to which the patient is exposed. Furthermore, the evaluation of the architecture of the intraosseous defect can be done after

reclination of a flap.

6. Conclusion :

Supra- and infra-bony periodontal bone lesions must be carefully diagnosed based on a well-conducted clinical examination and well-interpreted radiographs.

7. Bibliographic references:

1. Bercy, Tenembum, periodontology from diagnosis to practice, deBoek, 2000.
2. Bouchard Philippe, periodontology and implant dentistry, vol. 2, Lavoisier, 2015.
3. Doucet P., Lowenstein M., Activation of osteoclasis by bacterial endotoxins during periodontal diseases, medicine/science review, July 2006.
4. Niklaus P. Lang, Lindhe Jan, clinical periodontology and implant dentistry, willey blackwell, 2015.

Periodontal bone defects: classification and diagnosis

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Periodontal bone defects: classification and diagnosis