## 9 Impact of Thermal Necrosis on Orthopedic Procedures and Tissue Regeneration  
The impact of thermal necrosis in orthopedic procedures is the slowing down of the bone healing process and osseointegration of implants. High temperatures, starting at 47 \({}^{\circ}\)C over a period of 60 s, lead to osteocyte death and impaired bone tissue healing [35; 62; 75]. Thermal damage has a disruptive effect on the bone remodeling process, impeding the healing process. Studies have shown that bone-to-implant contact can be significantly impacted by exposing the bone tissue to a temperature of 50 \({}^{\circ}\)C for 1 min. This also leads to the formation of small pockets next to the contact surface, which is a sign of poor osseointegration. With the regenerative capabilities of the bone compromised, we can observe a delayed periosteal membrane regeneration and an increase in osteocyte apoptosis [37; 44; 62; 75; 76]. The compromised bone-cement interface can lead to early mobilization and eventual failure of the implant. This weakened bone structure lacks the necessary mechanical properties to support the implant, leading to micromovements that eventually cause loosening. This is a major problem in orthopedics, especially in the case of hip and knee implants, these being weight-bearing implants, where implant stability is important for the function of the lower limb and longevity of the implant [77; 78]. Clinically, this thermal necrosis may present itself through pain, swelling, and impaired function at the sight of the implant. During routine imaging procedures, such as radiographs or CT, we may encounter areas of osteolysis, peri-implant radiolucent lines, and lack of signs of osseointegration or new bone formation around the implant. Histological findings often reveal necrotic bone tissue and empty lacunae with the notable absence of viable osteocytes (Table 5) [35; 62; 79]. [PERSON] et al. demonstrated a significant decrease in osteocyte viability at varying depths, depending on the thickness of the cement mantle utilized during implantation, with greater thicknesses causing more extensive damage during polymerization. This can weaken the bone-cement interface, leading to early mobilization and implant failure through aseptic loosening [26]. \begin{table}
\begin{tabular}{c c c c} \hline \hline
**Clinical Impact** & & **Description** & **Diagnostic Signs** \\ \hline Delayed bone healing & - & Slowed bone remodeling and repair processes & - & Prolonged recovery time \\ \hline Impaired osseointegration & - & Reduced bone-to-implant contact & - & Radiolucent lines, lack of new bone formation on X-ray \\ \hline Implant loosening and failure & - & Compromised bone–cement interface, leading to micromovements of the implant & - & Early mobilization, pain, implant instability \\ \hline Clinical symptoms & - & Pain, swelling, impaired function at implant site & - & Patient reports discomfort, decreased mobility \\ \hline Histological findings & - & Necrotic bone tissue, empty lacunae, absence of osteocytes & - & Confirmed through biopsy and microscopic examination \\ \hline \hline \end{tabular}
\end{table} 
Table 5: The impact of thermal necrosis on tissue regeneration at implant site. [PERSON] and [PERSON] have explored thermal isotherms in PMMA and have suggested that using a 3-5 mm thick cement mantle is optimal for preventing bone cell necrosis during total hip arthroplasty while maintaining a strong fixation. Thinner mantles may not provide sufficient support for the implant [80]. [PERSON] et al. have stated that variations in the PMMA formula can affect the peak temperature of the cement and the duration of heat exposure, influencing the extent of thermal necrosis [78]. Thermal damage can initiate a remodeling cascade, as evidenced by [PERSON] et al., where osteocytes damaged by the heat released during polymerization can alter gene expression and influence the bone remodeling processes [78].